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https://microbewiki.kenyon.edu/index.php?title=Streptococcus_mutans-_Tooth_Decay&diff=91525
Streptococcus mutans- Tooth Decay
2013-07-24T23:44:24Z
<p>Kelley.L.Raines-1: /* Diagnosis */</p>
<hr />
<div>{{Curated}}<br />
[[Image:OULOGOBIANCO.JPEG|thumb|400px|right|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]<br />
<br />
=<b>Etiology/Bacteriology</b>=<br />
[[Image:Streptococcus-mutans.jpeg|thumb|275|px|left|''Streptococcus mutans'' From:http://microbiologyglossary.wikispaces.com [http://microbiologyglossary.wikispaces.com/Streptococcus+mutans]]<br />
<br />
===Taxonomy===<br />
<br />
Kingdom: Bacteria | Phylum: Firmicutes | Class: Bacilli | Order: Lactobacillales | Family: Streptococcaceae | Genus: Streptococcus | Species: <i> S. mutans </i><br />
<br />
===Description===<br />
<br />
<i> Streptococcus mutans </i> are gram-positive cocci shaped bacteria. These facultative anaerobes are commonly found in the human oral cavity, and is a significantly contributor of tooth decay. The result of decay can greatly affect the overall health of the individual. [[#References|[1]]] <i> S. mutans </i> are mesophilic and grow at temperatures between 18-40 degrees Celsius. <i> Streptococcus mutans </i> is a cariogenic microorganism that breaks down sugar for energy and produces an acidic environment, which demineralizes the superficial structure of the tooth. The result of the conversion disintegrates the coating of the tooth then later dissolves the Calcium molecule creating a hole. Transmission of <i> S. mutans </i> can be found in people of all ages although it is more common for infants and children. The transfer of genotypes are responsible for the transmission of <i> S. mutans </i> from mothers to their children although, there is a genotypic variation from one population to the next.[[#References|[2]]] Someone with a healthy oral flora will roughly contain 10,000 CFU per ml of <i> Streptococcus mutans </i> in their mouth.[[#References|[3]]] <i> Streptococcus mutans </i> possesses three virulence factors: water insoluble glycans, acid tolerance, and production of lactic acid. [[#References|[4]]] A toothache is the most common symptom of tooth decay. An infection or irritation of the tooth pulp usually causes the pain. The dentist is usually the person to diagnose tooth decay by taking X-Rays, and sometimes the X-Rays can detect the formation of a cavity before it is fully intact. If diagnosed with tooth decay, there are many treatment options such as: fillings, crowns and root canals. Since every human has bacteria in their mouth, the only prevention is to lessen the impact of acid fermentation by practicing adequate oral hygiene. [[#References|[5]]]<br />
<br />
=<b>Pathogenesis</b>=<br />
<br />
===Transmission===<br />
<br />
<i> Streptococcus mutans </i> is considered to be part of the "normal" flora of the human mouth, which is associated with dental caries also known as tooth decay. Dental caries is an infectious and communicable dental disease that affects people of all ages. <i> Streptococcus mutans </i> can be passed from one person to the next via horizontal or vertical transmission. The transmission route of <i> Streptococcus mutans </i> is to colonize itself among human hosts. Children and infants are more prone to the diagnosis of <i> Streptococcus mutans </i> and studies show that many receive it from their primary caregivers. [[#References|[2]]] <i> S. mutans </i> favors hard non-shedding surfaces to establish permanent colonies, which implies that levels of <i> S. mutans </i> are undetected in infants until the primary teeth extravasate;although, recent studies have shown that <i> S. mutans </i> is able to colonize the furrows of the tongue in pre-denate infants. Typically between the ages of one and two, teeth erupt, which allows <i> S. mutans </i> to establish flourishing colonies on teeth, and causes cavities. The indication of cavity formation is the appearance of detectable levels of bacteria on teeth. When <i> S. mutans </i> is detected in the furrows of the tongue it is concluded that the vertical transmission route for the bacteria from mother to child arises shortly after birth. To prove this, saliva samples of two to five year old children were taken, which revealed a high fidelity in genetic make-up of each host's <i> S. mutans </i> population. These experiments also concluded that plasmid DNA correlates to different rates, which primarily implies vertical transmission. Mothers with large amounts of bacteria or those who have suffered from many dental caries themselves are likely to transmit the same virulence factors to their children. When the mother's salivary S. mutans levels exceed 105 Colony Forming Units they are nine times more likely to pass bacteria on to their children. [[#References|[6]]]<br />
<br />
===Colonization===<br />
[[Image:biofilm on teeth.jpeg|thumb|200px|right|''biofilm on teeth'' From:http://www.advancedhealing.com [http://www.advancedhealing.com/biofilm-basics/]]]<br />
<br />
The growth and metabolism of <i> S. mutanss </i> changes the environmental conditions of the oral flora, which enables fastidious organisms to colonize and causes the formation of dental plaque. <i> Streptococcus mutans </i> is a specialized microorganism equipped with receptors that allow it to adhere to the surface of the tooth creating a slimy environment. After adherence to the tooth, <i> S. mutans </i> begin to divide and produce microcolonies within the slime layer to construct a biofilm. <i> S. mutans </i> begin to grow and synthesize dextran with the enzyme dextransucrase. Dextran contains a capsule that binds to the enamel and forms a biofilm that consists of 300-500 bacterial cells. The biofilm metabolizes <i> S. mutans </i> and is able to cleave sucrose with the enzyme Glucansucrase in the reaction: n sucrose -------> (glucose) n + n fructose. With these products fructose is fermented as an energy source for bacterial growth while glucose is polymerized to an extracellular dextran polymer. This is important because the polymer cements <i> S. mutans </i> at the enamel and becomes the matrix of dental plaque. The dextrin can also depolymerize to glucose and use the monosaccharide as a carbon source, which produces lactic acid in the biofilm by decalcifying the enamel, and leads to dental caries. The combination of acid and plaque results in the causative agent of decay. [[#References|[7]]]<br />
<br />
===Infectious Dose===<br />
<br />
Bacteria are the most numerous microbes in the mouth. It has been estimated that there are over 100 million in every milliliter of saliva from more than 600 different species.[[#References|[8]]] In order to decrease the bacterial challenge, it is encouraged for people to have 10,000 CFU per ml of saliva <i> Streptococcus mutans </i> in their mouth. [[#References|[3]]]<br />
<br />
{| class="wikitable"<br />
|-<br />
! Colony Forming Units CFU <i> S. mutans </i>/ml saliva !! <br />
|-<br />
| class 0-1 || <100,000 || <br />
|-<br />
| class 2 || 100,000< CFU/ml <1,000,000 || <br />
|-<br />
| class 3 || >1,000,000 CFU/ml || <br />
|}<br />
<br />
In the table, class 0-3 is referring to how many <i> Streptococcus mutans </i> reside in the mouth with class 0-1 acting as best case with good oral hygiene, while class 3 acts as the worst case. [[#References|[3]]]<br />
<br />
===Epidemiology===<br />
<br />
The Decayed Missing Filled also known as the DMF index is the key to measuring the caries that are caused by the bacterial strain <i> Streptococcus </i> mutans. The DMF index expresses the total number of teeth or surfaces that have decayed. When the index is applied specifically to teeth, it is called the DMFT index. The DMFT index scores the individual tooth from 0-28 or 32 depending on the presence or absence of the third molars. When the index is applied to the tooth surface it is called the DMFS index and scores from a range of 0-128 or 148 also depending on the assumption if the third molar is included or not. [[#References|[9]]]<br />
<br />
===Virulence Factors===<br />
<br />
There are three virulence factors that are associated with the cariogenicity of <i> Streptococcus mutans </i>. The first property is dependent on the synthesis of water-soluble glycans from the disaccharide sucrose. Next, <i> S. mutans </i> possesses the ability to become more acid tolerant. This leads to the third characteristic, which displays a production of lactic acid from dietary sugars. [[#References|[4]]]<br />
<br />
=<b>Clinical features</b>=<br />
[[Image:cavity.jpeg|thumb|100px|left| "cavity image" From:oralanswers.com [http://www.oralanswers.com/2011/07/risk-factors-dental-cavities/]]<br />
<br />
===Signs and Symptoms===<br />
<i> Streptococcus mutans </i> can be identified by a chalky white spot on the surface of the tooth indicating an area of demineralization of enamel, which is commonly referred to as a carious lesion. A carious lesion is the earliest diagnosis of tooth decay formation. As the lesion further demineralizes, it can turn brown and will eventually result in a cavity. Before the formation of the cavity, the process is reversible, but once the <i> Streptococcus mutans </i> forms the cavity, the tooth structure is lost and cannot be regenerated. A lesion that appears shiny and dark brown suggests that a lesion was once present but the demineralization has stopped leaving a stain. As the enamel and dentin are destroyed, the cavity becomes more noticeable. The effected area of the tooth changes color and becomes sensitive. When the decay passes through the enamel, the dentin tubules allow passages to the nerves making the tooth exposed, which results in pain that temporarily worsens with exposure to heat, cold,sweet food or drinks. If the tooth is weakened by substantial amounts of internal decay a fracture may occur under normal chewing forces. Pain will arise more constant when the decay has progressed enough to where the bacteria can overwhelm the pulp tissue that is located in the center of the tooth. <br />
<br> In addition to cavity formation of the bacterial strain <i> Streptococcus mutans </i>, dental caries can also cause bad breath and foul tastes, and gum disease. In highly progressed states, the infection can spread to the soft tissue from the tooth. Life-threatening complications may arise such as cavernous sinus thrombosis and Ludwig's angina. [[#References|[10]]]<br />
<br />
=<b>Diagnosis</b>=<br />
<br />
<i> Streptococcus mutans </i> and <i> Streptococcus sobrinus </i> are two microorganisms that reside in the mouth of a human. <i> S. mutans </i> is carried by everyone while <i> S. sobrinus </i> is carried between 8 and 35 % of people in different countries. These different bacterial strains can be distinguished by laboratory tests although the procedure is expensive and time consuming; therefore, it is not always practicable to identify the species in a large epidemiological scale. Researchers not invented a selective media that would allow one to look at the presence of a single species in saliva samples. Because of this, researchers have combined the two species together as mutans streptococci also known as (MS). Since <i> Streptococcus mutans</i> is more prevalent than <i> Streptococcus sobrinus </i> most of the isolates will solely be <i> S. mutans</i>. Mutans streptococci can be cultured in a laboratory by taking a sample of the microorganisms in the mouth. The microbiologist can then use two types of selective media that are widely used to isolate caries-related <i> Streptococcus </i> on Mitis- Salivarius agar and TYC agar in which antibiotic Bacitracin is added. These types of media suppress the growth of most microorganisms but allows the growth of <i> Streptococcus mutans</i> and <i> Streptococcus sobrinus </i>. The inclusion of sucrose leads to the formation of glucans and the appearance of colony formation to aid identification. Diagnostic kits used in dental clinics are based on similar selective media, but it is important to note that they are measuring for total MS, not just <i> S. mutans </i>. [[#References|[11]]] <br> If the strain of <i> Streptococcus mutans </i> has already invaded the tooth enamel, a dentist will diagnose the tooth decay. The dentist begin by asking questions about the patient's dental history and medical problems. Next, the dentist will examine the patient's teeth by using an explorer and a small mirror. To confirm that a tooth has decayed the dentist will take X-Rays of the mouth to examine the teeth as well as the gums. [[#References|[12]]]<br />
<br />
=<b>Treatment</b>=<br />
[[Image:Composite Vs. Amalgam.jpeg|thumb|250px|right|''Composite Vs. Amalgam'' From:http://www.bauerfamilydental.com [http://www.bauerfamilydental.com/services-2/cleanings/]]<br />
<br />
Treatment for tooth decay depends on how severe the decay is. One may simply be able to reverse slight tooth decay by the application of fluoride. [[#References|[12]]] When a processed sugar is consumed, the bacteria from the mouth combine with the sugar to produce an acid.This acid can erode the tooth enamel and damage teeth. Fluoride is used to protect teeth from the demineralization caused by the acid. Fluoride does this by accumulating the demineralized areas of the tooth and strengthening the enamel in a process called remineralization. Fluoride is efficient in preventing tooth decay and making teeth stronger however, it is much less effective if a cavity has already formed. [[#References|[13]]]<br />
<br>To fix cavities caused by the bacterial strain <i> Streptococcus mutans </i> a dentist will need to adequately perform either a composite filling or an amalgam filling- two of the most common fillings used today. In both types of fillings, the dentist will remove the decayed portion of the tooth and fill in the area of the tooth where the decayed area once resided. Amalgam fillings are made from a mixture of silver, tin, zinc, copper and mercury. An advantage of the amalgam filling is durability, strength and expense. Amalgam fillings are durable in the fact that they usually outlast composite fillings, and do not need to be replaced for approximately 10-15 years. These fillings are strong since they can withstand the chewing forces, and are less expensive than composite fillings. A disadvantage of the amalgam fillings is that they cause: discoloration, cracks and fractures, allergic reactions, and destroys more tooth structure. These fillings also have poor aesthetics since the silver fillings are not the color of one's natural tooth. Composite fillings are made from a mixture of plastic and fine glass particles. Some advantages of composite fillings are: aesthetics the fact that the filling closely matches the color of the tooth, the ability to bond to the tooth structure since composite fillings are chemically bonded to the tooth they provide better support, versatility not only does the material fill cavities it is also used to repair chipped, broken down teeth. Tooth-sparing preparation is also an advantage of composite fillings this is because, sometimes less tooth structure needs to be removed than what the amalgam filling will provide. Disadvantages of tooth decay include: lack of durability. Composite fillings wear out sooner than amalgam fillings lasting 5 years as opposed to 10-15 years. There is also an increase in chair time because the process to apply the filling is longer vs. the amalgam filling. Additional visits are required, chipping the composite material from the tooth, and the fact that composite fillings are double the cost of amalgam fillings. [[#References|[14]]]<br />
<br> If one experiences an extreme case of tooth decay a root canal or crown may be used. If the decay exceeds a certain level the dentist may end up needing to extract the tooth.[[#References|[14]]] The dentist will use a crown to treat the decay if the structure of the tooth is weaker than it should be. A tooth should be crowned if the filling would make up more than half the surface area of the clinical crown. A crown should also be installed if the tooth decay has traveled deep under the gum line. The dentist will choose the root canal procedure when the decayed tooth is deep and has reached the pulp of the tooth, which is the center of the tooth where the nerves are. [[#References|[15]]]<br />
<br />
=<b>Prevention</b>=<br />
[[Image:how to prevent tooth decay.jpeg|thumb|210px|right| [http://www.drchetan.com/different-plaque-removal-procedures.html]]<br />
<br />
It is a fact that every human has bacteria already existing in their mouth. The only prevention is to lessen the impact of the fermentation by product lactic acid. Brushing, flossing and reducing the intake of refined and processed sugars can accomplish this. These processed sugars come in the form of sweets, colas and processed powered sweeteners. Studies have shown that rinsing one's mouth out with water can greatly reduce the probability of cavities after the consumption of these sugars. It is almost impossible to completely reduce the effects of <i> S. mutans </i> but there is an option to control it. [[#References|[16]]]<br />
<br />
=<b>Host Immune Response</b>=<br />
<br />
<i> Streptococcus mutans </i> is the major pathogen of dental caries due to the ability to adhere and accumulate to the tooth surface. The Innate Immune Response and the Adaptive Immune Response are two fundamental aspects of the immune system that respond to infections such as dental caries. <i> Streptococcus mutans </i> enters the host through the oral route. The mucosal tissue associated with the exocrine glands and saliva contributes to the production of the oral cavity. This is because; these regions contain cells responsible for antigen internalization and antibodies specific to oral bacteria. The secretory antibodies that protect against dental caries are IgA and IgG. The Macrophages of the innate immune response are phagocytic cells that can internalize and kill bacteria by several mechanisms of internalization, which includes macropinocytosis and phagocytosis. If <i> Streptococcus mutans </i> initiates dental caries after the teeth have erupted either the host did not undergo the effective immune response of secretory IgA played a small role in preventing colonization and subsequent plaque development. [[#References|[7]]]<br />
<br />
=<b>References</b>=<br />
<br />
<br />
1 [http://www.ncl.ac.uk/dental/oralbiol/oralenv/tutorials/streps.htm Whiley, R.A., and Beighton, D. "Streptococci and Oral Streptococci." Bite-Sized Tutorials. N.p.. Web. 23 Jul 2013.]<br />
<br />2 [http://www.podj.com.pk/Dec_2012/p-28.pdf Javed, M., Chaudhry, S., Butt, S., Ijaz, S., Asad, R., Awais, F., and Khan, A., "Transmission of Streptococcus mutans from Mother to Child." Review Article. Pakistan and Oral Dental Journal vol 32, No.3, n.d. Web. 24 Jul 2013.]<br />
<br />3 [http://xenophilia.com/tooth-health-cure-for-cavities "Tooth Health: Cure for Cavities." Xenophilia.]<br />
<br />4 [http://cro.sagepub.com/content/4/2/159.full.pdf Howard, K. "Virulence factors of Mutans Streptococci: Role of Molecular genetics." Critical Reviews in Oral Biology and Medicine.] <br />
<br />5 [http://health.nytimes.com/health/guides/disease/dental-cavities) "Dental Cavities." The New York Times.]<br />
<br />6 [http://www.jyi.org/issue/the-role-of-streptococcus-mutans-and-oral-ecology-in-the-formation-of-dental-caries/) Simon, L., " The Role of Streptococcus mutans & Oral Ecology in the Formation of Dental Caries." Journal of the Young Investigators.] <br />
<br />7 [http://textbookofbacteriology.net/structure.html Todar, K. "Structure and Function of Prokaryotic Cells." Todar's Online Textbook of Bacteriology]<br />
<br />8 [http://www.brighthub.com/science/genetics/articles/45935.asp Arnold, P. "Mouth Bacteria. It's a Jungle in There." Bright Hub.]<br />
<br />9 [http://www.dentalcare.com/media/en-us/education/ce368/ce368.pdf Edward, L. "Caries Process & Prevention Strategies: Epidemiology." Dentalcare.com Continuing Education.]<br />
<br />10 [https://en.wikipedia.org/wiki/Dental_caries "Dental Caries." Wikipedia The Free Encyclopedia.] <br />
<br /> 11 [http://www.ncl.ac.uk/dental/oralbiol/oralenv/tutorials/mutans.htm "Streptococcus mutans and the mutan Streptococci."]<br />
<br /> 12 [http://www.webmd.com/oral-health/tc/tooth-decay-topic-overview "Tooth Decay-Topic Overview." Web MD.]<br />
<br /> 13 [http://www.medicalnewstoday.com/articles/154164.php "What is Fluoride? What does Fluoride Do?" Medical News Today.]<br />
<br /> 14 [http://www.webmd.com/oral-health/guide/dental-health-fillings?page=2 "Dental Health & Tooth Fillings." Web MD]<br />
<br /> 15 [http://doctorspiller.com/Fillings/fillings_5.htm Spiller, M. "When is it more appropriate to place a crown on a tooth instead of a filling?" DoctorSpiller.Com]<br />
<br /> 16 [http://web.mst.edu/~microbio/bio221_2006/S_mutans.htm Bassett, A. "Streptococcus mutans."]<br />
<br />
Created by Taylor Zelnicek, student of Tyrrell Conway at the University of Oklahoma.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Streptococcus_mutans-_Tooth_Decay&diff=91523
Streptococcus mutans- Tooth Decay
2013-07-24T23:39:45Z
<p>Kelley.L.Raines-1: /* Signs and Symptoms */</p>
<hr />
<div>{{Curated}}<br />
[[Image:OULOGOBIANCO.JPEG|thumb|400px|right|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]<br />
<br />
=<b>Etiology/Bacteriology</b>=<br />
[[Image:Streptococcus-mutans.jpeg|thumb|275|px|left|''Streptococcus mutans'' From:http://microbiologyglossary.wikispaces.com [http://microbiologyglossary.wikispaces.com/Streptococcus+mutans]]<br />
<br />
===Taxonomy===<br />
<br />
Kingdom: Bacteria | Phylum: Firmicutes | Class: Bacilli | Order: Lactobacillales | Family: Streptococcaceae | Genus: Streptococcus | Species: <i> S. mutans </i><br />
<br />
===Description===<br />
<br />
