https://microbewiki.kenyon.edu/api.php?action=feedcontributions&user=Magdalene.C.Shaughnessy-1&feedformat=atommicrobewiki - User contributions [en]2024-03-28T10:40:05ZUser contributionsMediaWiki 1.39.6https://microbewiki.kenyon.edu/index.php?title=H5N1_Influenza_A&diff=91476H5N1 Influenza A2013-07-24T21:39:27Z<p>Magdalene.C.Shaughnessy-1: /* Antiviral Chemoprohylaxis */</p>
<hr />
<div>{{Curated}}<br />
<br />
[[Image:OULOGOBIANCO.JPEG|thumb|230px|right|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]<br />
<br />
==Etiology/Bacteriology==<br />
===<i>Taxonomy</i>===<br />
<br>| Domain = [[Viruses]] <br />
<br>| Class = [[ssRNA viruses]]<br />
<br>| Order = [[ssRNA negative strand viruses]]<br />
<br>| Family = [[Orthomyxoviridae]]<br />
<br>| Genus = [[Influenzavirus A]]<br />
<br>| species = [[Influenza A virus]]<br />
<br />
{|<br />
| height="10" bgcolor="#FFDF95" |<br />
'''NCBI: [http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=102793&lvl=3&lin=f&keep=1&srchmode=1&unlock] Genome: [[Influenza A Virus H5N1]] <font size="2">[http://www.ncbi.nlm.nih.gov/genome/10290?project_id=15617]</font>'''<br />
|}<br />
<br />
===<i>Description</i>===<br />
<br />
[[Image: H5N1 Flu.jpg |thumb|400px|right| Avian Influenza A (H5N1) virus particles, TEM <br /> From: http://urbantimes.co/magazine/2010/12/artificial-intelligents/h5n1-avian-influenza-virus-particles-tem/]]<br />
<br />
Avian Influenza A (H5N1) is a type of influenza virus responsible for causing severe respiratory disease in birds, generally waterfowl, and humans. However, researchers have yet to definitively document human-to-human transmission and victims of avian-to-human transmission generally spend substantial amounts of time around birds (like poultry farm workers, migratory duck herders, etc.) There is a growing level of concern about the virus because of its high mortality rate and its predisposition to mutation. This renders the human adaptive immune response fairly inadequate against the infection, and the virus has the potential to be devastating to the human population if it were to mutate to a strain capable of human-to-human transmission. Symptoms of H5N1 infection include high fever (>38°C), malaise, cough, sore throat, muscle aches, abdominal or chest pain, and diarrhea. The sequelae of H5N1 infection are often severe respiratory illness including pneumonia and acute respiratory distress syndrome as well as neurological changes like altered mental state and seizures. Treatment often involves implementation of the antiviral medication oseltamivir. At this stage, all vaccinations are still experimental [[#References|[1]]].<br />
<br />
==Pathogenesis==<br />
===<i>Transmission</i>===<br />
Transmission of H5N1 primarily occurs via direct avian-to-human contact. Major risk factors include handling diseased poultry and the consumption of raw or undercooked poultry products. The exact mode and sites of infection in the respiratory tract remain unknown. H5N1 also has several mammalian hosts including cats, dogs, and ferrets. None have been shown to transmit the disease to humans. However, a genetically modified strain of the virus was capable of airborne transmission in ferrets, which gives insight into the possibility of human-to-human transmission [[#References|[2]]]. The mode of transmission remains unclear for about one quarter of infected patients and environment-to-human transmission has not been ruled out. It is still uncertain whether infection can begin in the gastrointestinal tract, but it has been implicated in other mammals and is an open area of research.<br />
<br />
===<i>Infectious Dose, Incubation, and Epidemiology</i>===<br />
====Infectious Dose====<br />
There is not a definitive known infectious dose for H5N1 and it is likely dependent on a number of host factors like age, race, genes, and location. However, it seems clear that a low number of viral particles can proliferate extremely successfully once they have become bound in the respiratory tract.<br />
<br />
====Incubation====<br />
The incubation period for H5N1 infection is generally 7 days or less, many times as little as 2-5 days. In cases where human-to-human transmission likely occurred the average is 3 days. However, some reports estimate as long as 8-9 days.<br />
<br />
====Epidemiology====<br />