<i> Streptococcus mutans </i> are gram-positive cocci shaped bacteria. These facultative anaerobes are commonly found in the human oral cavity, and is a significantly contributor of tooth decay. The result of decay can greatly affect the overall health of the individual. [[#References|[1]]] <i> S. mutans </i> are mesophilic and grow at temperatures between 18-40 degrees Celsius. <i> Streptococcus mutans </i> is a cariogenic microorganism that breaks down sugar for energy and produces an acidic environment, which demineralizes the superficial structure of the tooth. The result of the conversion disintegrates the coating of the tooth then later dissolves the Calcium molecule creating a hole. Transmission of <i> S. mutans </i> can be found in people of all ages although it is more common for infants and children. The transfer of genotypes are responsible for the transmission of <i> S. mutans </i> from mothers to their children although, there is a genotypic variation from one population to the next.[[#References|[2]]] Someone with a healthy oral flora will roughly contain 10,000 CFU per ml of <i> Streptococcus mutans </i> in their mouth.[[#References|[3]]] <i> Streptococcus mutans </i> possesses three virulence factors: water insoluble glycans, acid tolerance, and production of lactic acid. [[#References|[4]]] A toothache is the most common symptom of tooth decay. An infection or irritation of the tooth pulp usually causes the pain. The dentist is usually the person to diagnose tooth decay by taking X-Rays, and sometimes the X-Rays can detect the formation of a cavity before it is fully intact. If diagnosed with tooth decay, there are many treatment options such as: fillings, crowns and root canals. Since every human has bacteria in their mouth, the only prevention is to lessen the impact of acid fermentation by practicing adequate oral hygiene. [[#References|[5]]]<br />
<br />
=<b>Pathogenesis</b>=<br />
<br />
===Transmission===<br />
<br />
<i> Streptococcus mutans </i> is considered to be part of the "normal" flora of the human mouth, which is associated with dental caries also known as tooth decay. Dental caries is an infectious and communicable dental disease that affects people of all ages. <i> Streptococcus mutans </i> can be passed from one person to the next via horizontal or vertical transmission. The transmission route of <i> Streptococcus mutans </i> is to colonize itself among human hosts. Children and infants are more prone to the diagnosis of <i> Streptococcus mutans </i> and studies show that many receive it from their primary caregivers. [[#References|[2]]] <i> S. mutans </i> favors hard non-shedding surfaces to establish permanent colonies, which implies that levels of <i> S. mutans </i> are undetected in infants until the primary teeth extravasate;although, recent studies have shown that <i> S. mutans </i> is able to colonize the furrows of the tongue in pre-denate infants. Typically between the ages of one and two, teeth erupt, which allows <i> S. mutans </i> to establish flourishing colonies on teeth, and causes cavities. The indication of cavity formation is the appearance of detectable levels of bacteria on teeth. When <i> S. mutans </i> is detected in the furrows of the tongue it is concluded that the vertical transmission route for the bacteria from mother to child arises shortly after birth. To prove this, saliva samples of two to five year old children were taken, which revealed a high fidelity in genetic make-up of each host's <i> S. mutans </i> population. These experiments also concluded that plasmid DNA correlates to different rates, which primarily implies vertical transmission. Mothers with large amounts of bacteria or those who have suffered from many dental caries themselves are likely to transmit the same virulence factors to their children. When the mother's salivary S. mutans levels exceed 105 Colony Forming Units they are nine times more likely to pass bacteria on to their children. [[#References|[6]]]<br />
<br />
===Colonization===<br />
[[Image:biofilm on teeth.jpeg|thumb|200px|right|''biofilm on teeth'' From:http://www.advancedhealing.com [http://www.advancedhealing.com/biofilm-basics/]]]<br />
<br />
The growth and metabolism of <i> S. mutanss </i> changes the environmental conditions of the oral flora, which enables fastidious organisms to colonize and causes the formation of dental plaque. <i> Streptococcus mutans </i> is a specialized microorganism equipped with receptors that allow it to adhere to the surface of the tooth creating a slimy environment. After adherence to the tooth, <i> S. mutans </i> begin to divide and produce microcolonies within the slime layer to construct a biofilm. <i> S. mutans </i> begin to grow and synthesize dextran with the enzyme dextransucrase. Dextran contains a capsule that binds to the enamel and forms a biofilm that consists of 300-500 bacterial cells. The biofilm metabolizes <i> S. mutans </i> and is able to cleave sucrose with the enzyme Glucansucrase in the reaction: n sucrose -------> (glucose) n + n fructose. With these products fructose is fermented as an energy source for bacterial growth while glucose is polymerized to an extracellular dextran polymer. This is important because the polymer cements <i> S. mutans </i> at the enamel and becomes the matrix of dental plaque. The dextrin can also depolymerize to glucose and use the monosaccharide as a carbon source, which produces lactic acid in the biofilm by decalcifying the enamel, and leads to dental caries. The combination of acid and plaque results in the causative agent of decay. [[#References|[7]]]<br />
<br />
===Infectious Dose===<br />
<br />
Bacteria are the most numerous microbes in the mouth. It has been estimated that there are over 100 million in every milliliter of saliva from more than 600 different species.[[#References|[8]]] In order to decrease the bacterial challenge, it is encouraged for people to have 10,000 CFU per ml of saliva <i> Streptococcus mutans </i> in their mouth. [[#References|[3]]]<br />
<br />
{| class="wikitable"<br />
|-<br />
! Colony Forming Units CFU <i> S. mutans </i>/ml saliva !! <br />
|-<br />
| class 0-1 || <100,000 || <br />
|-<br />
| class 2 || 100,000< CFU/ml <1,000,000 || <br />
|-<br />
| class 3 || >1,000,000 CFU/ml || <br />
|}<br />
<br />
In the table, class 0-3 is referring to how many <i> Streptococcus mutans </i> reside in the mouth with class 0-1 acting as best case with good oral hygiene, while class 3 acts as the worst case. [[#References|[3]]]<br />
<br />
===Epidemiology===<br />
<br />
The Decayed Missing Filled also known as the DMF index is the key to measuring the caries that are caused by the bacterial strain <i> Streptococcus </i> mutans. The DMF index expresses the total number of teeth or surfaces that have decayed. When the index is applied specifically to teeth, it is called the DMFT index. The DMFT index scores the individual tooth from 0-28 or 32 depending on the presence or absence of the third molars. When the index is applied to the tooth surface it is called the DMFS index and scores from a range of 0-128 or 148 also depending on the assumption if the third molar is included or not. [[#References|[9]]]<br />
<br />
===Virulence Factors===<br />
<br />
There are three virulence factors that are associated with the cariogenicity of <i> Streptococcus mutans </i>. The first property is dependent on the synthesis of water-soluble glycans from the disaccharide sucrose. Next, <i> S. mutans </i> possesses the ability to become more acid tolerant. This leads to the third characteristic, which displays a production of lactic acid from dietary sugars. [[#References|[4]]]<br />
<br />
=<b>Clinical features</b>=<br />
[[Image:cavity.jpeg|thumb|100px|left| "cavity image" From:oralanswers.com [http://www.oralanswers.com/2011/07/risk-factors-dental-cavities/]]<br />
<br />
===Signs and Symptoms===<br />
<i> Streptococcus mutans </i> can be identified by a chalky white spot on the surface of the tooth indicating an area of demineralization of enamel, which is commonly referred to as a carious lesion. A carious lesion is the earliest diagnosis of tooth decay formation. As the lesion further demineralizes, it can turn brown and will eventually result in a cavity. Before the formation of the cavity, the process is reversible, but once the <i> Streptococcus mutans </i> forms the cavity, the tooth structure is lost and cannot be regenerated. A lesion that appears shiny and dark brown suggests that a lesion was once present but the demineralization has stopped leaving a stain. As the enamel and dentin are destroyed, the cavity becomes more noticeable. The effected area of the tooth changes color and becomes sensitive. When the decay passes through the enamel, the dentin tubules allow passages to the nerves making the tooth exposed, which results in pain that temporarily worsens with exposure to heat, cold,sweet food or drinks. If the tooth is weakened by substantial amounts of internal decay a fracture may occur under normal chewing forces. Pain will arise more constant when the decay has progressed enough to where the bacteria can overwhelm the pulp tissue that is located in the center of the tooth. <br />
<br> In addition to cavity formation of the bacterial strain <i> Streptococcus mutans </i>, dental caries can also cause bad breath and foul tastes, and gum disease. In highly progressed states, the infection can spread to the soft tissue from the tooth. Life-threatening complications may arise such as cavernous sinus thrombosis and Ludwig's angina. [[#References|[10]]]<br />
<br />
=<b>Diagnosis</b>=<br />
<br />
<i> Streptococcus mutans </i> and <i> Streptococcus sobrinus </i> are two microorganisms that reside in the mouth of a human. <i> S. mutans </i> is carried by everyone while <i> S. sobrinus </i> is carried between 8 and 35 % of people in different countries. These different bacterial strains can be distinguished by laboratory tests although the procedure is expensive and time consuming therefore; it is not always practicable to identify the species in a large epidemiological scale. Researchers have lacked to invent a selective media that would allow one to look at the presence of a single species in saliva samples. Because of this, researchers have combined the two species together as mutans streptococci also known as (MS). Since <i> Streptococcus mutans</i> is more prevalent than <i> Streptococcus sobrinus </i> most of the isolates will solely be <i> S. mutans</i>. Mutans streptococci can be cultured in a laboratory by taking a sample of the microorganisms in the mouth. The microbiologist can then use two types of selective media that are widely used to isolate caries-related <i> Streptococcus </i> on Mitis- Salivarius agar and TYC agar in which antibiotic Bacitracin is added. These types of media suppress the growth of most microorganisms but allows the growth of <i> Streptococcus mutans</i> and <i> Streptococcus sobrinus </i>. The inclusion of sucrose leads to the formation of glucans and the appearance of colony formation to aid identification. Diagnostic kits used in dental clinics are based on similar selective media, but it is important to note that they are measuring for total MS, not just <i> S. mutans </i>. [[#References|[11]]] <br> If the strain of <i> Streptococcus mutans </i> has already invaded the tooth enamel, a dentist will diagnose the tooth decay. The dentist will start out by asking questions about the patient's dental history and medical problems. Next, the dentist will examine the patient's teeth by using an explorer and a small mirror. To confirm that a tooth has decayed the dentist will take X-Rays of the mouth to examine the teeth as well as the gums. [[#References|[12]]]<br />
<br />
=<b>Treatment</b>=<br />
[[Image:Composite Vs. Amalgam.jpeg|thumb|250px|right|''Composite Vs. Amalgam'' From:http://www.bauerfamilydental.com [http://www.bauerfamilydental.com/services-2/cleanings/]]<br />
<br />
Treatment for tooth decay depends on how severe the decay is. One may simply be able to reverse slight tooth decay by the application of fluoride. [[#References|[12]]] When a processed sugar is consumed, the bacteria from the mouth combine with the sugar to produce an acid.This acid can erode the tooth enamel and damage teeth. Fluoride is used to protect teeth from the demineralization caused by the acid. Fluoride does this by accumulating the demineralized areas of the tooth and strengthening the enamel in a process called remineralization. Fluoride is efficient in preventing tooth decay and making teeth stronger however, it is much less effective if a cavity has already formed. [[#References|[13]]]<br />
<br>To fix cavities caused by the bacterial strain <i> Streptococcus mutans </i> a dentist will need to adequately perform either a composite filling or an amalgam filling- two of the most common fillings used today. In both types of fillings, the dentist will remove the decayed portion of the tooth and fill in the area of the tooth where the decayed area once resided. Amalgam fillings are made from a mixture of silver, tin, zinc, copper and mercury. An advantage of the amalgam filling is durability, strength and expense. Amalgam fillings are durable in the fact that they usually outlast composite fillings, and do not need to be replaced for approximately 10-15 years. These fillings are strong since they can withstand the chewing forces, and are less expensive than composite fillings. A disadvantage of the amalgam fillings is that they cause: discoloration, cracks and fractures, allergic reactions, and destroys more tooth structure. These fillings also have poor aesthetics since the silver fillings are not the color of one's natural tooth. Composite fillings are made from a mixture of plastic and fine glass particles. Some advantages of composite fillings are: aesthetics the fact that the filling closely matches the color of the tooth, the ability to bond to the tooth structure since composite fillings are chemically bonded to the tooth they provide better support, versatility not only does the material fill cavities it is also used to repair chipped, broken down teeth. Tooth-sparing preparation is also an advantage of composite fillings this is because, sometimes less tooth structure needs to be removed than what the amalgam filling will provide. Disadvantages of tooth decay include: lack of durability. Composite fillings wear out sooner than amalgam fillings lasting 5 years as opposed to 10-15 years. There is also an increase in chair time because the process to apply the filling is longer vs. the amalgam filling. Additional visits are required, chipping the composite material from the tooth, and the fact that composite fillings are double the cost of amalgam fillings. [[#References|[14]]]<br />
<br> If one experiences an extreme case of tooth decay a root canal or crown may be used. If the decay exceeds a certain level the dentist may end up needing to extract the tooth.[[#References|[14]]] The dentist will use a crown to treat the decay if the structure of the tooth is weaker than it should be. A tooth should be crowned if the filling would make up more than half the surface area of the clinical crown. A crown should also be installed if the tooth decay has traveled deep under the gum line. The dentist will choose the root canal procedure when the decayed tooth is deep and has reached the pulp of the tooth, which is the center of the tooth where the nerves are. [[#References|[15]]]<br />
<br />
=<b>Prevention</b>=<br />
[[Image:how to prevent tooth decay.jpeg|thumb|210px|right| [http://www.drchetan.com/different-plaque-removal-procedures.html]]<br />
<br />
It is a fact that every human has bacteria already existing in their mouth. The only prevention is to lessen the impact of the fermentation by product lactic acid. Brushing, flossing and reducing the intake of refined and processed sugars can accomplish this. These processed sugars come in the form of sweets, colas and processed powered sweeteners. Studies have shown that rinsing one's mouth out with water can greatly reduce the probability of cavities after the consumption of these sugars. It is almost impossible to completely reduce the effects of <i> S. mutans </i> but there is an option to control it. [[#References|[16]]]<br />
<br />
=<b>Host Immune Response</b>=<br />
<br />
<i> Streptococcus mutans </i> is the major pathogen of dental caries due to the ability to adhere and accumulate to the tooth surface. The Innate Immune Response and the Adaptive Immune Response are two fundamental aspects of the immune system that respond to infections such as dental caries. <i> Streptococcus mutans </i> enters the host through the oral route. The mucosal tissue associated with the exocrine glands and saliva contributes to the production of the oral cavity. This is because; these regions contain cells responsible for antigen internalization and antibodies specific to oral bacteria. The secretory antibodies that protect against dental caries are IgA and IgG. The Macrophages of the innate immune response are phagocytic cells that can internalize and kill bacteria by several mechanisms of internalization, which includes macropinocytosis and phagocytosis. If <i> Streptococcus mutans </i> initiates dental caries after the teeth have erupted either the host did not undergo the effective immune response of secretory IgA played a small role in preventing colonization and subsequent plaque development. [[#References|[7]]]<br />
<br />
=<b>References</b>=<br />
<br />
<br />
1 [http://www.ncl.ac.uk/dental/oralbiol/oralenv/tutorials/streps.htm Whiley, R.A., and Beighton, D. "Streptococci and Oral Streptococci." Bite-Sized Tutorials. N.p.. Web. 23 Jul 2013.]<br />
<br />2 [http://www.podj.com.pk/Dec_2012/p-28.pdf Javed, M., Chaudhry, S., Butt, S., Ijaz, S., Asad, R., Awais, F., and Khan, A., "Transmission of Streptococcus mutans from Mother to Child." Review Article. Pakistan and Oral Dental Journal vol 32, No.3, n.d. Web. 24 Jul 2013.]<br />
<br />3 [http://xenophilia.com/tooth-health-cure-for-cavities "Tooth Health: Cure for Cavities." Xenophilia.]<br />
<br />4 [http://cro.sagepub.com/content/4/2/159.full.pdf Howard, K. "Virulence factors of Mutans Streptococci: Role of Molecular genetics." Critical Reviews in Oral Biology and Medicine.] <br />
<br />5 [http://health.nytimes.com/health/guides/disease/dental-cavities) "Dental Cavities." The New York Times.]<br />
<br />6 [http://www.jyi.org/issue/the-role-of-streptococcus-mutans-and-oral-ecology-in-the-formation-of-dental-caries/) Simon, L., " The Role of Streptococcus mutans & Oral Ecology in the Formation of Dental Caries." Journal of the Young Investigators.] <br />
<br />7 [http://textbookofbacteriology.net/structure.html Todar, K. "Structure and Function of Prokaryotic Cells." Todar's Online Textbook of Bacteriology]<br />
<br />8 [http://www.brighthub.com/science/genetics/articles/45935.asp Arnold, P. "Mouth Bacteria. It's a Jungle in There." Bright Hub.]<br />
<br />9 [http://www.dentalcare.com/media/en-us/education/ce368/ce368.pdf Edward, L. "Caries Process & Prevention Strategies: Epidemiology." Dentalcare.com Continuing Education.]<br />
<br />10 [https://en.wikipedia.org/wiki/Dental_caries "Dental Caries." Wikipedia The Free Encyclopedia.] <br />
<br /> 11 [http://www.ncl.ac.uk/dental/oralbiol/oralenv/tutorials/mutans.htm "Streptococcus mutans and the mutan Streptococci."]<br />
<br /> 12 [http://www.webmd.com/oral-health/tc/tooth-decay-topic-overview "Tooth Decay-Topic Overview." Web MD.]<br />
<br /> 13 [http://www.medicalnewstoday.com/articles/154164.php "What is Fluoride? What does Fluoride Do?" Medical News Today.]<br />
<br /> 14 [http://www.webmd.com/oral-health/guide/dental-health-fillings?page=2 "Dental Health & Tooth Fillings." Web MD]<br />
<br /> 15 [http://doctorspiller.com/Fillings/fillings_5.htm Spiller, M. "When is it more appropriate to place a crown on a tooth instead of a filling?" DoctorSpiller.Com]<br />
<br /> 16 [http://web.mst.edu/~microbio/bio221_2006/S_mutans.htm Bassett, A. "Streptococcus mutans."]<br />
<br />
Created by Taylor Zelnicek, student of Tyrrell Conway at the University of Oklahoma.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Streptococcus_mutans-_Tooth_Decay&diff=91522
Streptococcus mutans- Tooth Decay
2013-07-24T23:35:03Z
<p>Kelley.L.Raines-1: /* Epidemiology */</p>
<hr />
<div>{{Curated}}<br />
[[Image:OULOGOBIANCO.JPEG|thumb|400px|right|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]<br />
<br />
=<b>Etiology/Bacteriology</b>=<br />
[[Image:Streptococcus-mutans.jpeg|thumb|275|px|left|''Streptococcus mutans'' From:http://microbiologyglossary.wikispaces.com [http://microbiologyglossary.wikispaces.com/Streptococcus+mutans]]<br />
<br />
===Taxonomy===<br />
<br />
Kingdom: Bacteria | Phylum: Firmicutes | Class: Bacilli | Order: Lactobacillales | Family: Streptococcaceae | Genus: Streptococcus | Species: <i> S. mutans </i><br />
<br />
===Description===<br />
<br />
<i> Streptococcus mutans </i> are gram-positive cocci shaped bacteria. These facultative anaerobes are commonly found in the human oral cavity, and is a significantly contributor of tooth decay. The result of decay can greatly affect the overall health of the individual. [[#References|[1]]] <i> S. mutans </i> are mesophilic and grow at temperatures between 18-40 degrees Celsius. <i> Streptococcus mutans </i> is a cariogenic microorganism that breaks down sugar for energy and produces an acidic environment, which demineralizes the superficial structure of the tooth. The result of the conversion disintegrates the coating of the tooth then later dissolves the Calcium molecule creating a hole. Transmission of <i> S. mutans </i> can be found in people of all ages although it is more common for infants and children. The transfer of genotypes are responsible for the transmission of <i> S. mutans </i> from mothers to their children although, there is a genotypic variation from one population to the next.[[#References|[2]]] Someone with a healthy oral flora will roughly contain 10,000 CFU per ml of <i> Streptococcus mutans </i> in their mouth.[[#References|[3]]] <i> Streptococcus mutans </i> possesses three virulence factors: water insoluble glycans, acid tolerance, and production of lactic acid. [[#References|[4]]] A toothache is the most common symptom of tooth decay. An infection or irritation of the tooth pulp usually causes the pain. The dentist is usually the person to diagnose tooth decay by taking X-Rays, and sometimes the X-Rays can detect the formation of a cavity before it is fully intact. If diagnosed with tooth decay, there are many treatment options such as: fillings, crowns and root canals. Since every human has bacteria in their mouth, the only prevention is to lessen the impact of acid fermentation by practicing adequate oral hygiene. [[#References|[5]]]<br />