The first documented case of H5N1 was in a 3-year-old boy in Hong Kong SAR that promptly died from respiratory failure in 1997. By the end of 1997, 18 people had succumbed to the virus. There have been about 600 reported cases of H5N1 infection since 1997 and the virus reemerges periodically, infecting clustered regions of people who are generally related or in very close proximity. The median age of infected persons is 18 and 90% of patients are under 40 and healthy. Mortality is estimated to be 61% and is highest in the 10-19 year age range. Interestingly, observed cases typically occur in cooler months but are often correlated with outbreaks in poultry. Despite likely widespread human exposure, human infections remain relatively rare [[#References|[3]]].<br />
<br />
===<i>Virulence Factors</i>===<br />
<br />
[[Image: Ha sialic acid.png |thumb|400px|right| A single amino acid change switches avian influenza H5N1 and H7N9 viruses to human receptors <br /> From: http://www.virology.ws/2013/06/11/a-single-amino-acid-change-switches-avian-influenza-h5n1-and-h7n9-viruses-to-human-receptors/]]<br />
<br />
Avian influenza A viruses are enveloped, single stranded negative sense RNA viruses that contain 8 segments of RNA that code for 10 proteins. They have surface antigens called haemagglutinin (HA) and neuraminidase (NA) that are responsible for binding to host tissue. There are 16 subtypes of haemagglutinin and neuraminidase and their genes appear to have a synergistic effect on virulence. Researchers have identified 15 amino acid residues from 4 influenza virus genes from the 1997 Hong Kong strain that seemed to determine high- versus low-pathogenic phenotypes. Furthermore, the absence of glycosylation sites at aa154 in the HA gene result in increased virulence. H5N1 strains isolated from humans have an acquired mutation that permits binding to both ∝2,3-linked sialic acid receptors and ∝2,6-linked sialic acid receptors that also produce increased virulence. However, it seems that the virus will require a mutations in a number of genes in order to confer effective human-to-human transmission.<br />
<br />
==Clinical features==<br />
H5N1 infections typically manifest as severe pneumonia that rapidly progresses in to acute respiratory distress syndrome. The time from on set of infection to death is generally 9 days with fatality percentages ranging from 50-80% depending on the region of the cluster outbreak. Some febrile upper respiratory illness has occurred without pneumonia more frequently since 2005, but this is likely due to increased administration of antivirals. Other commonly related conditions include leucopenia, lymphopenia, mild-to-moderate thrombocytopenia, and elevated levels of aminotransferases as well as elevated levels of lactate dehydrogenase, creatine phosphokinase, hypoalbuminemia, and d-dimer levels. The very non-specific nature of the clinical presentation often results in misdiagnosis [[#References|[4]]]. <br />
<br />
==Diagnosis==<br />
<br />
[[Image: Diagnostic.gif |thumb|400px|right| Viral titers obtained from various regions of red foxes infected with H5N1 <br /> From: http://www.medscape.com/viewarticle/584804_3]]<br />
<br />
Conventional or real-time reverse-transcriptase PCR is the best method under biohazard level 2 conditions. Primers need to be continuously updated, given the high rate at which the virus mutates. Most often primers are engineered to target mutations in the H5 haemagglutinin gene. Diagnostic yields are generally highest from throat specimens rather than nasal swabs because viral loads are usually highest in the throat. A single negative result should not rule out H5N1 infection and multiple samples should be taken. Samples can also be taken from the blood and stool, but they generally have lower diagnostic sensitivity. The detection of anti-H5 antibodies is requisite for diagnosis and microneutralization assays are typically the most reliable method for recognition. However, it should be noted that microneutralization is labor intensive and required biohazard level 3 conditions. Furthermore, haemagglutinin-inhibition assays that use erythrocytes from horses are a promising diagnostic option, but require further investigation.<br />
<br />
==Treatment==<br />
===<i>Antiviral Agents</i>===<br />
Many forms of influenza A virus are susceptible, at least to some extent, to antiviral agents. Oseltamivir, marketed under the tradename Tamiflu, is a neurominidase inhibitor that is most often administered in H5N1 infection cases. However, the dosage is dependent on the strain’s rate of replication, as many oseltamivir-susceptible strains have high rates of replication. The general regimen presecribed for H5N1 infection, when prescribed early (1-3 days after onset of infection), is 75 mg twice daily for 5 days. Other potential treatment involve a combination of oseltamivir and amantadine or zanamivir (in cases where strains are oseltamivirR) depending on the nature of the infecting strain and the stage of the patient’s illness.<br />