<br />
=<b>Pathogenesis</b>=<br />
<br />
===Transmission===<br />
<br />
<i> Streptococcus mutans </i> is considered to be part of the "normal" flora of the human mouth, which is associated with dental caries also known as tooth decay. Dental caries is an infectious and communicable dental disease that affects people of all ages. <i> Streptococcus mutans </i> can be passed from one person to the next via horizontal or vertical transmission. The transmission route of <i> Streptococcus mutans </i> is to colonize itself among human hosts. Children and infants are more prone to the diagnosis of <i> Streptococcus mutans </i> and studies show that many receive it from their primary caregivers. [[#References|[2]]] <i> S. mutans </i> favors hard non-shedding surfaces to establish permanent colonies, which implies that levels of <i> S. mutans </i> are undetected in infants until the primary teeth extravasate;although, recent studies have shown that <i> S. mutans </i> is able to colonize the furrows of the tongue in pre-denate infants. Typically between the ages of one and two, teeth erupt, which allows <i> S. mutans </i> to establish flourishing colonies on teeth, and causes cavities. The indication of cavity formation is the appearance of detectable levels of bacteria on teeth. When <i> S. mutans </i> is detected in the furrows of the tongue it is concluded that the vertical transmission route for the bacteria from mother to child arises shortly after birth. To prove this, saliva samples of two to five year old children were taken, which revealed a high fidelity in genetic make-up of each host's <i> S. mutans </i> population. These experiments also concluded that plasmid DNA correlates to different rates, which primarily implies vertical transmission. Mothers with large amounts of bacteria or those who have suffered from many dental caries themselves are likely to transmit the same virulence factors to their children. When the mother's salivary S. mutans levels exceed 105 Colony Forming Units they are nine times more likely to pass bacteria on to their children. [[#References|[6]]]<br />
<br />
===Colonization===<br />
[[Image:biofilm on teeth.jpeg|thumb|200px|right|''biofilm on teeth'' From:http://www.advancedhealing.com [http://www.advancedhealing.com/biofilm-basics/]]]<br />
<br />
The growth and metabolism of <i> S. mutanss </i> changes the environmental conditions of the oral flora, which enables fastidious organisms to colonize and causes the formation of dental plaque. <i> Streptococcus mutans </i> is a specialized microorganism equipped with receptors that allow it to adhere to the surface of the tooth creating a slimy environment. After adherence to the tooth, <i> S. mutans </i> begin to divide and produce microcolonies within the slime layer to construct a biofilm. <i> S. mutans </i> begin to grow and synthesize dextran with the enzyme dextransucrase. Dextran contains a capsule that binds to the enamel and forms a biofilm that consists of 300-500 bacterial cells. The biofilm metabolizes <i> S. mutans </i> and is able to cleave sucrose with the enzyme Glucansucrase in the reaction: n sucrose -------> (glucose) n + n fructose. With these products fructose is fermented as an energy source for bacterial growth while glucose is polymerized to an extracellular dextran polymer. This is important because the polymer cements <i> S. mutans </i> at the enamel and becomes the matrix of dental plaque. The dextrin can also depolymerize to glucose and use the monosaccharide as a carbon source, which produces lactic acid in the biofilm by decalcifying the enamel, and leads to dental caries. The combination of acid and plaque results in the causative agent of decay. [[#References|[7]]]<br />
<br />
===Infectious Dose===<br />
<br />
Bacteria are the most numerous microbes in the mouth. It has been estimated that there are over 100 million in every milliliter of saliva from more than 600 different species.[[#References|[8]]] In order to decrease the bacterial challenge, it is encouraged for people to have 10,000 CFU per ml of saliva <i> Streptococcus mutans </i> in their mouth. [[#References|[3]]]<br />
<br />
{| class="wikitable"<br />
|-<br />
! Colony Forming Units CFU <i> S. mutans </i>/ml saliva !! <br />
|-<br />
| class 0-1 || <100,000 || <br />
|-<br />
| class 2 || 100,000< CFU/ml <1,000,000 || <br />
|-<br />
| class 3 || >1,000,000 CFU/ml || <br />
|}<br />
<br />
In the table, class 0-3 is referring to how many <i> Streptococcus mutans </i> reside in the mouth with class 0-1 acting as best case with good oral hygiene, while class 3 acts as the worst case. [[#References|[3]]]<br />
<br />
===Epidemiology===<br />
<br />
The Decayed Missing Filled also known as the DMF index is the key to measuring the caries that are caused by the bacterial strain <i> Streptococcus </i> mutans. The DMF index expresses the total number of teeth or surfaces that have decayed. When the index is applied specifically to teeth, it is called the DMFT index. The DMFT index scores the individual tooth from 0-28 or 32 depending on the presence or absence of the third molars. When the index is applied to the tooth surface it is called the DMFS index and scores from a range of 0-128 or 148 also depending on the assumption if the third molar is included or not. [[#References|[9]]]<br />
<br />
===Virulence Factors===<br />
<br />
There are three virulence factors that are associated with the cariogenicity of <i> Streptococcus mutans </i>. The first property is dependent on the synthesis of water-soluble glycans from the disaccharide sucrose. Next, <i> S. mutans </i> possesses the ability to become more acid tolerant. This leads to the third characteristic, which displays a production of lactic acid from dietary sugars. [[#References|[4]]]<br />
<br />
=<b>Clinical features</b>=<br />
[[Image:cavity.jpeg|thumb|100px|left| "cavity image" From:oralanswers.com [http://www.oralanswers.com/2011/07/risk-factors-dental-cavities/]]<br />
<br />
===Signs and Symptoms===<br />
<br />
If <i> Streptococcus mutans </i> leads to dental caries, one may not be aware they are diagnosed with the disease. A chalky white spot on the surface of the tooth indicates an area of demineralization of enamel, which is commonly referred to as a carious lesion. A carious lesion is the earliest diagnosis of tooth decay formation. As the lesion further demineralizes, it can turn brown and will eventually result in a cavity. Before the formation of the cavity, the process is reversible, but once the <i> Streptococcus mutans </i> forms the cavity, the tooth structure is lost and cannot be regenerated. A lesion that appears shiny and dark brown suggests that a lesion was once present but the demineralization has stopped leaving a stain. As the enamel and dentin are destroyed, the cavity becomes more noticeable. The effected area of the tooth changes color and becomes sensitive. When the decay passes through the enamel, the dentin tubules allow passages to the nerves making the tooth exposed, which results in pain that temporarily worsens with exposure to heat, cold, or sweet food or drinks. If the tooth is weakened by substantial amounts of internal decay a fracture may occur under normal chewing forces. Pain will arise more constant when the decay has progressed enough to where the bacteria can overwhelm the pulp tissue that is located in the center of the tooth. <br />
<br> In addition to cavity formation of the bacterial strain <i> Streptococcus mutans </i>, dental caries can also cause bad breath and foul tastes, and gum disease. In highly progressed states, the infection can spread to the soft tissue from the tooth. Life-threatening complications may arise such as cavernous sinus thrombosis and Ludwig's angina. [[#References|[10]]]<br />
<br />
=<b>Diagnosis</b>=<br />
<br />
<i> Streptococcus mutans </i> and <i> Streptococcus sobrinus </i> are two microorganisms that reside in the mouth of a human. <i> S. mutans </i> is carried by everyone while <i> S. sobrinus </i> is carried between 8 and 35 % of people in different countries. These different bacterial strains can be distinguished by laboratory tests although the procedure is expensive and time consuming therefore; it is not always practicable to identify the species in a large epidemiological scale. Researchers have lacked to invent a selective media that would allow one to look at the presence of a single species in saliva samples. Because of this, researchers have combined the two species together as mutans streptococci also known as (MS). Since <i> Streptococcus mutans</i> is more prevalent than <i> Streptococcus sobrinus </i> most of the isolates will solely be <i> S. mutans</i>. Mutans streptococci can be cultured in a laboratory by taking a sample of the microorganisms in the mouth. The microbiologist can then use two types of selective media that are widely used to isolate caries-related <i> Streptococcus </i> on Mitis- Salivarius agar and TYC agar in which antibiotic Bacitracin is added. These types of media suppress the growth of most microorganisms but allows the growth of <i> Streptococcus mutans</i> and <i> Streptococcus sobrinus </i>. The inclusion of sucrose leads to the formation of glucans and the appearance of colony formation to aid identification. Diagnostic kits used in dental clinics are based on similar selective media, but it is important to note that they are measuring for total MS, not just <i> S. mutans </i>. [[#References|[11]]] <br> If the strain of <i> Streptococcus mutans </i> has already invaded the tooth enamel, a dentist will diagnose the tooth decay. The dentist will start out by asking questions about the patient's dental history and medical problems. Next, the dentist will examine the patient's teeth by using an explorer and a small mirror. To confirm that a tooth has decayed the dentist will take X-Rays of the mouth to examine the teeth as well as the gums. [[#References|[12]]]<br />
<br />
=<b>Treatment</b>=<br />
[[Image:Composite Vs. Amalgam.jpeg|thumb|250px|right|''Composite Vs. Amalgam'' From:http://www.bauerfamilydental.com [http://www.bauerfamilydental.com/services-2/cleanings/]]<br />
<br />
Treatment for tooth decay depends on how severe the decay is. One may simply be able to reverse slight tooth decay by the application of fluoride. [[#References|[12]]] When a processed sugar is consumed, the bacteria from the mouth combine with the sugar to produce an acid.This acid can erode the tooth enamel and damage teeth. Fluoride is used to protect teeth from the demineralization caused by the acid. Fluoride does this by accumulating the demineralized areas of the tooth and strengthening the enamel in a process called remineralization. Fluoride is efficient in preventing tooth decay and making teeth stronger however, it is much less effective if a cavity has already formed. [[#References|[13]]]<br />
<br>To fix cavities caused by the bacterial strain <i> Streptococcus mutans </i> a dentist will need to adequately perform either a composite filling or an amalgam filling- two of the most common fillings used today. In both types of fillings, the dentist will remove the decayed portion of the tooth and fill in the area of the tooth where the decayed area once resided. Amalgam fillings are made from a mixture of silver, tin, zinc, copper and mercury. An advantage of the amalgam filling is durability, strength and expense. Amalgam fillings are durable in the fact that they usually outlast composite fillings, and do not need to be replaced for approximately 10-15 years. These fillings are strong since they can withstand the chewing forces, and are less expensive than composite fillings. A disadvantage of the amalgam fillings is that they cause: discoloration, cracks and fractures, allergic reactions, and destroys more tooth structure. These fillings also have poor aesthetics since the silver fillings are not the color of one's natural tooth. Composite fillings are made from a mixture of plastic and fine glass particles. Some advantages of composite fillings are: aesthetics the fact that the filling closely matches the color of the tooth, the ability to bond to the tooth structure since composite fillings are chemically bonded to the tooth they provide better support, versatility not only does the material fill cavities it is also used to repair chipped, broken down teeth. Tooth-sparing preparation is also an advantage of composite fillings this is because, sometimes less tooth structure needs to be removed than what the amalgam filling will provide. Disadvantages of tooth decay include: lack of durability. Composite fillings wear out sooner than amalgam fillings lasting 5 years as opposed to 10-15 years. There is also an increase in chair time because the process to apply the filling is longer vs. the amalgam filling. Additional visits are required, chipping the composite material from the tooth, and the fact that composite fillings are double the cost of amalgam fillings. [[#References|[14]]]<br />
<br> If one experiences an extreme case of tooth decay a root canal or crown may be used. If the decay exceeds a certain level the dentist may end up needing to extract the tooth.[[#References|[14]]] The dentist will use a crown to treat the decay if the structure of the tooth is weaker than it should be. A tooth should be crowned if the filling would make up more than half the surface area of the clinical crown. A crown should also be installed if the tooth decay has traveled deep under the gum line. The dentist will choose the root canal procedure when the decayed tooth is deep and has reached the pulp of the tooth, which is the center of the tooth where the nerves are. [[#References|[15]]]<br />
<br />
=<b>Prevention</b>=<br />
[[Image:how to prevent tooth decay.jpeg|thumb|210px|right| [http://www.drchetan.com/different-plaque-removal-procedures.html]]<br />
<br />
It is a fact that every human has bacteria already existing in their mouth. The only prevention is to lessen the impact of the fermentation by product lactic acid. Brushing, flossing and reducing the intake of refined and processed sugars can accomplish this. These processed sugars come in the form of sweets, colas and processed powered sweeteners. Studies have shown that rinsing one's mouth out with water can greatly reduce the probability of cavities after the consumption of these sugars. It is almost impossible to completely reduce the effects of <i> S. mutans </i> but there is an option to control it. [[#References|[16]]]<br />
<br />
=<b>Host Immune Response</b>=<br />
<br />
<i> Streptococcus mutans </i> is the major pathogen of dental caries due to the ability to adhere and accumulate to the tooth surface. The Innate Immune Response and the Adaptive Immune Response are two fundamental aspects of the immune system that respond to infections such as dental caries. <i> Streptococcus mutans </i> enters the host through the oral route. The mucosal tissue associated with the exocrine glands and saliva contributes to the production of the oral cavity. This is because; these regions contain cells responsible for antigen internalization and antibodies specific to oral bacteria. The secretory antibodies that protect against dental caries are IgA and IgG. The Macrophages of the innate immune response are phagocytic cells that can internalize and kill bacteria by several mechanisms of internalization, which includes macropinocytosis and phagocytosis. If <i> Streptococcus mutans </i> initiates dental caries after the teeth have erupted either the host did not undergo the effective immune response of secretory IgA played a small role in preventing colonization and subsequent plaque development. [[#References|[7]]]<br />
<br />
=<b>References</b>=<br />
<br />
<br />
1 [http://www.ncl.ac.uk/dental/oralbiol/oralenv/tutorials/streps.htm Whiley, R.A., and Beighton, D. "Streptococci and Oral Streptococci." Bite-Sized Tutorials. N.p.. Web. 23 Jul 2013.]<br />
<br />2 [http://www.podj.com.pk/Dec_2012/p-28.pdf Javed, M., Chaudhry, S., Butt, S., Ijaz, S., Asad, R., Awais, F., and Khan, A., "Transmission of Streptococcus mutans from Mother to Child." Review Article. Pakistan and Oral Dental Journal vol 32, No.3, n.d. Web. 24 Jul 2013.]<br />
<br />3 [http://xenophilia.com/tooth-health-cure-for-cavities "Tooth Health: Cure for Cavities." Xenophilia.]<br />
<br />4 [http://cro.sagepub.com/content/4/2/159.full.pdf Howard, K. "Virulence factors of Mutans Streptococci: Role of Molecular genetics." Critical Reviews in Oral Biology and Medicine.] <br />
<br />5 [http://health.nytimes.com/health/guides/disease/dental-cavities) "Dental Cavities." The New York Times.]<br />
<br />6 [http://www.jyi.org/issue/the-role-of-streptococcus-mutans-and-oral-ecology-in-the-formation-of-dental-caries/) Simon, L., " The Role of Streptococcus mutans & Oral Ecology in the Formation of Dental Caries." Journal of the Young Investigators.] <br />
<br />7 [http://textbookofbacteriology.net/structure.html Todar, K. "Structure and Function of Prokaryotic Cells." Todar's Online Textbook of Bacteriology]<br />
<br />8 [http://www.brighthub.com/science/genetics/articles/45935.asp Arnold, P. "Mouth Bacteria. It's a Jungle in There." Bright Hub.]<br />
<br />9 [http://www.dentalcare.com/media/en-us/education/ce368/ce368.pdf Edward, L. "Caries Process & Prevention Strategies: Epidemiology." Dentalcare.com Continuing Education.]<br />
<br />10 [https://en.wikipedia.org/wiki/Dental_caries "Dental Caries." Wikipedia The Free Encyclopedia.] <br />
<br /> 11 [http://www.ncl.ac.uk/dental/oralbiol/oralenv/tutorials/mutans.htm "Streptococcus mutans and the mutan Streptococci."]<br />
<br /> 12 [http://www.webmd.com/oral-health/tc/tooth-decay-topic-overview "Tooth Decay-Topic Overview." Web MD.]<br />
<br /> 13 [http://www.medicalnewstoday.com/articles/154164.php "What is Fluoride? What does Fluoride Do?" Medical News Today.]<br />
<br /> 14 [http://www.webmd.com/oral-health/guide/dental-health-fillings?page=2 "Dental Health & Tooth Fillings." Web MD]<br />
<br /> 15 [http://doctorspiller.com/Fillings/fillings_5.htm Spiller, M. "When is it more appropriate to place a crown on a tooth instead of a filling?" DoctorSpiller.Com]<br />
<br /> 16 [http://web.mst.edu/~microbio/bio221_2006/S_mutans.htm Bassett, A. "Streptococcus mutans."]<br />
<br />
Created by Taylor Zelnicek, student of Tyrrell Conway at the University of Oklahoma.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Streptococcus_mutans-_Tooth_Decay&diff=91520
Streptococcus mutans- Tooth Decay
2013-07-24T23:33:07Z
<p>Kelley.L.Raines-1: /* Colonization */</p>
<hr />
<div>{{Curated}}<br />
[[Image:OULOGOBIANCO.JPEG|thumb|400px|right|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]<br />
<br />
=<b>Etiology/Bacteriology</b>=<br />
[[Image:Streptococcus-mutans.jpeg|thumb|275|px|left|''Streptococcus mutans'' From:http://microbiologyglossary.wikispaces.com [http://microbiologyglossary.wikispaces.com/Streptococcus+mutans]]<br />
<br />
===Taxonomy===<br />
<br />
Kingdom: Bacteria | Phylum: Firmicutes | Class: Bacilli | Order: Lactobacillales | Family: Streptococcaceae | Genus: Streptococcus | Species: <i> S. mutans </i><br />
<br />
===Description===<br />
<br />
<i> Streptococcus mutans </i> are gram-positive cocci shaped bacteria. These facultative anaerobes are commonly found in the human oral cavity, and is a significantly contributor of tooth decay. The result of decay can greatly affect the overall health of the individual. [[#References|[1]]] <i> S. mutans </i> are mesophilic and grow at temperatures between 18-40 degrees Celsius. <i> Streptococcus mutans </i> is a cariogenic microorganism that breaks down sugar for energy and produces an acidic environment, which demineralizes the superficial structure of the tooth. The result of the conversion disintegrates the coating of the tooth then later dissolves the Calcium molecule creating a hole. Transmission of <i> S. mutans </i> can be found in people of all ages although it is more common for infants and children. The transfer of genotypes are responsible for the transmission of <i> S. mutans </i> from mothers to their children although, there is a genotypic variation from one population to the next.[[#References|[2]]] Someone with a healthy oral flora will roughly contain 10,000 CFU per ml of <i> Streptococcus mutans </i> in their mouth.[[#References|[3]]] <i> Streptococcus mutans </i> possesses three virulence factors: water insoluble glycans, acid tolerance, and production of lactic acid. [[#References|[4]]] A toothache is the most common symptom of tooth decay. An infection or irritation of the tooth pulp usually causes the pain. The dentist is usually the person to diagnose tooth decay by taking X-Rays, and sometimes the X-Rays can detect the formation of a cavity before it is fully intact. If diagnosed with tooth decay, there are many treatment options such as: fillings, crowns and root canals. Since every human has bacteria in their mouth, the only prevention is to lessen the impact of acid fermentation by practicing adequate oral hygiene. [[#References|[5]]]<br />
<br />
=<b>Pathogenesis</b>=<br />
<br />
===Transmission===<br />
<br />
<i> Streptococcus mutans </i> is considered to be part of the "normal" flora of the human mouth, which is associated with dental caries also known as tooth decay. Dental caries is an infectious and communicable dental disease that affects people of all ages. <i> Streptococcus mutans </i> can be passed from one person to the next via horizontal or vertical transmission. The transmission route of <i> Streptococcus mutans </i> is to colonize itself among human hosts. Children and infants are more prone to the diagnosis of <i> Streptococcus mutans </i> and studies show that many receive it from their primary caregivers. [[#References|[2]]] <i> S. mutans </i> favors hard non-shedding surfaces to establish permanent colonies, which implies that levels of <i> S. mutans </i> are undetected in infants until the primary teeth extravasate;although, recent studies have shown that <i> S. mutans </i> is able to colonize the furrows of the tongue in pre-denate infants. Typically between the ages of one and two, teeth erupt, which allows <i> S. mutans </i> to establish flourishing colonies on teeth, and causes cavities. The indication of cavity formation is the appearance of detectable levels of bacteria on teeth. When <i> S. mutans </i> is detected in the furrows of the tongue it is concluded that the vertical transmission route for the bacteria from mother to child arises shortly after birth. To prove this, saliva samples of two to five year old children were taken, which revealed a high fidelity in genetic make-up of each host's <i> S. mutans </i> population. These experiments also concluded that plasmid DNA correlates to different rates, which primarily implies vertical transmission. Mothers with large amounts of bacteria or those who have suffered from many dental caries themselves are likely to transmit the same virulence factors to their children. When the mother's salivary S. mutans levels exceed 105 Colony Forming Units they are nine times more likely to pass bacteria on to their children. [[#References|[6]]]<br />