<br />
===<i>Other Treatments</i>===<br />
Management of hypoxemia and treatment of nosocomial complications generally supplement antiviral treatments. Furthermore, the use of corticosteroids for any period for the duration of the infection is discouraged, as it may render the patient more susceptible to infection.<br />
<br />
==Prevention==<br />
===<i>General Hygiene</i>===<br />
Avian influenza A viruses can be inactivated by general hygiene measures involving chemical agents and physical conditions like the use of soaps, detergents, and alcohols. <br />
<br />
===<i>Antiviral Chemoprohylaxis</i>===<br />
There are published recommendations for the prophylactic administration of antiviral agents to persons who may have been exposed to the virus [[#References|[5]]]. The World Health Organization (WHO) has developed mathematical models that indicate that the spread of pandemic strains may be stemmed or contained to manageable regions through prophylactic administration of oseltamivin.<br />
<br />
===<i>Immunization</i>===<br />
Some literature suggests that safe immunogenic inactivated H5 vaccines have been developed [[#References|[6]]]. However, the antibody levels required for protection against H5N1 is unclear and the duration of the antibody response is limited. Additionally, there is serious concern about the cross-reactivity of Avian Influenza A (H5N1) and memory T cells established by seasonal human influenza A infections in healthy individuals, although the risk appears to be lower for children and the elderly[[#References|[7]]]. Various investigational approaches, including conserved antigen vaccines, vectored H5 vaccines, and other adjuvants are currently being investigated. <br />
<br />
==Host Immune Response==<br />
To date, very little is known about the details of the host immune response to H5N1. However, it seems clear that T cell cross-reactivity with conserved portions of H5N1 are responsible for the severity of the disease. Patients typically have exaggerated levels of expression of cytokines and chemokines, which in turn produce a massive inflammatory response, thereby rendering the host more prone to additional infection [[#References|[7]]]. Furthermore, it appears that the serum antibody responses of H5N1 survivors are significantly impaired, suggesting that T cell-based heterosubtypic immunity may be implicated as an important preventative measure [[#References|[8]]].<br />
<br />
<br />
==References==<br />
1. [World Health Organization FAQs: H5N1 influenza. April, 2011. (Accessed July 21, 2013 at http://who.int/influenza/human_animal_interface/avian_influenza/h5n1_research/faqs/en/)]<br />
<br />
2. [Herfst S, Schrauwen JA, Linster M, et al. Airborne Transmission of Influenza A/H5N1 Virus Between Ferrets. Science June 22, 2012; 336 (6088): 1534-41.]<br />
<br />
3. [World Health Organization: Update of Avian Influenza A (H5N1) Virus Infection in Humans. N Engl J Med Jan 17, 2008; 358: 261-273.]<br />
<br />
4. [Yee KS, Carpenter TE, Cardona CJ. Epidemiology of H5N1 avian influenza. J Comp Immun Micro Infec Dis. July 2009; 32(4): 325-340.]<br />
<br />
5. [WHO Rapid Advice Guidelines on pharmacological management of humans infected with avian influenza A (H5N1) virus. May 2006 (Accessed July 22, 2013 at http://www.who.int/influenza/resources/documents/pharmacological_management_h5n1_05_2006/en/)]<br />
<br />
6. Girard MP, Katz J, Pervikov Y, et al. Report of the 6th meeting on the evaluation of pandemic influenza vaccines in clinical trials World Health Organization, Geneva, Switzerland, 17-18 February 2010. Vaccine October 4, 2010; 28(42): 6811-6820.<br />
<br />
7. Yong-Hwa Lee L, Anh Ha DL, Dong T. Memory T cells established by seasonal human influenza A infection cross-react with avian influenza A (H5N1) in healthy individuals. J Clin Invest November 1, 2012; 122(11): 4301.<br />
<br />
8. de Jong MD, Simmons CP, Thanh TT, et al. Fatal outcome of human influenza A (H5N1) is associated with high viral load and hypercytokinemia. Nature Medicine September 10, 2006; 12(2006): 1203-07.<br />
<br />
<br />
Created by Marrett Hild, student of Tyrrell Conway at the University of Oklahoma.</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=H5N1_Influenza_A&diff=91467H5N1 Influenza A2013-07-24T21:33:52Z<p>Magdalene.C.Shaughnessy-1: /* Virulence Factors */</p>