<br />
===Colonization===<br />
[[Image:biofilm on teeth.jpeg|thumb|200px|right|''biofilm on teeth'' From:http://www.advancedhealing.com [http://www.advancedhealing.com/biofilm-basics/]]]<br />
<br />
The growth and metabolism of <i> S. mutanss </i> changes the environmental conditions of the oral flora, which enables fastidious organisms to colonize and causes the formation of dental plaque. <i> Streptococcus mutans </i> is a specialized microorganism equipped with receptors that allow it to adhere to the surface of the tooth creating a slimy environment. After adherence to the tooth, <i> S. mutans </i> begin to divide and produce microcolonies within the slime layer to construct a biofilm. <i> S. mutans </i> begin to grow and synthesize dextran with the enzyme dextransucrase. Dextran contains a capsule that binds to the enamel and forms a biofilm that consists of 300-500 bacterial cells. The biofilm metabolizes <i> S. mutans </i> and is able to cleave sucrose with the enzyme Glucansucrase in the reaction: n sucrose -------> (glucose) n + n fructose. With these products fructose is fermented as an energy source for bacterial growth while glucose is polymerized to an extracellular dextran polymer. This is important because the polymer cements <i> S. mutans </i> at the enamel and becomes the matrix of dental plaque. The dextrin can also depolymerize to glucose and use the monosaccharide as a carbon source, which produces lactic acid in the biofilm by decalcifying the enamel, and leads to dental caries. The combination of acid and plaque results in the causative agent of decay. [[#References|[7]]]<br />
<br />
===Infectious Dose===<br />
<br />
Bacteria are the most numerous microbes in the mouth. It has been estimated that there are over 100 million in every milliliter of saliva from more than 600 different species.[[#References|[8]]] In order to decrease the bacterial challenge, it is encouraged for people to have 10,000 CFU per ml of saliva <i> Streptococcus mutans </i> in their mouth. [[#References|[3]]]<br />
<br />
{| class="wikitable"<br />
|-<br />
! Colony Forming Units CFU <i> S. mutans </i>/ml saliva !! <br />
|-<br />
| class 0-1 || <100,000 || <br />
|-<br />
| class 2 || 100,000< CFU/ml <1,000,000 || <br />
|-<br />
| class 3 || >1,000,000 CFU/ml || <br />
|}<br />
<br />
In the table, class 0-3 is referring to how many <i> Streptococcus mutans </i> reside in the mouth with class 0-1 acting as best case with good oral hygiene, while class 3 acts as the worst case. [[#References|[3]]]<br />
<br />
===Epidemiology===<br />
<br />
The Decayed Missing Filled also known as the DMF index is the key to measuring the caries that is caused by the bacterial strain <i> Streptococcus </i> mutans. The DMF index expresses the total number of teeth or surfaces that have decayed. When the index is applied specifically to teeth, it is called the DMFT index. The DMFT index scores the individual tooth from 0-28 or 32 depending on the presence or absence of the third molars. When the index is applied to the tooth surface it is called the DMFS index and scores from a range of 0-128 or 148 also depending on the assumption if the third molar is included or not. [[#References|[9]]]<br />
<br />
===Virulence Factors===<br />
<br />
There are three virulence factors that are associated with the cariogenicity of <i> Streptococcus mutans </i>. The first property is dependent on the synthesis of water-soluble glycans from the disaccharide sucrose. Next, <i> S. mutans </i> possesses the ability to become more acid tolerant. This leads to the third characteristic, which displays a production of lactic acid from dietary sugars. [[#References|[4]]]<br />
<br />
=<b>Clinical features</b>=<br />
[[Image:cavity.jpeg|thumb|100px|left| "cavity image" From:oralanswers.com [http://www.oralanswers.com/2011/07/risk-factors-dental-cavities/]]<br />
<br />
===Signs and Symptoms===<br />
<br />
If <i> Streptococcus mutans </i> leads to dental caries, one may not be aware they are diagnosed with the disease. A chalky white spot on the surface of the tooth indicates an area of demineralization of enamel, which is commonly referred to as a carious lesion. A carious lesion is the earliest diagnosis of tooth decay formation. As the lesion further demineralizes, it can turn brown and will eventually result in a cavity. Before the formation of the cavity, the process is reversible, but once the <i> Streptococcus mutans </i> forms the cavity, the tooth structure is lost and cannot be regenerated. A lesion that appears shiny and dark brown suggests that a lesion was once present but the demineralization has stopped leaving a stain. As the enamel and dentin are destroyed, the cavity becomes more noticeable. The effected area of the tooth changes color and becomes sensitive. When the decay passes through the enamel, the dentin tubules allow passages to the nerves making the tooth exposed, which results in pain that temporarily worsens with exposure to heat, cold, or sweet food or drinks. If the tooth is weakened by substantial amounts of internal decay a fracture may occur under normal chewing forces. Pain will arise more constant when the decay has progressed enough to where the bacteria can overwhelm the pulp tissue that is located in the center of the tooth. <br />
<br> In addition to cavity formation of the bacterial strain <i> Streptococcus mutans </i>, dental caries can also cause bad breath and foul tastes, and gum disease. In highly progressed states, the infection can spread to the soft tissue from the tooth. Life-threatening complications may arise such as cavernous sinus thrombosis and Ludwig's angina. [[#References|[10]]]<br />
<br />
=<b>Diagnosis</b>=<br />
<br />
<i> Streptococcus mutans </i> and <i> Streptococcus sobrinus </i> are two microorganisms that reside in the mouth of a human. <i> S. mutans </i> is carried by everyone while <i> S. sobrinus </i> is carried between 8 and 35 % of people in different countries. These different bacterial strains can be distinguished by laboratory tests although the procedure is expensive and time consuming therefore; it is not always practicable to identify the species in a large epidemiological scale. Researchers have lacked to invent a selective media that would allow one to look at the presence of a single species in saliva samples. Because of this, researchers have combined the two species together as mutans streptococci also known as (MS). Since <i> Streptococcus mutans</i> is more prevalent than <i> Streptococcus sobrinus </i> most of the isolates will solely be <i> S. mutans</i>. Mutans streptococci can be cultured in a laboratory by taking a sample of the microorganisms in the mouth. The microbiologist can then use two types of selective media that are widely used to isolate caries-related <i> Streptococcus </i> on Mitis- Salivarius agar and TYC agar in which antibiotic Bacitracin is added. These types of media suppress the growth of most microorganisms but allows the growth of <i> Streptococcus mutans</i> and <i> Streptococcus sobrinus </i>. The inclusion of sucrose leads to the formation of glucans and the appearance of colony formation to aid identification. Diagnostic kits used in dental clinics are based on similar selective media, but it is important to note that they are measuring for total MS, not just <i> S. mutans </i>. [[#References|[11]]] <br> If the strain of <i> Streptococcus mutans </i> has already invaded the tooth enamel, a dentist will diagnose the tooth decay. The dentist will start out by asking questions about the patient's dental history and medical problems. Next, the dentist will examine the patient's teeth by using an explorer and a small mirror. To confirm that a tooth has decayed the dentist will take X-Rays of the mouth to examine the teeth as well as the gums. [[#References|[12]]]<br />
<br />
=<b>Treatment</b>=<br />
[[Image:Composite Vs. Amalgam.jpeg|thumb|250px|right|''Composite Vs. Amalgam'' From:http://www.bauerfamilydental.com [http://www.bauerfamilydental.com/services-2/cleanings/]]<br />
<br />
Treatment for tooth decay depends on how severe the decay is. One may simply be able to reverse slight tooth decay by the application of fluoride. [[#References|[12]]] When a processed sugar is consumed, the bacteria from the mouth combine with the sugar to produce an acid.This acid can erode the tooth enamel and damage teeth. Fluoride is used to protect teeth from the demineralization caused by the acid. Fluoride does this by accumulating the demineralized areas of the tooth and strengthening the enamel in a process called remineralization. Fluoride is efficient in preventing tooth decay and making teeth stronger however, it is much less effective if a cavity has already formed. [[#References|[13]]]<br />
<br>To fix cavities caused by the bacterial strain <i> Streptococcus mutans </i> a dentist will need to adequately perform either a composite filling or an amalgam filling- two of the most common fillings used today. In both types of fillings, the dentist will remove the decayed portion of the tooth and fill in the area of the tooth where the decayed area once resided. Amalgam fillings are made from a mixture of silver, tin, zinc, copper and mercury. An advantage of the amalgam filling is durability, strength and expense. Amalgam fillings are durable in the fact that they usually outlast composite fillings, and do not need to be replaced for approximately 10-15 years. These fillings are strong since they can withstand the chewing forces, and are less expensive than composite fillings. A disadvantage of the amalgam fillings is that they cause: discoloration, cracks and fractures, allergic reactions, and destroys more tooth structure. These fillings also have poor aesthetics since the silver fillings are not the color of one's natural tooth. Composite fillings are made from a mixture of plastic and fine glass particles. Some advantages of composite fillings are: aesthetics the fact that the filling closely matches the color of the tooth, the ability to bond to the tooth structure since composite fillings are chemically bonded to the tooth they provide better support, versatility not only does the material fill cavities it is also used to repair chipped, broken down teeth. Tooth-sparing preparation is also an advantage of composite fillings this is because, sometimes less tooth structure needs to be removed than what the amalgam filling will provide. Disadvantages of tooth decay include: lack of durability. Composite fillings wear out sooner than amalgam fillings lasting 5 years as opposed to 10-15 years. There is also an increase in chair time because the process to apply the filling is longer vs. the amalgam filling. Additional visits are required, chipping the composite material from the tooth, and the fact that composite fillings are double the cost of amalgam fillings. [[#References|[14]]]<br />
<br> If one experiences an extreme case of tooth decay a root canal or crown may be used. If the decay exceeds a certain level the dentist may end up needing to extract the tooth.[[#References|[14]]] The dentist will use a crown to treat the decay if the structure of the tooth is weaker than it should be. A tooth should be crowned if the filling would make up more than half the surface area of the clinical crown. A crown should also be installed if the tooth decay has traveled deep under the gum line. The dentist will choose the root canal procedure when the decayed tooth is deep and has reached the pulp of the tooth, which is the center of the tooth where the nerves are. [[#References|[15]]]<br />
<br />
=<b>Prevention</b>=<br />
[[Image:how to prevent tooth decay.jpeg|thumb|210px|right| [http://www.drchetan.com/different-plaque-removal-procedures.html]]<br />
<br />
It is a fact that every human has bacteria already existing in their mouth. The only prevention is to lessen the impact of the fermentation by product lactic acid. Brushing, flossing and reducing the intake of refined and processed sugars can accomplish this. These processed sugars come in the form of sweets, colas and processed powered sweeteners. Studies have shown that rinsing one's mouth out with water can greatly reduce the probability of cavities after the consumption of these sugars. It is almost impossible to completely reduce the effects of <i> S. mutans </i> but there is an option to control it. [[#References|[16]]]<br />
<br />
=<b>Host Immune Response</b>=<br />
<br />
<i> Streptococcus mutans </i> is the major pathogen of dental caries due to the ability to adhere and accumulate to the tooth surface. The Innate Immune Response and the Adaptive Immune Response are two fundamental aspects of the immune system that respond to infections such as dental caries. <i> Streptococcus mutans </i> enters the host through the oral route. The mucosal tissue associated with the exocrine glands and saliva contributes to the production of the oral cavity. This is because; these regions contain cells responsible for antigen internalization and antibodies specific to oral bacteria. The secretory antibodies that protect against dental caries are IgA and IgG. The Macrophages of the innate immune response are phagocytic cells that can internalize and kill bacteria by several mechanisms of internalization, which includes macropinocytosis and phagocytosis. If <i> Streptococcus mutans </i> initiates dental caries after the teeth have erupted either the host did not undergo the effective immune response of secretory IgA played a small role in preventing colonization and subsequent plaque development. [[#References|[7]]]<br />
<br />
=<b>References</b>=<br />
<br />
<br />
1 [http://www.ncl.ac.uk/dental/oralbiol/oralenv/tutorials/streps.htm Whiley, R.A., and Beighton, D. "Streptococci and Oral Streptococci." Bite-Sized Tutorials. N.p.. Web. 23 Jul 2013.]<br />
<br />2 [http://www.podj.com.pk/Dec_2012/p-28.pdf Javed, M., Chaudhry, S., Butt, S., Ijaz, S., Asad, R., Awais, F., and Khan, A., "Transmission of Streptococcus mutans from Mother to Child." Review Article. Pakistan and Oral Dental Journal vol 32, No.3, n.d. Web. 24 Jul 2013.]<br />
<br />3 [http://xenophilia.com/tooth-health-cure-for-cavities "Tooth Health: Cure for Cavities." Xenophilia.]<br />
<br />4 [http://cro.sagepub.com/content/4/2/159.full.pdf Howard, K. "Virulence factors of Mutans Streptococci: Role of Molecular genetics." Critical Reviews in Oral Biology and Medicine.] <br />
<br />5 [http://health.nytimes.com/health/guides/disease/dental-cavities) "Dental Cavities." The New York Times.]<br />
<br />6 [http://www.jyi.org/issue/the-role-of-streptococcus-mutans-and-oral-ecology-in-the-formation-of-dental-caries/) Simon, L., " The Role of Streptococcus mutans & Oral Ecology in the Formation of Dental Caries." Journal of the Young Investigators.] <br />
<br />7 [http://textbookofbacteriology.net/structure.html Todar, K. "Structure and Function of Prokaryotic Cells." Todar's Online Textbook of Bacteriology]<br />
<br />8 [http://www.brighthub.com/science/genetics/articles/45935.asp Arnold, P. "Mouth Bacteria. It's a Jungle in There." Bright Hub.]<br />
<br />9 [http://www.dentalcare.com/media/en-us/education/ce368/ce368.pdf Edward, L. "Caries Process & Prevention Strategies: Epidemiology." Dentalcare.com Continuing Education.]<br />
<br />10 [https://en.wikipedia.org/wiki/Dental_caries "Dental Caries." Wikipedia The Free Encyclopedia.] <br />
<br /> 11 [http://www.ncl.ac.uk/dental/oralbiol/oralenv/tutorials/mutans.htm "Streptococcus mutans and the mutan Streptococci."]<br />
<br /> 12 [http://www.webmd.com/oral-health/tc/tooth-decay-topic-overview "Tooth Decay-Topic Overview." Web MD.]<br />
<br /> 13 [http://www.medicalnewstoday.com/articles/154164.php "What is Fluoride? What does Fluoride Do?" Medical News Today.]<br />
<br /> 14 [http://www.webmd.com/oral-health/guide/dental-health-fillings?page=2 "Dental Health & Tooth Fillings." Web MD]<br />
<br /> 15 [http://doctorspiller.com/Fillings/fillings_5.htm Spiller, M. "When is it more appropriate to place a crown on a tooth instead of a filling?" DoctorSpiller.Com]<br />
<br /> 16 [http://web.mst.edu/~microbio/bio221_2006/S_mutans.htm Bassett, A. "Streptococcus mutans."]<br />
<br />
Created by Taylor Zelnicek, student of Tyrrell Conway at the University of Oklahoma.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Streptococcus_mutans-_Tooth_Decay&diff=91519
Streptococcus mutans- Tooth Decay
2013-07-24T23:29:32Z
<p>Kelley.L.Raines-1: /* Transmission */</p>
<hr />
<div>{{Curated}}<br />
[[Image:OULOGOBIANCO.JPEG|thumb|400px|right|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]<br />
<br />
=<b>Etiology/Bacteriology</b>=<br />
[[Image:Streptococcus-mutans.jpeg|thumb|275|px|left|''Streptococcus mutans'' From:http://microbiologyglossary.wikispaces.com [http://microbiologyglossary.wikispaces.com/Streptococcus+mutans]]<br />
<br />
===Taxonomy===<br />
<br />
Kingdom: Bacteria | Phylum: Firmicutes | Class: Bacilli | Order: Lactobacillales | Family: Streptococcaceae | Genus: Streptococcus | Species: <i> S. mutans </i><br />
<br />
===Description===<br />
<br />
<i> Streptococcus mutans </i> are gram-positive cocci shaped bacteria. These facultative anaerobes are commonly found in the human oral cavity, and is a significantly contributor of tooth decay. The result of decay can greatly affect the overall health of the individual. [[#References|[1]]] <i> S. mutans </i> are mesophilic and grow at temperatures between 18-40 degrees Celsius. <i> Streptococcus mutans </i> is a cariogenic microorganism that breaks down sugar for energy and produces an acidic environment, which demineralizes the superficial structure of the tooth. The result of the conversion disintegrates the coating of the tooth then later dissolves the Calcium molecule creating a hole. Transmission of <i> S. mutans </i> can be found in people of all ages although it is more common for infants and children. The transfer of genotypes are responsible for the transmission of <i> S. mutans </i> from mothers to their children although, there is a genotypic variation from one population to the next.[[#References|[2]]] Someone with a healthy oral flora will roughly contain 10,000 CFU per ml of <i> Streptococcus mutans </i> in their mouth.[[#References|[3]]] <i> Streptococcus mutans </i> possesses three virulence factors: water insoluble glycans, acid tolerance, and production of lactic acid. [[#References|[4]]] A toothache is the most common symptom of tooth decay. An infection or irritation of the tooth pulp usually causes the pain. The dentist is usually the person to diagnose tooth decay by taking X-Rays, and sometimes the X-Rays can detect the formation of a cavity before it is fully intact. If diagnosed with tooth decay, there are many treatment options such as: fillings, crowns and root canals. Since every human has bacteria in their mouth, the only prevention is to lessen the impact of acid fermentation by practicing adequate oral hygiene. [[#References|[5]]]<br />
<br />
=<b>Pathogenesis</b>=<br />
<br />
===Transmission===<br />
<br />
<i> Streptococcus mutans </i> is considered to be part of the "normal" flora of the human mouth, which is associated with dental caries also known as tooth decay. Dental caries is an infectious and communicable dental disease that affects people of all ages. <i> Streptococcus mutans </i> can be passed from one person to the next via horizontal or vertical transmission. The transmission route of <i> Streptococcus mutans </i> is to colonize itself among human hosts. Children and infants are more prone to the diagnosis of <i> Streptococcus mutans </i> and studies show that many receive it from their primary caregivers. [[#References|[2]]] <i> S. mutans </i> favors hard non-shedding surfaces to establish permanent colonies, which implies that levels of <i> S. mutans </i> are undetected in infants until the primary teeth extravasate;although, recent studies have shown that <i> S. mutans </i> is able to colonize the furrows of the tongue in pre-denate infants. Typically between the ages of one and two, teeth erupt, which allows <i> S. mutans </i> to establish flourishing colonies on teeth, and causes cavities. The indication of cavity formation is the appearance of detectable levels of bacteria on teeth. When <i> S. mutans </i> is detected in the furrows of the tongue it is concluded that the vertical transmission route for the bacteria from mother to child arises shortly after birth. To prove this, saliva samples of two to five year old children were taken, which revealed a high fidelity in genetic make-up of each host's <i> S. mutans </i> population. These experiments also concluded that plasmid DNA correlates to different rates, which primarily implies vertical transmission. Mothers with large amounts of bacteria or those who have suffered from many dental caries themselves are likely to transmit the same virulence factors to their children. When the mother's salivary S. mutans levels exceed 105 Colony Forming Units they are nine times more likely to pass bacteria on to their children. [[#References|[6]]]<br />
<br />
===Colonization===<br />
[[Image:biofilm on teeth.jpeg|thumb|200px|right|''biofilm on teeth'' From:http://www.advancedhealing.com [http://www.advancedhealing.com/biofilm-basics/]]]<br />
<br />