<hr />
<div>{{Curated}}<br />
<br />
[[Image:OULOGOBIANCO.JPEG|thumb|230px|right|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]<br />
<br />
==Etiology/Bacteriology==<br />
===<i>Taxonomy</i>===<br />
<br>| Domain = [[Viruses]] <br />
<br>| Class = [[ssRNA viruses]]<br />
<br>| Order = [[ssRNA negative strand viruses]]<br />
<br>| Family = [[Orthomyxoviridae]]<br />
<br>| Genus = [[Influenzavirus A]]<br />
<br>| species = [[Influenza A virus]]<br />
<br />
{|<br />
| height="10" bgcolor="#FFDF95" |<br />
'''NCBI: [http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=102793&lvl=3&lin=f&keep=1&srchmode=1&unlock] Genome: [[Influenza A Virus H5N1]] <font size="2">[http://www.ncbi.nlm.nih.gov/genome/10290?project_id=15617]</font>'''<br />
|}<br />
<br />
===<i>Description</i>===<br />
<br />
[[Image: H5N1 Flu.jpg |thumb|400px|right| Avian Influenza A (H5N1) virus particles, TEM <br /> From: http://urbantimes.co/magazine/2010/12/artificial-intelligents/h5n1-avian-influenza-virus-particles-tem/]]<br />
<br />
Avian Influenza A (H5N1) is a type of influenza virus responsible for causing severe respiratory disease in birds, generally waterfowl, and humans. However, researchers have yet to definitively document human-to-human transmission and victims of avian-to-human transmission generally spend substantial amounts of time around birds (like poultry farm workers, migratory duck herders, etc.) There is a growing level of concern about the virus because of its high mortality rate and its predisposition to mutation. This renders the human adaptive immune response fairly inadequate against the infection, and the virus has the potential to be devastating to the human population if it were to mutate to a strain capable of human-to-human transmission. Symptoms of H5N1 infection include high fever (>38°C), malaise, cough, sore throat, muscle aches, abdominal or chest pain, and diarrhea. The sequelae of H5N1 infection are often severe respiratory illness including pneumonia and acute respiratory distress syndrome as well as neurological changes like altered mental state and seizures. Treatment often involves implementation of the antiviral medication oseltamivir. At this stage, all vaccinations are still experimental [[#References|[1]]].<br />
<br />
==Pathogenesis==<br />
===<i>Transmission</i>===<br />
Transmission of H5N1 primarily occurs via direct avian-to-human contact. Major risk factors include handling diseased poultry and the consumption of raw or undercooked poultry products. The exact mode and sites of infection in the respiratory tract remain unknown. H5N1 also has several mammalian hosts including cats, dogs, and ferrets. None have been shown to transmit the disease to humans. However, a genetically modified strain of the virus was capable of airborne transmission in ferrets, which gives insight into the possibility of human-to-human transmission [[#References|[2]]]. The mode of transmission remains unclear for about one quarter of infected patients and environment-to-human transmission has not been ruled out. It is still uncertain whether infection can begin in the gastrointestinal tract, but it has been implicated in other mammals and is an open area of research.<br />
<br />
===<i>Infectious Dose, Incubation, and Epidemiology</i>===<br />
====Infectious Dose====<br />
There is not a definitive known infectious dose for H5N1 and it is likely dependent on a number of host factors like age, race, genes, and location. However, it seems clear that a low number of viral particles can proliferate extremely successfully once they have become bound in the respiratory tract.<br />
<br />
====Incubation====<br />
The incubation period for H5N1 infection is generally 7 days or less, many times as little as 2-5 days. In cases where human-to-human transmission likely occurred the average is 3 days. However, some reports estimate as long as 8-9 days.<br />
<br />
====Epidemiology====<br />
The first documented case of H5N1 was in a 3-year-old boy in Hong Kong SAR that promptly died from respiratory failure in 1997. By the end of 1997, 18 people had succumbed to the virus. There have been about 600 reported cases of H5N1 infection since 1997 and the virus reemerges periodically, infecting clustered regions of people who are generally related or in very close proximity. The median age of infected persons is 18 and 90% of patients are under 40 and healthy. Mortality is estimated to be 61% and is highest in the 10-19 year age range. Interestingly, observed cases typically occur in cooler months but are often correlated with outbreaks in poultry. Despite likely widespread human exposure, human infections remain relatively rare [[#References|[3]]].<br />
<br />
===<i>Virulence Factors</i>===<br />
<br />
[[Image: Ha sialic acid.png |thumb|400px|right| A single amino acid change switches avian influenza H5N1 and H7N9 viruses to human receptors <br /> From: http://www.virology.ws/2013/06/11/a-single-amino-acid-change-switches-avian-influenza-h5n1-and-h7n9-viruses-to-human-receptors/]]<br />
<br />
Avian influenza A viruses are enveloped, single stranded negative sense RNA viruses that contain 8 segments of RNA that code for 10 proteins. They have surface antigens called haemagglutinin (HA) and neuraminidase (NA) that are responsible for binding to host tissue. There are 16 subtypes of haemagglutinin and neuraminidase and their genes appear to have a synergistic effect on virulence. Researchers have identified 15 amino acid residues from 4 influenza virus genes from the 1997 Hong Kong strain that seemed to determine high- versus low-pathogenic phenotypes. Furthermore, the absence of glycosylation sites at aa154 in the HA gene result in increased virulence. H5N1 strains isolated from humans have an acquired mutation that permits binding to both ∝2,3-linked sialic acid receptors and ∝2,6-linked sialic acid receptors that also produce increased virulence. However, it seems that the virus will require a mutations in a number of genes in order to confer effective human-to-human transmission.<br />
<br />
==Clinical features==<br />
H5N1 infections typically manifest as severe pneumonia that rapidly progresses in to acute respiratory distress syndrome. The time from on set of infection to death is generally 9 days with fatality percentages ranging from 50-80% depending on the region of the cluster outbreak. Some febrile upper respiratory illness has occurred without pneumonia more frequently since 2005, but this is likely due to increased administration of antivirals. Other commonly related conditions include leucopenia, lymphopenia, mild-to-moderate thrombocytopenia, and elevated levels of aminotransferases as well as elevated levels of lactate dehydrogenase, creatine phosphokinase, hypoalbuminemia, and d-dimer levels. The very non-specific nature of the clinical presentation often results in misdiagnosis [[#References|[4]]]. <br />
<br />
==Diagnosis==<br />
<br />
[[Image: Diagnostic.gif |thumb|400px|right| Viral titers obtained from various regions of red foxes infected with H5N1 <br /> From: http://www.medscape.com/viewarticle/584804_3]]<br />
<br />
Conventional or real-time reverse-transcriptase PCR is the best method under biohazard level 2 conditions. Primers need to be continuously updated, given the high rate at which the virus mutates. Most often primers are engineered to target mutations in the H5 haemagglutinin gene. Diagnostic yields are generally highest from throat specimens rather than nasal swabs because viral loads are usually highest in the throat. A single negative result should not rule out H5N1 infection and multiple samples should be taken. Samples can also be taken from the blood and stool, but they generally have lower diagnostic sensitivity. The detection of anti-H5 antibodies is requisite for diagnosis and microneutralization assays are typically the most reliable method for recognition. However, it should be noted that microneutralization is labor intensive and required biohazard level 3 conditions. Furthermore, haemagglutinin-inhibition assays that use erythrocytes from horses are a promising diagnostic option, but require further investigation.<br />
<br />
==Treatment==<br />
===<i>Antiviral Agents</i>===<br />
Many forms of influenza A virus are susceptible, at least to some extent, to antiviral agents. Oseltamivir, marketed under the tradename Tamiflu, is a neurominidase inhibitor that is most often administered in H5N1 infection cases. However, the dosage is dependent on the strain’s rate of replication, as many oseltamivir-susceptible strains have high rates of replication. The general regimen presecribed for H5N1 infection, when prescribed early (1-3 days after onset of infection), is 75 mg twice daily for 5 days. Other potential treatment involve a combination of oseltamivir and amantadine or zanamivir (in cases where strains are oseltamivirR) depending on the nature of the infecting strain and the stage of the patient’s illness.<br />
<br />
===<i>Other Treatments</i>===<br />