The growth and metabolism of <i> S. mutanss </i> changes the environmental conditions of the oral flora, which enables fastidious organisms to colonize and causes the formation of dental plaque. <i> Streptococcus mutans </i> is a specialized microorganism equipped with receptors that allow it to adhere to the surface of the tooth creating a slimy environment. After adherence to the tooth, <i> S. mutans </i> begins to divide and produce microcolonies within the slime layer to construct a biofilm. <i> S. mutans </i> begins to grow and synthesize dextran with the enzyme dextransucrase. Dextran contains a capsule that binds to the enamel and forms a biofilm that consists of 300-500 bacterial cells. The biofilm metabolizes <i> S. mutans </i> and is able to cleave sucrose with the enzyme Glucansucrase in the reaction: n sucrose -------> (glucose) n + n fructose. With these products fructose is fermented as an energy source for bacterial growth while glucose is polymerized to an extracellular dextran polymer. This is important because the polymer cements <i> S. mutans </i> at the enamel and becomes the matrix of dental plaque. The dextrin can also depolymerize to glucose and use the monosaccharide as a carbon source, which produces lactic acid in the biofilm by decalcifying the enamel, and leads to dental caries. The combination of acid and plaque results in the causative agent of decay. [[#References|[7]]]<br />
<br />
===Infectious Dose===<br />
<br />
Bacteria are the most numerous microbes in the mouth. It has been estimated that there are over 100 million in every milliliter of saliva from more than 600 different species.[[#References|[8]]] In order to decrease the bacterial challenge, it is encouraged for people to have 10,000 CFU per ml of saliva <i> Streptococcus mutans </i> in their mouth. [[#References|[3]]]<br />
<br />
{| class="wikitable"<br />
|-<br />
! Colony Forming Units CFU <i> S. mutans </i>/ml saliva !! <br />
|-<br />
| class 0-1 || <100,000 || <br />
|-<br />
| class 2 || 100,000< CFU/ml <1,000,000 || <br />
|-<br />
| class 3 || >1,000,000 CFU/ml || <br />
|}<br />
<br />
In the table, class 0-3 is referring to how many <i> Streptococcus mutans </i> reside in the mouth with class 0-1 acting as best case with good oral hygiene, while class 3 acts as the worst case. [[#References|[3]]]<br />
<br />
===Epidemiology===<br />
<br />
The Decayed Missing Filled also known as the DMF index is the key to measuring the caries that is caused by the bacterial strain <i> Streptococcus </i> mutans. The DMF index expresses the total number of teeth or surfaces that have decayed. When the index is applied specifically to teeth, it is called the DMFT index. The DMFT index scores the individual tooth from 0-28 or 32 depending on the presence or absence of the third molars. When the index is applied to the tooth surface it is called the DMFS index and scores from a range of 0-128 or 148 also depending on the assumption if the third molar is included or not. [[#References|[9]]]<br />
<br />
===Virulence Factors===<br />
<br />
There are three virulence factors that are associated with the cariogenicity of <i> Streptococcus mutans </i>. The first property is dependent on the synthesis of water-soluble glycans from the disaccharide sucrose. Next, <i> S. mutans </i> possesses the ability to become more acid tolerant. This leads to the third characteristic, which displays a production of lactic acid from dietary sugars. [[#References|[4]]]<br />
<br />
=<b>Clinical features</b>=<br />
[[Image:cavity.jpeg|thumb|100px|left| "cavity image" From:oralanswers.com [http://www.oralanswers.com/2011/07/risk-factors-dental-cavities/]]<br />
<br />
===Signs and Symptoms===<br />
<br />
If <i> Streptococcus mutans </i> leads to dental caries, one may not be aware they are diagnosed with the disease. A chalky white spot on the surface of the tooth indicates an area of demineralization of enamel, which is commonly referred to as a carious lesion. A carious lesion is the earliest diagnosis of tooth decay formation. As the lesion further demineralizes, it can turn brown and will eventually result in a cavity. Before the formation of the cavity, the process is reversible, but once the <i> Streptococcus mutans </i> forms the cavity, the tooth structure is lost and cannot be regenerated. A lesion that appears shiny and dark brown suggests that a lesion was once present but the demineralization has stopped leaving a stain. As the enamel and dentin are destroyed, the cavity becomes more noticeable. The effected area of the tooth changes color and becomes sensitive. When the decay passes through the enamel, the dentin tubules allow passages to the nerves making the tooth exposed, which results in pain that temporarily worsens with exposure to heat, cold, or sweet food or drinks. If the tooth is weakened by substantial amounts of internal decay a fracture may occur under normal chewing forces. Pain will arise more constant when the decay has progressed enough to where the bacteria can overwhelm the pulp tissue that is located in the center of the tooth. <br />
<br> In addition to cavity formation of the bacterial strain <i> Streptococcus mutans </i>, dental caries can also cause bad breath and foul tastes, and gum disease. In highly progressed states, the infection can spread to the soft tissue from the tooth. Life-threatening complications may arise such as cavernous sinus thrombosis and Ludwig's angina. [[#References|[10]]]<br />
<br />
=<b>Diagnosis</b>=<br />
<br />
<i> Streptococcus mutans </i> and <i> Streptococcus sobrinus </i> are two microorganisms that reside in the mouth of a human. <i> S. mutans </i> is carried by everyone while <i> S. sobrinus </i> is carried between 8 and 35 % of people in different countries. These different bacterial strains can be distinguished by laboratory tests although the procedure is expensive and time consuming therefore; it is not always practicable to identify the species in a large epidemiological scale. Researchers have lacked to invent a selective media that would allow one to look at the presence of a single species in saliva samples. Because of this, researchers have combined the two species together as mutans streptococci also known as (MS). Since <i> Streptococcus mutans</i> is more prevalent than <i> Streptococcus sobrinus </i> most of the isolates will solely be <i> S. mutans</i>. Mutans streptococci can be cultured in a laboratory by taking a sample of the microorganisms in the mouth. The microbiologist can then use two types of selective media that are widely used to isolate caries-related <i> Streptococcus </i> on Mitis- Salivarius agar and TYC agar in which antibiotic Bacitracin is added. These types of media suppress the growth of most microorganisms but allows the growth of <i> Streptococcus mutans</i> and <i> Streptococcus sobrinus </i>. The inclusion of sucrose leads to the formation of glucans and the appearance of colony formation to aid identification. Diagnostic kits used in dental clinics are based on similar selective media, but it is important to note that they are measuring for total MS, not just <i> S. mutans </i>. [[#References|[11]]] <br> If the strain of <i> Streptococcus mutans </i> has already invaded the tooth enamel, a dentist will diagnose the tooth decay. The dentist will start out by asking questions about the patient's dental history and medical problems. Next, the dentist will examine the patient's teeth by using an explorer and a small mirror. To confirm that a tooth has decayed the dentist will take X-Rays of the mouth to examine the teeth as well as the gums. [[#References|[12]]]<br />
<br />
=<b>Treatment</b>=<br />
[[Image:Composite Vs. Amalgam.jpeg|thumb|250px|right|''Composite Vs. Amalgam'' From:http://www.bauerfamilydental.com [http://www.bauerfamilydental.com/services-2/cleanings/]]<br />
<br />
Treatment for tooth decay depends on how severe the decay is. One may simply be able to reverse slight tooth decay by the application of fluoride. [[#References|[12]]] When a processed sugar is consumed, the bacteria from the mouth combine with the sugar to produce an acid.This acid can erode the tooth enamel and damage teeth. Fluoride is used to protect teeth from the demineralization caused by the acid. Fluoride does this by accumulating the demineralized areas of the tooth and strengthening the enamel in a process called remineralization. Fluoride is efficient in preventing tooth decay and making teeth stronger however, it is much less effective if a cavity has already formed. [[#References|[13]]]<br />
<br>To fix cavities caused by the bacterial strain <i> Streptococcus mutans </i> a dentist will need to adequately perform either a composite filling or an amalgam filling- two of the most common fillings used today. In both types of fillings, the dentist will remove the decayed portion of the tooth and fill in the area of the tooth where the decayed area once resided. Amalgam fillings are made from a mixture of silver, tin, zinc, copper and mercury. An advantage of the amalgam filling is durability, strength and expense. Amalgam fillings are durable in the fact that they usually outlast composite fillings, and do not need to be replaced for approximately 10-15 years. These fillings are strong since they can withstand the chewing forces, and are less expensive than composite fillings. A disadvantage of the amalgam fillings is that they cause: discoloration, cracks and fractures, allergic reactions, and destroys more tooth structure. These fillings also have poor aesthetics since the silver fillings are not the color of one's natural tooth. Composite fillings are made from a mixture of plastic and fine glass particles. Some advantages of composite fillings are: aesthetics the fact that the filling closely matches the color of the tooth, the ability to bond to the tooth structure since composite fillings are chemically bonded to the tooth they provide better support, versatility not only does the material fill cavities it is also used to repair chipped, broken down teeth. Tooth-sparing preparation is also an advantage of composite fillings this is because, sometimes less tooth structure needs to be removed than what the amalgam filling will provide. Disadvantages of tooth decay include: lack of durability. Composite fillings wear out sooner than amalgam fillings lasting 5 years as opposed to 10-15 years. There is also an increase in chair time because the process to apply the filling is longer vs. the amalgam filling. Additional visits are required, chipping the composite material from the tooth, and the fact that composite fillings are double the cost of amalgam fillings. [[#References|[14]]]<br />
<br> If one experiences an extreme case of tooth decay a root canal or crown may be used. If the decay exceeds a certain level the dentist may end up needing to extract the tooth.[[#References|[14]]] The dentist will use a crown to treat the decay if the structure of the tooth is weaker than it should be. A tooth should be crowned if the filling would make up more than half the surface area of the clinical crown. A crown should also be installed if the tooth decay has traveled deep under the gum line. The dentist will choose the root canal procedure when the decayed tooth is deep and has reached the pulp of the tooth, which is the center of the tooth where the nerves are. [[#References|[15]]]<br />
<br />
=<b>Prevention</b>=<br />
[[Image:how to prevent tooth decay.jpeg|thumb|210px|right| [http://www.drchetan.com/different-plaque-removal-procedures.html]]<br />
<br />
It is a fact that every human has bacteria already existing in their mouth. The only prevention is to lessen the impact of the fermentation by product lactic acid. Brushing, flossing and reducing the intake of refined and processed sugars can accomplish this. These processed sugars come in the form of sweets, colas and processed powered sweeteners. Studies have shown that rinsing one's mouth out with water can greatly reduce the probability of cavities after the consumption of these sugars. It is almost impossible to completely reduce the effects of <i> S. mutans </i> but there is an option to control it. [[#References|[16]]]<br />
<br />
=<b>Host Immune Response</b>=<br />
<br />
<i> Streptococcus mutans </i> is the major pathogen of dental caries due to the ability to adhere and accumulate to the tooth surface. The Innate Immune Response and the Adaptive Immune Response are two fundamental aspects of the immune system that respond to infections such as dental caries. <i> Streptococcus mutans </i> enters the host through the oral route. The mucosal tissue associated with the exocrine glands and saliva contributes to the production of the oral cavity. This is because; these regions contain cells responsible for antigen internalization and antibodies specific to oral bacteria. The secretory antibodies that protect against dental caries are IgA and IgG. The Macrophages of the innate immune response are phagocytic cells that can internalize and kill bacteria by several mechanisms of internalization, which includes macropinocytosis and phagocytosis. If <i> Streptococcus mutans </i> initiates dental caries after the teeth have erupted either the host did not undergo the effective immune response of secretory IgA played a small role in preventing colonization and subsequent plaque development. [[#References|[7]]]<br />
<br />
=<b>References</b>=<br />
<br />
<br />
1 [http://www.ncl.ac.uk/dental/oralbiol/oralenv/tutorials/streps.htm Whiley, R.A., and Beighton, D. "Streptococci and Oral Streptococci." Bite-Sized Tutorials. N.p.. Web. 23 Jul 2013.]<br />
<br />2 [http://www.podj.com.pk/Dec_2012/p-28.pdf Javed, M., Chaudhry, S., Butt, S., Ijaz, S., Asad, R., Awais, F., and Khan, A., "Transmission of Streptococcus mutans from Mother to Child." Review Article. Pakistan and Oral Dental Journal vol 32, No.3, n.d. Web. 24 Jul 2013.]<br />
<br />3 [http://xenophilia.com/tooth-health-cure-for-cavities "Tooth Health: Cure for Cavities." Xenophilia.]<br />
<br />4 [http://cro.sagepub.com/content/4/2/159.full.pdf Howard, K. "Virulence factors of Mutans Streptococci: Role of Molecular genetics." Critical Reviews in Oral Biology and Medicine.] <br />
<br />5 [http://health.nytimes.com/health/guides/disease/dental-cavities) "Dental Cavities." The New York Times.]<br />
<br />6 [http://www.jyi.org/issue/the-role-of-streptococcus-mutans-and-oral-ecology-in-the-formation-of-dental-caries/) Simon, L., " The Role of Streptococcus mutans & Oral Ecology in the Formation of Dental Caries." Journal of the Young Investigators.] <br />
<br />7 [http://textbookofbacteriology.net/structure.html Todar, K. "Structure and Function of Prokaryotic Cells." Todar's Online Textbook of Bacteriology]<br />
<br />8 [http://www.brighthub.com/science/genetics/articles/45935.asp Arnold, P. "Mouth Bacteria. It's a Jungle in There." Bright Hub.]<br />
<br />9 [http://www.dentalcare.com/media/en-us/education/ce368/ce368.pdf Edward, L. "Caries Process & Prevention Strategies: Epidemiology." Dentalcare.com Continuing Education.]<br />
<br />10 [https://en.wikipedia.org/wiki/Dental_caries "Dental Caries." Wikipedia The Free Encyclopedia.] <br />
<br /> 11 [http://www.ncl.ac.uk/dental/oralbiol/oralenv/tutorials/mutans.htm "Streptococcus mutans and the mutan Streptococci."]<br />
<br /> 12 [http://www.webmd.com/oral-health/tc/tooth-decay-topic-overview "Tooth Decay-Topic Overview." Web MD.]<br />
<br /> 13 [http://www.medicalnewstoday.com/articles/154164.php "What is Fluoride? What does Fluoride Do?" Medical News Today.]<br />
<br /> 14 [http://www.webmd.com/oral-health/guide/dental-health-fillings?page=2 "Dental Health & Tooth Fillings." Web MD]<br />
<br /> 15 [http://doctorspiller.com/Fillings/fillings_5.htm Spiller, M. "When is it more appropriate to place a crown on a tooth instead of a filling?" DoctorSpiller.Com]<br />
<br /> 16 [http://web.mst.edu/~microbio/bio221_2006/S_mutans.htm Bassett, A. "Streptococcus mutans."]<br />
<br />
Created by Taylor Zelnicek, student of Tyrrell Conway at the University of Oklahoma.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Streptococcus_mutans-_Tooth_Decay&diff=91518
Streptococcus mutans- Tooth Decay
2013-07-24T23:25:45Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
[[Image:OULOGOBIANCO.JPEG|thumb|400px|right|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]<br />
<br />
=<b>Etiology/Bacteriology</b>=<br />
[[Image:Streptococcus-mutans.jpeg|thumb|275|px|left|''Streptococcus mutans'' From:http://microbiologyglossary.wikispaces.com [http://microbiologyglossary.wikispaces.com/Streptococcus+mutans]]<br />
<br />
===Taxonomy===<br />
<br />
Kingdom: Bacteria | Phylum: Firmicutes | Class: Bacilli | Order: Lactobacillales | Family: Streptococcaceae | Genus: Streptococcus | Species: <i> S. mutans </i><br />
<br />
===Description===<br />
<br />
<i> Streptococcus mutans </i> are gram-positive cocci shaped bacteria. These facultative anaerobes are commonly found in the human oral cavity, and is a significantly contributor of tooth decay. The result of decay can greatly affect the overall health of the individual. [[#References|[1]]] <i> S. mutans </i> are mesophilic and grow at temperatures between 18-40 degrees Celsius. <i> Streptococcus mutans </i> is a cariogenic microorganism that breaks down sugar for energy and produces an acidic environment, which demineralizes the superficial structure of the tooth. The result of the conversion disintegrates the coating of the tooth then later dissolves the Calcium molecule creating a hole. Transmission of <i> S. mutans </i> can be found in people of all ages although it is more common for infants and children. The transfer of genotypes are responsible for the transmission of <i> S. mutans </i> from mothers to their children although, there is a genotypic variation from one population to the next.[[#References|[2]]] Someone with a healthy oral flora will roughly contain 10,000 CFU per ml of <i> Streptococcus mutans </i> in their mouth.[[#References|[3]]] <i> Streptococcus mutans </i> possesses three virulence factors: water insoluble glycans, acid tolerance, and production of lactic acid. [[#References|[4]]] A toothache is the most common symptom of tooth decay. An infection or irritation of the tooth pulp usually causes the pain. The dentist is usually the person to diagnose tooth decay by taking X-Rays, and sometimes the X-Rays can detect the formation of a cavity before it is fully intact. If diagnosed with tooth decay, there are many treatment options such as: fillings, crowns and root canals. Since every human has bacteria in their mouth, the only prevention is to lessen the impact of acid fermentation by practicing adequate oral hygiene. [[#References|[5]]]<br />
<br />
=<b>Pathogenesis</b>=<br />
<br />
===Transmission===<br />
<br />
<i> Streptococcus mutans </i> is considered to be part of the "normal" flora of the human mouth, which is associated with dental caries also known as tooth decay. Dental caries is an infectious and communicable dental disease that affects people of all ages. <i> Streptococcus mutans </i> can be passed from one person to the next via horizontal or vertical transmission. The transmission route of <i> Streptococcus mutans </i> is to colonize itself among human hosts. Children and infants are more prone to the diagnosis of <i> Streptococcus mutans </i> and studies show that many receive it from their primary caregivers. [[#References|[2]]] <i> S. mutans </i> favors hard non-shedding surfaces to establish permanent colonies, which implies that levels of <i> S. mutans </i> are undetected in infants until the primary teeth extravasate;although, recent studies have shown that <i> S. mutans </i> is able to colonize the furrows of the tongue in pre-denate infants. Typically between the ages of one and two, teeth erupt, which allows <i> S. mutans </i> to establish flourishing colonies on teeth, and causes cavities. The indication of cavity formation is the appearance of detectable levels of bacteria on teeth. When <i> S. mutans </i> is detected in the furrows of the tongue it is concluded that the vertical transmission route for the bacteria from mother to child arises shortly after birth. To prove this, saliva samples of two to five year old children were taken, which revealed a high fidelity in genetic make-up of each host's <i> S. mutans </i> population. These experiments also concluded that plasmid DNA correlates to different rates, which primarily implies vertical transmission. Mothers with large amounts of bacteria or those who have suffered from many dental caries themselves are likely to transmit the same virulence factors to their children. When the mother's salivary S. mutans levels exceed 105 Colony Forming Units are nine times more likely to pass bacteria on to their children. [[#References|[6]]]<br />
<br />
===Colonization===<br />
[[Image:biofilm on teeth.jpeg|thumb|200px|right|''biofilm on teeth'' From:http://www.advancedhealing.com [http://www.advancedhealing.com/biofilm-basics/]]]<br />
<br />
The growth and metabolism of <i> S. mutanss </i> changes the environmental conditions of the oral flora, which enables fastidious organisms to colonize and causes the formation of dental plaque. <i> Streptococcus mutans </i> is a specialized microorganism equipped with receptors that allow it to adhere to the surface of the tooth creating a slimy environment. After adherence to the tooth, <i> S. mutans </i> begins to divide and produce microcolonies within the slime layer to construct a biofilm. <i> S. mutans </i> begins to grow and synthesize dextran with the enzyme dextransucrase. Dextran contains a capsule that binds to the enamel and forms a biofilm that consists of 300-500 bacterial cells. The biofilm metabolizes <i> S. mutans </i> and is able to cleave sucrose with the enzyme Glucansucrase in the reaction: n sucrose -------> (glucose) n + n fructose. With these products fructose is fermented as an energy source for bacterial growth while glucose is polymerized to an extracellular dextran polymer. This is important because the polymer cements <i> S. mutans </i> at the enamel and becomes the matrix of dental plaque. The dextrin can also depolymerize to glucose and use the monosaccharide as a carbon source, which produces lactic acid in the biofilm by decalcifying the enamel, and leads to dental caries. The combination of acid and plaque results in the causative agent of decay. [[#References|[7]]]<br />
<br />
===Infectious Dose===<br />
<br />
Bacteria are the most numerous microbes in the mouth. It has been estimated that there are over 100 million in every milliliter of saliva from more than 600 different species.[[#References|[8]]] In order to decrease the bacterial challenge, it is encouraged for people to have 10,000 CFU per ml of saliva <i> Streptococcus mutans </i> in their mouth. [[#References|[3]]]<br />
<br />
{| class="wikitable"<br />
|-<br />
! Colony Forming Units CFU <i> S. mutans </i>/ml saliva !! <br />
|-<br />
| class 0-1 || <100,000 || <br />
|-<br />
| class 2 || 100,000< CFU/ml <1,000,000 || <br />
|-<br />
| class 3 || >1,000,000 CFU/ml || <br />
|}<br />
<br />
In the table, class 0-3 is referring to how many <i> Streptococcus mutans </i> reside in the mouth with class 0-1 acting as best case with good oral hygiene, while class 3 acts as the worst case. [[#References|[3]]]<br />
<br />
===Epidemiology===<br />
<br />
The Decayed Missing Filled also known as the DMF index is the key to measuring the caries that is caused by the bacterial strain <i> Streptococcus </i> mutans. The DMF index expresses the total number of teeth or surfaces that have decayed. When the index is applied specifically to teeth, it is called the DMFT index. The DMFT index scores the individual tooth from 0-28 or 32 depending on the presence or absence of the third molars. When the index is applied to the tooth surface it is called the DMFS index and scores from a range of 0-128 or 148 also depending on the assumption if the third molar is included or not. [[#References|[9]]]<br />
<br />
===Virulence Factors===<br />
<br />
There are three virulence factors that are associated with the cariogenicity of <i> Streptococcus mutans </i>. The first property is dependent on the synthesis of water-soluble glycans from the disaccharide sucrose. Next, <i> S. mutans </i> possesses the ability to become more acid tolerant. This leads to the third characteristic, which displays a production of lactic acid from dietary sugars. [[#References|[4]]]<br />
<br />
=<b>Clinical features</b>=<br />
[[Image:cavity.jpeg|thumb|100px|left| "cavity image" From:oralanswers.com [http://www.oralanswers.com/2011/07/risk-factors-dental-cavities/]]<br />
<br />
===Signs and Symptoms===<br />
<br />
If <i> Streptococcus mutans </i> leads to dental caries, one may not be aware they are diagnosed with the disease. A chalky white spot on the surface of the tooth indicates an area of demineralization of enamel, which is commonly referred to as a carious lesion. A carious lesion is the earliest diagnosis of tooth decay formation. As the lesion further demineralizes, it can turn brown and will eventually result in a cavity. Before the formation of the cavity, the process is reversible, but once the <i> Streptococcus mutans </i> forms the cavity, the tooth structure is lost and cannot be regenerated. A lesion that appears shiny and dark brown suggests that a lesion was once present but the demineralization has stopped leaving a stain. As the enamel and dentin are destroyed, the cavity becomes more noticeable. The effected area of the tooth changes color and becomes sensitive. When the decay passes through the enamel, the dentin tubules allow passages to the nerves making the tooth exposed, which results in pain that temporarily worsens with exposure to heat, cold, or sweet food or drinks. If the tooth is weakened by substantial amounts of internal decay a fracture may occur under normal chewing forces. Pain will arise more constant when the decay has progressed enough to where the bacteria can overwhelm the pulp tissue that is located in the center of the tooth. <br />
<br> In addition to cavity formation of the bacterial strain <i> Streptococcus mutans </i>, dental caries can also cause bad breath and foul tastes, and gum disease. In highly progressed states, the infection can spread to the soft tissue from the tooth. Life-threatening complications may arise such as cavernous sinus thrombosis and Ludwig's angina. [[#References|[10]]]<br />
<br />
=<b>Diagnosis</b>=<br />
<br />
<i> Streptococcus mutans </i> and <i> Streptococcus sobrinus </i> are two microorganisms that reside in the mouth of a human. <i> S. mutans </i> is carried by everyone while <i> S. sobrinus </i> is carried between 8 and 35 % of people in different countries. These different bacterial strains can be distinguished by laboratory tests although the procedure is expensive and time consuming therefore; it is not always practicable to identify the species in a large epidemiological scale. Researchers have lacked to invent a selective media that would allow one to look at the presence of a single species in saliva samples. Because of this, researchers have combined the two species together as mutans streptococci also known as (MS). Since <i> Streptococcus mutans</i> is more prevalent than <i> Streptococcus sobrinus </i> most of the isolates will solely be <i> S. mutans</i>. Mutans streptococci can be cultured in a laboratory by taking a sample of the microorganisms in the mouth. The microbiologist can then use two types of selective media that are widely used to isolate caries-related <i> Streptococcus </i> on Mitis- Salivarius agar and TYC agar in which antibiotic Bacitracin is added. These types of media suppress the growth of most microorganisms but allows the growth of <i> Streptococcus mutans</i> and <i> Streptococcus sobrinus </i>. The inclusion of sucrose leads to the formation of glucans and the appearance of colony formation to aid identification. Diagnostic kits used in dental clinics are based on similar selective media, but it is important to note that they are measuring for total MS, not just <i> S. mutans </i>. [[#References|[11]]] <br> If the strain of <i> Streptococcus mutans </i> has already invaded the tooth enamel, a dentist will diagnose the tooth decay. The dentist will start out by asking questions about the patient's dental history and medical problems. Next, the dentist will examine the patient's teeth by using an explorer and a small mirror. To confirm that a tooth has decayed the dentist will take X-Rays of the mouth to examine the teeth as well as the gums. [[#References|[12]]]<br />
<br />
=<b>Treatment</b>=<br />
[[Image:Composite Vs. Amalgam.jpeg|thumb|250px|right|''Composite Vs. Amalgam'' From:http://www.bauerfamilydental.com [http://www.bauerfamilydental.com/services-2/cleanings/]]<br />
<br />
Treatment for tooth decay depends on how severe the decay is. One may simply be able to reverse slight tooth decay by the application of fluoride. [[#References|[12]]] When a processed sugar is consumed, the bacteria from the mouth combine with the sugar to produce an acid.This acid can erode the tooth enamel and damage teeth. Fluoride is used to protect teeth from the demineralization caused by the acid. Fluoride does this by accumulating the demineralized areas of the tooth and strengthening the enamel in a process called remineralization. Fluoride is efficient in preventing tooth decay and making teeth stronger however, it is much less effective if a cavity has already formed. [[#References|[13]]]<br />
<br>To fix cavities caused by the bacterial strain <i> Streptococcus mutans </i> a dentist will need to adequately perform either a composite filling or an amalgam filling- two of the most common fillings used today. In both types of fillings, the dentist will remove the decayed portion of the tooth and fill in the area of the tooth where the decayed area once resided. Amalgam fillings are made from a mixture of silver, tin, zinc, copper and mercury. An advantage of the amalgam filling is durability, strength and expense. Amalgam fillings are durable in the fact that they usually outlast composite fillings, and do not need to be replaced for approximately 10-15 years. These fillings are strong since they can withstand the chewing forces, and are less expensive than composite fillings. A disadvantage of the amalgam fillings is that they cause: discoloration, cracks and fractures, allergic reactions, and destroys more tooth structure. These fillings also have poor aesthetics since the silver fillings are not the color of one's natural tooth. Composite fillings are made from a mixture of plastic and fine glass particles. Some advantages of composite fillings are: aesthetics the fact that the filling closely matches the color of the tooth, the ability to bond to the tooth structure since composite fillings are chemically bonded to the tooth they provide better support, versatility not only does the material fill cavities it is also used to repair chipped, broken down teeth. Tooth-sparing preparation is also an advantage of composite fillings this is because, sometimes less tooth structure needs to be removed than what the amalgam filling will provide. Disadvantages of tooth decay include: lack of durability. Composite fillings wear out sooner than amalgam fillings lasting 5 years as opposed to 10-15 years. There is also an increase in chair time because the process to apply the filling is longer vs. the amalgam filling. Additional visits are required, chipping the composite material from the tooth, and the fact that composite fillings are double the cost of amalgam fillings. [[#References|[14]]]<br />
<br> If one experiences an extreme case of tooth decay a root canal or crown may be used. If the decay exceeds a certain level the dentist may end up needing to extract the tooth.[[#References|[14]]] The dentist will use a crown to treat the decay if the structure of the tooth is weaker than it should be. A tooth should be crowned if the filling would make up more than half the surface area of the clinical crown. A crown should also be installed if the tooth decay has traveled deep under the gum line. The dentist will choose the root canal procedure when the decayed tooth is deep and has reached the pulp of the tooth, which is the center of the tooth where the nerves are. [[#References|[15]]]<br />
<br />
=<b>Prevention</b>=<br />
[[Image:how to prevent tooth decay.jpeg|thumb|210px|right| [http://www.drchetan.com/different-plaque-removal-procedures.html]]<br />
<br />
It is a fact that every human has bacteria already existing in their mouth. The only prevention is to lessen the impact of the fermentation by product lactic acid. Brushing, flossing and reducing the intake of refined and processed sugars can accomplish this. These processed sugars come in the form of sweets, colas and processed powered sweeteners. Studies have shown that rinsing one's mouth out with water can greatly reduce the probability of cavities after the consumption of these sugars. It is almost impossible to completely reduce the effects of <i> S. mutans </i> but there is an option to control it. [[#References|[16]]]<br />
<br />
=<b>Host Immune Response</b>=<br />
<br />
<i> Streptococcus mutans </i> is the major pathogen of dental caries due to the ability to adhere and accumulate to the tooth surface. The Innate Immune Response and the Adaptive Immune Response are two fundamental aspects of the immune system that respond to infections such as dental caries. <i> Streptococcus mutans </i> enters the host through the oral route. The mucosal tissue associated with the exocrine glands and saliva contributes to the production of the oral cavity. This is because; these regions contain cells responsible for antigen internalization and antibodies specific to oral bacteria. The secretory antibodies that protect against dental caries are IgA and IgG. The Macrophages of the innate immune response are phagocytic cells that can internalize and kill bacteria by several mechanisms of internalization, which includes macropinocytosis and phagocytosis. If <i> Streptococcus mutans </i> initiates dental caries after the teeth have erupted either the host did not undergo the effective immune response of secretory IgA played a small role in preventing colonization and subsequent plaque development. [[#References|[7]]]<br />
<br />
=<b>References</b>=<br />
<br />
<br />
1 [http://www.ncl.ac.uk/dental/oralbiol/oralenv/tutorials/streps.htm Whiley, R.A., and Beighton, D. "Streptococci and Oral Streptococci." Bite-Sized Tutorials. N.p.. Web. 23 Jul 2013.]<br />
<br />2 [http://www.podj.com.pk/Dec_2012/p-28.pdf Javed, M., Chaudhry, S., Butt, S., Ijaz, S., Asad, R., Awais, F., and Khan, A., "Transmission of Streptococcus mutans from Mother to Child." Review Article. Pakistan and Oral Dental Journal vol 32, No.3, n.d. Web. 24 Jul 2013.]<br />
<br />3 [http://xenophilia.com/tooth-health-cure-for-cavities "Tooth Health: Cure for Cavities." Xenophilia.]<br />
<br />4 [http://cro.sagepub.com/content/4/2/159.full.pdf Howard, K. "Virulence factors of Mutans Streptococci: Role of Molecular genetics." Critical Reviews in Oral Biology and Medicine.] <br />
<br />5 [http://health.nytimes.com/health/guides/disease/dental-cavities) "Dental Cavities." The New York Times.]<br />
<br />6 [http://www.jyi.org/issue/the-role-of-streptococcus-mutans-and-oral-ecology-in-the-formation-of-dental-caries/) Simon, L., " The Role of Streptococcus mutans & Oral Ecology in the Formation of Dental Caries." Journal of the Young Investigators.] <br />
<br />7 [http://textbookofbacteriology.net/structure.html Todar, K. "Structure and Function of Prokaryotic Cells." Todar's Online Textbook of Bacteriology]<br />
<br />8 [http://www.brighthub.com/science/genetics/articles/45935.asp Arnold, P. "Mouth Bacteria. It's a Jungle in There." Bright Hub.]<br />
<br />9 [http://www.dentalcare.com/media/en-us/education/ce368/ce368.pdf Edward, L. "Caries Process & Prevention Strategies: Epidemiology." Dentalcare.com Continuing Education.]<br />
<br />10 [https://en.wikipedia.org/wiki/Dental_caries "Dental Caries." Wikipedia The Free Encyclopedia.] <br />
<br /> 11 [http://www.ncl.ac.uk/dental/oralbiol/oralenv/tutorials/mutans.htm "Streptococcus mutans and the mutan Streptococci."]<br />
<br /> 12 [http://www.webmd.com/oral-health/tc/tooth-decay-topic-overview "Tooth Decay-Topic Overview." Web MD.]<br />
<br /> 13 [http://www.medicalnewstoday.com/articles/154164.php "What is Fluoride? What does Fluoride Do?" Medical News Today.]<br />
<br /> 14 [http://www.webmd.com/oral-health/guide/dental-health-fillings?page=2 "Dental Health & Tooth Fillings." Web MD]<br />
<br /> 15 [http://doctorspiller.com/Fillings/fillings_5.htm Spiller, M. "When is it more appropriate to place a crown on a tooth instead of a filling?" DoctorSpiller.Com]<br />
<br /> 16 [http://web.mst.edu/~microbio/bio221_2006/S_mutans.htm Bassett, A. "Streptococcus mutans."]<br />
<br />
Created by Taylor Zelnicek, student of Tyrrell Conway at the University of Oklahoma.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91411
Plasmodium falciparum
2013-07-24T19:46:47Z
<p>Kelley.L.Raines-1: /* Life Cycle */</p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax</i>, <i>P. ovale</i>, and <i>P. malariae</i>. Humans become infected by a female Anopheles mosquito which transfers a parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. [[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <i>P. falciparum</i> to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax</i> and <i>P. ovale</i>, rather then <i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and enter erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarges followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum the infected erythrocytes do not rupture, but instead use their virulent nobs to sequester into the tissue. Due to this symptoms can be vastly more complicated leading possibly lethal symptoms.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by <i>P. falciparum</i>. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key.<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
<br/>1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
<br/>2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
<br/>3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
<br/>4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
<br/>5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
<br/>6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
<br/>7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
<br/>8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
<br/>9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
<br/>10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
<br/>11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
<br/>12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91408
Plasmodium falciparum
2013-07-24T19:43:53Z
<p>Kelley.L.Raines-1: /* Life Cycle */</p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax</i>, <i>P. ovale</i>, and <i>P. malariae</i>. Humans become infected by a female Anopheles mosquito which transfers a parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. [[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <i>P. falciparum</i> to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax</i> and <i>P. ovale</i>, rather then <i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and enter erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarges followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by <i>P. falciparum</i>. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key.<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
<br/>1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
<br/>2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
<br/>3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
<br/>4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
<br/>5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
<br/>6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
<br/>7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
<br/>8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
<br/>9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
<br/>10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
<br/>11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
<br/>12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91407
Plasmodium falciparum
2013-07-24T19:42:49Z
<p>Kelley.L.Raines-1: /* Virulence Factors */</p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax</i>, <i>P. ovale</i>, and <i>P. malariae</i>. Humans become infected by a female Anopheles mosquito which transfers a parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. [[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <i>P. falciparum</i> to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax</i> and <i>P. ovale</i>, rather then <i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and enter erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by <i>P. falciparum</i>. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key.<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
<br/>1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
<br/>2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
<br/>3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
<br/>4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
<br/>5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
<br/>6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
<br/>7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
<br/>8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
<br/>9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
<br/>10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
<br/>11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
<br/>12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91405
Plasmodium falciparum
2013-07-24T19:40:57Z
<p>Kelley.L.Raines-1: /* Infectious Dose, Incubation, Colonization */</p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax</i>, <i>P. ovale</i>, and <i>P. malariae</i>. Humans become infected by a female Anopheles mosquito which transfers a parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. [[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <i>P. falciparum</i> to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax</i> and <i>P. ovale</i>, rather then <i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and enter erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by <i>P. falciparum</i>. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key.<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
<br/>1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
<br/>2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
<br/>3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
<br/>4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
<br/>5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
<br/>6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
<br/>7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
<br/>8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
<br/>9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
<br/>10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
<br/>11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
<br/>12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91404
Plasmodium falciparum
2013-07-24T19:39:19Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax</i>, <i>P. ovale</i>, and <i>P. malariae</i>. Humans become infected by a female Anopheles mosquito which transfers a parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. [[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <i>P. falciparum</i> to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax</i> and <i>P. ovale</i>, rather then <i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by <i>P. falciparum</i>. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key.<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
<br/>1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
<br/>2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
<br/>3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
<br/>4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
<br/>5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
<br/>6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
<br/>7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
<br/>8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
<br/>9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
<br/>10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
<br/>11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
<br/>12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91403
Plasmodium falciparum
2013-07-24T19:37:33Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax</i>, <i>P. ovale</i>, and <i>P. malariae</i>. Humans become infected by a female Anopheles mosquito which transfers a parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <i>P. falciparum</i> to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax</i> and <i>P. ovale</i>, rather then <i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by <i>P. falciparum</i>. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key.<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
<br/>1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
<br/>2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
<br/>3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
<br/>4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
<br/>5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
<br/>6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
<br/>7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
<br/>8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
<br/>9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
<br/>10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
<br/>11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
<br/>12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91402
Plasmodium falciparum
2013-07-24T19:36:02Z
<p>Kelley.L.Raines-1: /* References */</p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax</i>, <i>P. ovale</i>, and <i>P. malariae</i>. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <i>P. falciparum</i> to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax</i> and <i>P. ovale</i>, rather then <i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by <i>P. falciparum</i>. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key.<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
<br/>1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
<br/>2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
<br/>3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
<br/>4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
<br/>5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
<br/>6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
<br/>7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
<br/>8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
<br/>9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
<br/>10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
<br/>11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
<br/>12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91401
Plasmodium falciparum
2013-07-24T19:35:37Z
<p>Kelley.L.Raines-1: /* References */</p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax</i>, <i>P. ovale</i>, and <i>P. malariae</i>. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <i>P. falciparum</i> to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax</i> and <i>P. ovale</i>, rather then <i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by <i>P. falciparum</i>. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key.<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
<br/>1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
<br/>2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
<br/>3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
<br/>4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
<br/>5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
<br/>6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
<br/>7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
<br/>8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
<br/>9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
<br/>10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
<br/>11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
<br/>12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91399
Plasmodium falciparum
2013-07-24T19:34:21Z
<p>Kelley.L.Raines-1: /* Transmission */</p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax</i>, <i>P. ovale</i>, and <i>P. malariae</i>. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <i>P. falciparum</i> to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax</i> and <i>P. ovale</i>, rather then <i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by <i>P. falciparum</i>. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key.<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91398
Plasmodium falciparum
2013-07-24T19:33:49Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax</i>, <i>P. ovale</i>, and <i>P. malariae</i>. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <br />
<i>P. falciparum</i><br />
to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax</i> and <i>P. ovale</i>, rather then <i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by <i>P. falciparum</i>. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key.<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91397
Plasmodium falciparum
2013-07-24T19:33:11Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax<i>, <I>P. ovale<i>, and <i>P. malariae<i>. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <br />
<i>P. falciparum</i><br />
to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax</i> and <i>P. ovale</i>, rather then <i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by <i>P. falciparum</i>. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key.<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91396
Plasmodium falciparum
2013-07-24T19:31:36Z
<p>Kelley.L.Raines-1: /* Treatment */</p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax<i>, <I>P. ovale<i>, and <i>P. malariae<i>. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <br />
<i>P. falciparum</i><br />
to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax<i> and <i>P. ovale<i>, other strains of Malaria, rather then <br />
<i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by <i>P. falciparum</i>. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key.<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91395
Plasmodium falciparum
2013-07-24T19:31:03Z
<p>Kelley.L.Raines-1: /* Morbidity and Mortality */</p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax<i>, <I>P. ovale<i>, and <i>P. malariae<i>. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <br />
<i>P. falciparum</i><br />
to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax<i> and <i>P. ovale<i>, other strains of Malaria, rather then <br />
<i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by <i>P. falciparum</i>. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. ==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91394
Plasmodium falciparum
2013-07-24T19:29:38Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
<i>Plasmodium falciparum</i> is a protozoan parasite that causes an infectious disease know as malaria. <i>P. falciparum</i> is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include <i>P. vivax<i>, <I>P. ovale<i>, and <i>P. malariae<i>. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. <i>P. falciparum</i> changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. <i>Plasmodium falciparum</i> mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of <i>P. falciparum</i> occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with <i>Plasmodium falciparum</i> it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass <br />
<i>P. falciparum</i><br />
to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in <i>P.vivax<i> and <i>P. ovale<i>, other strains of Malaria, rather then <br />
<i>P. falciparum</i>.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of <br />
<i>P. falciparum</i> are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. <i>Plasmodium falciparum</i> continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1,<i>P. falciparum</i> erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a <i>P. falciparum</i> infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each <i>Plasmodium falciparum</i> has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of <i>Plasmodium falciparum</i> mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of <i>P. falciparum</i> actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
<i>P. falciparum</i> normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine <i>Plasmodium falciparum</i> as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of <i>P.falciparum</i>are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of <i>P. falciparum</i> depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. ==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for <i>Plasmodium falciparum</i>. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of <i>Plasmodium falciparum</i> is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of <i>P. falciparum</i> have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91393
Plasmodium falciparum
2013-07-24T19:17:35Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each Plasmodium falciparum has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.[[#References|[11]]]<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection. [[#References|[3]]]<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of Plasmodium falciparum is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of P. falciparum have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications. [[#References|[12]]]<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
12 Hommel, M, P H David, and L D Oligino. "Surface Alterations Of Erythrocytes In Plasmodium Falciparum Malaria. Antigenic Variation, Antigenic Diversity, And The Role Of The Spleen." The Journal Of Experimental Medicine 157.4 (1983): 1137-1148. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91392
Plasmodium falciparum
2013-07-24T19:09:36Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each Plasmodium falciparum has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance.[[#References|[11]]] <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of Plasmodium falciparum is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of P. falciparum have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications.<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
11 Kakkilaya, . "Treatment of Malaria." Malaria Site. N.p., 16 05 2012. Web. 24 Jul 2013. <http://www.malariasite.com/malaria/Treatment4.htm>. <br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91391
Plasmodium falciparum
2013-07-24T18:56:39Z
<p>Kelley.L.Raines-1: /* Diagnosis */</p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each Plasmodium falciparum has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots. [[#References|[1]]]<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of Plasmodium falciparum is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of P. falciparum have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications.<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91390
Plasmodium falciparum
2013-07-24T18:55:55Z
<p>Kelley.L.Raines-1: /* Morbidity and Mortality */</p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each Plasmodium falciparum has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum. [[#References|[1]]]<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of Plasmodium falciparum is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of P. falciparum have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications.<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91389
Plasmodium falciparum
2013-07-24T18:53:41Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each Plasmodium falciparum has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.[[#References|[8]]]<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people.[[#References|[9]]] <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.[[#References|[10]]]<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.[[#References|[1]]]<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of Plasmodium falciparum is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of P. falciparum have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications.<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
8 Ogobara K. Doumbo, et al. "The Pathogenic Basis Of Malaria." Nature 415.6872 (2002): 673. Academic Search Premier. Web. 24 July 2013. <br />
9 Wiser, . "Plasmodium Life Cycle." . N.p.. Web. 24 Jul 2013. <http://www.tulane.edu/~wiser/malaria/mal_lc.PDF>. <br />
10 Rick M Fairhurst, et al. "Impaired Cytoadherence Of Plasmodium Falciparum-Infected Erythrocytes Containing Sickle Hemoglobin." Proceedings Of The National Academy Of Sciences Of The United States Of America 105.3 (2008): 991-996. MEDLINE. Web. 24 July 2013.<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91387
Plasmodium falciparum
2013-07-24T18:41:03Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each Plasmodium falciparum has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation.[[#References|[6]]]Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes.[[#References|[6]]] RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria.[[#References|[7]]] <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of Plasmodium falciparum is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of P. falciparum have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications.<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>. <br />
6 Bultrini, Emanuele . "Revisiting the Plasmodium falciparum RIFIN family: from comparative genomics to 3D-model prediction." BMC Genomics. N.p., 20 09 2009. Web. 24 Jul 2013. <http://www.biomedcentral.com/1471-2164/10/445>.<br />
7 Ho M, Davis TME, Silamut K, Bunnang D, White NJ. Rosette formation of Plasmodium falciparum-infected erythrocytes from patients with acute malaria. Infect Immun. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC257977/><br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91386
Plasmodium falciparum
2013-07-24T18:23:56Z
<p>Kelley.L.Raines-1: /* Virulence Factors */</p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. The protein is responsible for sequestration within the vital organs. In some case were sequestration occurs in the brain this will lead to the cerebral form of malaria. Each Plasmodium falciparum has multiple versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]]<br />
<br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of Plasmodium falciparum is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of P. falciparum have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications.<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>.<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91385
Plasmodium falciparum
2013-07-24T18:12:54Z
<p>Kelley.L.Raines-1: /* Host Immune Response */</p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
A key feature to the virulence of Plasmodium falciparum is antigenic diversity. This is the parasites ability to switch erythrocyte- associated antigens, thus evading the immune system. The alteration between antibodies only occurs in the trophozoite/schizont stage in the erythrocyte. The switch in erythrocites surface antigens as well as multiple strains of P. falciparum have prevented the creation of a vaccine. Plasmodium falciparum's clever avoidance of the spleen and immune system has created a parasite almost impossible to eradicate from the host without anti-malaria medications.<br />
<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>.<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91166
Plasmodium falciparum
2013-07-24T07:25:39Z
<p>Kelley.L.Raines-1: /* References */</p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html>.<br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.>. <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm>. <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm>.<br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637>.<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91165
Plasmodium falciparum
2013-07-24T07:23:17Z
<p>Kelley.L.Raines-1: /* Epidemiology */</p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts.[[#References|[1]]] Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889.[[#References|[3]]] There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html><br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.> <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm> <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm><br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637><br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91164
Plasmodium falciparum
2013-07-24T07:20:00Z
<p>Kelley.L.Raines-1: /* Infectious Dose, Incubation, Colonization */</p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication.[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum.[[#References|[1]]] The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html><br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.> <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm> <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm><br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637><br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91163
Plasmodium falciparum
2013-07-24T07:17:53Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication..[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html><br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.> <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm> <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm><br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. <https://www.ncbi.nlm.nih.gov/pubmed/22632637><br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91162
Plasmodium falciparum
2013-07-24T07:16:59Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication..[[#References|[5]]] The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html><br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.> <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm> <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm><br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. doi:10.1016/j.idc.2012.03.010. PMID 22632637<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91161
Plasmodium falciparum
2013-07-24T07:15:34Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html><br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.> <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm> <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm><br />
5 Nadjm B, Behrens RH (2012). "Malaria: An update for physicians". Infectious Disease Clinics of North America 26 (2): 243–59. doi:10.1016/j.idc.2012.03.010. PMID 22632637<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91160
Plasmodium falciparum
2013-07-24T07:11:52Z
<p>Kelley.L.Raines-1: /* Transmission */</p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by mosquito vectors from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. [[#References|[1]]] Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence.<br />
<br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html><br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.> <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm> <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm><br />
5 <br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91159
Plasmodium falciparum
2013-07-24T07:10:23Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by vectors such as Anopheles gambiae, Anopheles albimanus, Anopheles freebomi, Anopheles maculatus, and Anopheles stephensi which transfer from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. [[#References|[4]]] Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. <br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html><br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.> <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm> <br />
4 Vareil M-O, Tandonnet O, Chemoul A, Bogreau H, Saint-Léger M, Micheau M, et al. Unusual transmission of Plasmodium falciparum, Bordeaux, France, 2009. Emerg Infect Dis [CDC Emerging Infectious Disease]. 2011 Feb [07/24/2013]. <http://wwwnc.cdc.gov/eid/article/17/2/10-0595_article.htm><br />
5 <br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91158
Plasmodium falciparum
2013-07-24T06:59:46Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by vectors such as Anopheles gambiae, Anopheles albimanus, Anopheles freebomi, Anopheles maculatus, and Anopheles stephensi which transfer from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. <br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html><br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.> <br />
3 Davis, Charles. "Medicine Net On Health." Malaria. William shiel. Web. 24 Jul 2013. <http://www.onhealth.com/malaria/article.htm> <br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91157
Plasmodium falciparum
2013-07-24T06:55:09Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by vectors such as Anopheles gambiae, Anopheles albimanus, Anopheles freebomi, Anopheles maculatus, and Anopheles stephensi which transfer from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. <br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html><br />
2 Cross, Caroline. "Welcome Trust." Malaria, Plasmodium flaciparum. N.p., 08 11 2004. Web. 24 Jul 2013. <http://malaria.wellcome.ac.uk.> <br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91153
Plasmodium falciparum
2013-07-23T22:39:27Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death.[[#References|[1]]] The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells.[[#References|[2]]] In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%.[[#References|[3]]] <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by vectors such as Anopheles gambiae, Anopheles albimanus, Anopheles freebomi, Anopheles maculatus, and Anopheles stephensi which transfer from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. <br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 Centers for Disease Control and Prevention (2012), Malaria <http://www.cdc.gov/malaria/about/disease.html><br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91084
Plasmodium falciparum
2013-07-23T18:12:31Z
<p>Kelley.L.Raines-1: /* Sickle Cell Resistance */</p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death. The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells. In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%. <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by vectors such as Anopheles gambiae, Anopheles albimanus, Anopheles freebomi, Anopheles maculatus, and Anopheles stephensi which transfer from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. <br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
Sickle cell individuals have shown to rarely contract malaria. Research has shown that this is partially due to weakened binding of parasite infested sickle cell erythrocytes to microvasculare endothelial cells when compared to normal hemoglobin parasite erythrocytes binding. The virulence factor PfEMP1 that normally conducts cytoadherence is altered creating a weekend attachment between it and the epithelial wall. Due to the ability to attach lacking, sequestration would also not occur limiting the severe malarial response. The mechanism for how this is done is still unknown and needs further research.<br />
<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
[Sample reference] [http://ijs.sgmjournals.org/cgi/reprint/50/2/489 Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "''Palaeococcus ferrophilus'' gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". ''International Journal of Systematic and Evolutionary Microbiology''. 2000. Volume 50. p. 489-500.]<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91065
Plasmodium falciparum
2013-07-23T17:39:43Z
<p>Kelley.L.Raines-1: /* Life Cycle */</p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death. The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells. In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%. <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by vectors such as Anopheles gambiae, Anopheles albimanus, Anopheles freebomi, Anopheles maculatus, and Anopheles stephensi which transfer from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. <br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue which can limit oxygen to other areas of the body.<br />
<br />
==Sickle Cell Resistance==<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
[Sample reference] [http://ijs.sgmjournals.org/cgi/reprint/50/2/489 Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "''Palaeococcus ferrophilus'' gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". ''International Journal of Systematic and Evolutionary Microbiology''. 2000. Volume 50. p. 489-500.]<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91060
Plasmodium falciparum
2013-07-23T17:29:45Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death. The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells. In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%. <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by vectors such as Anopheles gambiae, Anopheles albimanus, Anopheles freebomi, Anopheles maculatus, and Anopheles stephensi which transfer from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. <br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin) is released during erythrocyte rupture. Cause the uncomplicated symptoms of malaria such as chills and fever.<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue.<br />
<br />
==Sickle Cell Resistance==<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
[Sample reference] [http://ijs.sgmjournals.org/cgi/reprint/50/2/489 Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "''Palaeococcus ferrophilus'' gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". ''International Journal of Systematic and Evolutionary Microbiology''. 2000. Volume 50. p. 489-500.]<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91059
Plasmodium falciparum
2013-07-23T17:25:44Z
<p>Kelley.L.Raines-1: /* Life Cycle */</p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death. The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells. In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%. <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by vectors such as Anopheles gambiae, Anopheles albimanus, Anopheles freebomi, Anopheles maculatus, and Anopheles stephensi which transfer from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. <br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin)<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
The life cycle of malaria is a complex process infecting two hosts, human and mosquito. The process begins when a infected mosquito transfering saliva as well as sporozoites into an individuals circulatory system. These sporozoites travel to the liver and invade hepatocytes. In the liver asexual reproduction occurs through exoerythrocytic schizogony, which produces merozoites that are released back into the blood. From here the merozoites invade an erythrocytes and begin the trophic period. During this period the trophozite enlarge followed buy multiple rounds of asexual nuclear division to a schizont. Merozoites bud from the schizont and eventually rupture the erythrocyte releasing toxins that cause the simple symptoms of malaria, fever and chills. Merozoites eventually invade another erythrocyte which begins another round of the blood stage replication. Some erythrocytes change into gametocytes capable of doing sexual reproduction. These cells do not lyse but instead are taken up but the next mosquito that bites, infecting the mosquito and possible more people. <br />
<br />
In severe cases caused by P. falciparum symptoms can be vastly more complicated leading to coma and possibly death. This is due to trophoziote and schizout be sequestered into deep tissue.<br />
<br />
==Sickle Cell Resistance==<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
[Sample reference] [http://ijs.sgmjournals.org/cgi/reprint/50/2/489 Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "''Palaeococcus ferrophilus'' gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". ''International Journal of Systematic and Evolutionary Microbiology''. 2000. Volume 50. p. 489-500.]<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91011
Plasmodium falciparum
2013-07-23T16:26:44Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death. The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells. In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%. <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by vectors such as Anopheles gambiae, Anopheles albimanus, Anopheles freebomi, Anopheles maculatus, and Anopheles stephensi which transfer from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. <br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin)<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
==Sickle Cell Resistance==<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
[Sample reference] [http://ijs.sgmjournals.org/cgi/reprint/50/2/489 Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "''Palaeococcus ferrophilus'' gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". ''International Journal of Systematic and Evolutionary Microbiology''. 2000. Volume 50. p. 489-500.]<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=91010
Plasmodium falciparum
2013-07-23T16:26:22Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death. The other 3 species that cause malaria include P. vivax, P. ovale, and P. malariae. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells. In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as pregnant women. With treatment of antimalarials the death rate drops drastically from almost 100% to 20%. <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
===History===<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by vectors such as Anopheles gambiae, Anopheles albimanus, Anopheles freebomi, Anopheles maculatus, and Anopheles stephensi which transfer from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. <br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin)<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
==Sickle Cell Resistance==<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
[Sample reference] [http://ijs.sgmjournals.org/cgi/reprint/50/2/489 Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "''Palaeococcus ferrophilus'' gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". ''International Journal of Systematic and Evolutionary Microbiology''. 2000. Volume 50. p. 489-500.]<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=90949
Plasmodium falciparum
2013-07-23T12:29:05Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells. In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as fetuses. With treatment of antimalarials the death rate drops drastically to 20%. <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
===History===<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by vectors such as Anopheles gambiae, Anopheles albimanus, Anopheles freebomi, Anopheles maculatus, and Anopheles stephensi which transfer from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. <br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin)<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Life Cycle==<br />
==Sickle Cell Resistance==<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
[Sample reference] [http://ijs.sgmjournals.org/cgi/reprint/50/2/489 Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "''Palaeococcus ferrophilus'' gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". ''International Journal of Systematic and Evolutionary Microbiology''. 2000. Volume 50. p. 489-500.]<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=90947
Plasmodium falciparum
2013-07-23T12:27:44Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells. In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as fetuses. With treatment of antimalarials the death rate drops drastically to 20%. <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
===History===<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by vectors such as Anopheles gambiae, Anopheles albimanus, Anopheles freebomi, Anopheles maculatus, and Anopheles stephensi which transfer from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. <br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin)<br />
==Life Cycle==<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Sickle Cell Resistance==<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]]<br />
===Risk Avoidance=== <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
[Sample reference] [http://ijs.sgmjournals.org/cgi/reprint/50/2/489 Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "''Palaeococcus ferrophilus'' gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". ''International Journal of Systematic and Evolutionary Microbiology''. 2000. Volume 50. p. 489-500.]<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=File:Control.jpg&diff=90944
File:Control.jpg
2013-07-23T12:25:31Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div></div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=Plasmodium_falciparum&diff=90943
Plasmodium falciparum
2013-07-23T12:24:41Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div>{{Curated}}<br />
Plasmodium falciparum is a protozoan parasite that causes an infectious disease know as malaria. P. falciparum is the most severe of the malaria species correlated with almost every malarial death. Humans become infected by a female Anopheles mosquito which transfers to parasitic vector through its saliva into the blood stream. The parasite then infects the liver and undergoes asexual reproduction followed by insertion into red blood cells where an additional round of replication takes place. P. falciparum changes the surface of an infected red blood cell causing it to stick to blood vessels, cytoadherence, as well as to other red blood cells. In severe cases this leads to obstructions of microcirculation resulting in dysfunction of many organs. Symptoms depend on severity of infection and can present a range of signs such as flulike symptoms, vomiting diarrhea, shock, kidney failure, coma, and death. Plasmodium falciparum mostly infects children under the age of 5 as well as fetuses. With treatment of antimalarials the death rate drops drastically to 20%. <br />
[[Image:Plasmodium_general.jpg|thumb|300px|right|Trophozoites of P. falciparum in thin blood smears. From: [http://www.dpd.cdc.gov/dpdx/HTML/Frames/M-R/Malaria/falciparum/body_malariadffalctrop.htm]]] <br />
__TOC__<br />
<br />
==Etiology/Bacteriology==<br />
===Taxonomy===<br />
| Domain = [[Eukarya]]<br />
| Kingdom = [[Chromalveolata]]<br />
| Phylum = [[Apicomplexa]]<br />
| Class = [[Aconoidasida]]<br />
| Order = [[Haemosporida]]<br />
| Family = [[Plasmodiidae]]<br />
| Genus = [[Plasmodium]]<br />
| Species = [[P. falciparum]]<br />
<br />
===History===<br />
==Pathogenesis==<br />
===Transmission===<br />
[[Image:Anopheles_stephensi_jpeg.jpeg|thumb|200px|right|An Anopheles stephensi mosquito. From: [https://en.wikipedia.org/wiki/Malaria]]]<br />
Transmission of P. falciparum occurs between humans and Anopheles mosquitos. Malaria is passed by vectors such as Anopheles gambiae, Anopheles albimanus, Anopheles freebomi, Anopheles maculatus, and Anopheles stephensi which transfer from host to host. The parasite can infect the mosquitos through the in take of human blood or a human by the mosquitos injection of saliva into the human. Once the mosquito becomes infected with Plasmodium falciparum it transfers the disease to each new host it penetrates. Humans can rarely transfer the parasite between each other. There have been rare cases of contaminated transfused blood infecting the recipient, but seldom does this occur because of screening that takes place pre-blood donation. Mothers can also pass P. falciparum to their child during birth, this is also a seldom occurrence. <br />
===Infectious Dose, Incubation, Colonization===<br />
Symptoms of Malaria typically begin 8-25 days following infection, in few cases it can take up to a year. The late onset of incubation is due to taking an inadequate amount of anti-malaria medication. The infectious dose is not precisely known, but it is understood to be a very low number. Malaria can be observed months to years after first set of symptoms are observed. This is due to the parasites ability to lie dormant in liver cells until the environment is right for a relapse. This is mainly seen in P.vivax and P. ovale, other strains of Malaria, rather then P. falciparum. The parasite colonizes in the liver and is then released into the blood stream and attached to erythrocytes.<br />
<br />
===Epidemiology===<br />
The key to Malaria-endemic is Anopheles mosquitos ability to live in an area. Temperature is also important having to stay above 20 degrees Celsius. The main areas of P. falciparum are South America, Africa, India, and few parts of Indonesia. The best possible location is along the equator in a warmer region. Transmission will not occur in high altitudes, colder seasons, and deserts. Malaria is thought to have been around since the beginning of mankind, but was first discovered in blood in 1880 and found to be transmitted by mosquitos in 1889. There are four common species of Malaria of which P. falciparum is the most severe. Plasmodium falciparum continues to increase in drug-resistant populations and insecticide-resistant mosquitos leading to the prediction that the disease will only worsen over time.<br />
<br />
===Virulence Factors===<br />
PfEMP1, P.falciparum erythrocye membrane protein 1, is an adhesive ligand protein which is created inside of a P. falciparum infected erythrocyte and presented on the surface. PfEMP1 is known as a knob and is encoded by the multigene segment, Var. Sequestration occurs when the parasite infected blood cells adhere to vascular endothelium which leads to further adherence of P. falciparum in deep microvasculature of tissues and organs. Each Plasmodium falciparum has roughly 50 versions of PfEMP1 with which it can alter its appearance by changing to another PfEMP1 when the immune system begins to create antibodies for the original PfEMP1 in a process known as antigenic variation. Changing of adherence molecules also means a change in the receptor on the epithelial. The change in receptor is hypothesized to possible change the disease outcome. <br />
<br />
RIFIN, repetitive interspersed family, is considered the most abundant multigene family. PfEMP1 along with RIFIN is considered a crucial cornerstones for the virulence of Plasmodium falciparum mainly due to its ability to avoid immune response through antigenic variability and ultimately colonizing and replicating in the liver and erythrocytes. RIFIN is also presented on the outer membrane of an parasite infected erythrocye as an adherence factor. <br />
<br />
Rosettes are uninfected red blood cells that form clumps with Malaria-infected erythrocytes. Clumping occurs when particularly sticky PfEMP1 attach to other red blood cells. Only a minority of P. falciparum actually creates rosettes, but when they do they are known to be linked to severe malaria. <br />
<br />
Malaria pigment (hemozoin)<br />
==Life Cycle==<br />
<br />
[[Image:malaria_lifecycle.gif|thumb|200px|right|CDC illustration of the life cycles of malaria parasites, Plasmodium spp. SOURCE: CDC. From: [http://www.onhealth.com/malaria/page3.htm#how_is_malaria_transmitted]]] <br />
==Sickle Cell Resistance==<br />
==Clinical features==<br />
===Symptoms===<br />
Malaria normally proceeds in two forms, uncomplicated or severe. In most occurrence the severe case is observed showing symptoms such as cerebral malaria, which cause abnormal behavior, seizures, coma, or impairment of consciousness. Severe symptoms also present anemia due to destruction of red blood cells, hemoglobinuria, acute respiratory distress, low blood pressure, acute kidney failure, metabolic acidosis, and hypoglycemia. These are all due to organ failure and abnormalities in patient's blood or metabolism. <br />
<br />
During a rare uncomplicated infection, symptoms appear flu-like. The attack lasts roughly 6-10 hours presenting a cold stage, hot stage, and sweat stage. During these stages one shows symptoms of fever, chills, sweats, headache, nausea, vomiting, body ached, and malaise.<br />
<br />
===Morbidity and Mortality===<br />
In 2010 malaria was diagnosed for 219 million people and killed 660,000 people. Roughly 70% being 5 years or younger and 75% of these cases were caused by P. falciparum.<br />
<br />
Pregnant women are at higher risk for a more severe reaction to themselves and the fetus. In some cases malaria my cause prematurity, abortion, and stillbirth.<br />
<br />
Young children are also at higher risk for more severe infections due to the immaturity of their immune systems.<br />
<br />
==Diagnosis==<br />
Rapid and accurate diagnosis using microscopic examination of blood smears is the most precise way to determine Plasmodium falciparum as the disease. CDC provides various references for microscope diagnosis along with serology, PCR, and drug resistance testing. Each species of P. falciparum has distinctive characteristics that can be see under a microscope. In only early form, trophozites and gametocytes of P. falciparum are seen in the blood as ring form inside the erythrocyte. There are normally multiple parasites in one erythrocytes appearing as several dots.<br />
<br />
==Treatment==<br />
The best line of defense against any form of malaria is preventative treatment, antimalarial, taken properly before, during, and after exposure to parasite. <br />
<br />
Treatment of P. falciparum depends on severity of infection as well as location where the infection took place. Treatment can also vary due to an individuals age, weight, and pregnancy status. <br />
<br />
In uncomplicated malaria, the first line of defense includes Artemisinin-based combination therapy (ACT). ACTs are used to improve treatment by overcoming the resistance by using more then one derivative of Artemisinin. The choice of which ACT to use depends on the region in which the infection took place. This is due to the varying level of resistance found in different areas. <br />
<br />
Non-ACTs such as sulfadoxine-pyrimethamin with chloroquine can also be used but are considered to have a limited sufficiency due to drug resistance. <br />
<br />
In severe malaria, the main focus is to keep the patient from dying. Rapid clinical assessment and confirmation are key. If P. falciparum goes untreated the death rate is 100%, but if treated with proper intravenous antimalarials the death rate drops to 15%-20%. The use of cinchona alkaloids and artemisinin derivatives are thought to be the best antimalarials and should be used immediately pending diagnosis.<br />
<br />
==Prevention==<br />
===Risk Avoidance===<br />
[[Image:control.jpg|thumb|230px|right| From: [http://www.malariasite.com/malaria/ControlOfMalaria.htm]]] <br />
In 1992, the W.H.O. redirected the strategy towards malaria from vector control to treatment. The control of malaria entails 3 living beings: human, mosquito, and vector. Each has its own complications and if treated properly ability to stop the cycle of malaria. For successful malaria control it is now believe to target man first, mosquitoes next followed by the parasite. The web of interact allows the control of malaria on one of these systems to complement the others.<br />
<br />
===Immunization===<br />
Studies are still on going for an immunization for Plasmodium falciparium. The prospects of a vaccine do not look promising due to infected individuals never developing sterilizing immunity. The parasite has an impressive ability to avoid and suppress the immune system never allowing it to create the proper antibodies to fight the infection.<br />
<br />
==Host Immune Response==<br />
==References==<br />
[Sample reference] [http://ijs.sgmjournals.org/cgi/reprint/50/2/489 Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "''Palaeococcus ferrophilus'' gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". ''International Journal of Systematic and Evolutionary Microbiology''. 2000. Volume 50. p. 489-500.]<br />
<br />
Created by {Kelley Raines}, students of Tyrrell Conway at the University of Oklahoma.<br />
<br />
This template is just a general guideline of how to design your site. You are not restricted to this format, so feel free to make changes to the headings and subheadings and to add or remove sections as appropriate.</div>
Kelley.L.Raines-1
https://microbewiki.kenyon.edu/index.php?title=File:Systom_Malaria.png&diff=90870
File:Systom Malaria.png
2013-07-23T10:09:01Z
<p>Kelley.L.Raines-1: </p>
<hr />
<div></div>
Kelley.L.Raines-1