Management of hypoxemia and treatment of nosocomial complications generally supplement antiviral treatments. Furthermore, the use of corticosteroids for any period for the duration of the infection is discouraged, as it may render the patient more susceptible to infection.<br />
<br />
==Prevention==<br />
===<i>General Hygiene</i>===<br />
Avian influenza A viruses can be inactivated by general hygiene measures involving chemical agents and physical conditions like the use of soaps, detergents, and alcohols. <br />
<br />
===<i>Antiviral Chemoprohylaxis</i>===<br />
There are published recommendations for the prophylactic administration of antiviral agents to persons who may have been exposed to the virus [[#References|[5]]]. The WHO has developed mathematical models that indicate that the spread of pandemic strains may be stemmed or contained to manageable regions through prophylactic administration of oseltamivin. <br />
<br />
===<i>Immunization</i>===<br />
Some literature suggests that safe immunogenic inactivated H5 vaccines have been developed [[#References|[6]]]. However, the antibody levels required for protection against H5N1 is unclear and the duration of the antibody response is limited. Additionally, there is serious concern about the cross-reactivity of Avian Influenza A (H5N1) and memory T cells established by seasonal human influenza A infections in healthy individuals, although the risk appears to be lower for children and the elderly[[#References|[7]]]. Various investigational approaches, including conserved antigen vaccines, vectored H5 vaccines, and other adjuvants are currently being investigated. <br />
<br />
==Host Immune Response==<br />
To date, very little is known about the details of the host immune response to H5N1. However, it seems clear that T cell cross-reactivity with conserved portions of H5N1 are responsible for the severity of the disease. Patients typically have exaggerated levels of expression of cytokines and chemokines, which in turn produce a massive inflammatory response, thereby rendering the host more prone to additional infection [[#References|[7]]]. Furthermore, it appears that the serum antibody responses of H5N1 survivors are significantly impaired, suggesting that T cell-based heterosubtypic immunity may be implicated as an important preventative measure [[#References|[8]]].<br />
<br />
<br />
==References==<br />
1. [World Health Organization FAQs: H5N1 influenza. April, 2011. (Accessed July 21, 2013 at http://who.int/influenza/human_animal_interface/avian_influenza/h5n1_research/faqs/en/)]<br />
<br />
2. [Herfst S, Schrauwen JA, Linster M, et al. Airborne Transmission of Influenza A/H5N1 Virus Between Ferrets. Science June 22, 2012; 336 (6088): 1534-41.]<br />
<br />
3. [World Health Organization: Update of Avian Influenza A (H5N1) Virus Infection in Humans. N Engl J Med Jan 17, 2008; 358: 261-273.]<br />
<br />
4. [Yee KS, Carpenter TE, Cardona CJ. Epidemiology of H5N1 avian influenza. J Comp Immun Micro Infec Dis. July 2009; 32(4): 325-340.]<br />
<br />
5. [WHO Rapid Advice Guidelines on pharmacological management of humans infected with avian influenza A (H5N1) virus. May 2006 (Accessed July 22, 2013 at http://www.who.int/influenza/resources/documents/pharmacological_management_h5n1_05_2006/en/)]<br />
<br />
6. Girard MP, Katz J, Pervikov Y, et al. Report of the 6th meeting on the evaluation of pandemic influenza vaccines in clinical trials World Health Organization, Geneva, Switzerland, 17-18 February 2010. Vaccine October 4, 2010; 28(42): 6811-6820.<br />
<br />
7. Yong-Hwa Lee L, Anh Ha DL, Dong T. Memory T cells established by seasonal human influenza A infection cross-react with avian influenza A (H5N1) in healthy individuals. J Clin Invest November 1, 2012; 122(11): 4301.<br />
<br />
8. de Jong MD, Simmons CP, Thanh TT, et al. Fatal outcome of human influenza A (H5N1) is associated with high viral load and hypercytokinemia. Nature Medicine September 10, 2006; 12(2006): 1203-07.<br />
<br />
<br />
Created by Marrett Hild, student of Tyrrell Conway at the University of Oklahoma.</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=H5N1_Influenza_A&diff=91466H5N1 Influenza A2013-07-24T21:32:55Z<p>Magdalene.C.Shaughnessy-1: /* Epidemiology */</p>
<hr />
<div>{{Curated}}<br />
<br />
[[Image:OULOGOBIANCO.JPEG|thumb|230px|right|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]<br />
<br />
==Etiology/Bacteriology==<br />
===<i>Taxonomy</i>===<br />
<br>| Domain = [[Viruses]] <br />
<br>| Class = [[ssRNA viruses]]<br />
<br>| Order = [[ssRNA negative strand viruses]]<br />
<br>| Family = [[Orthomyxoviridae]]<br />
<br>| Genus = [[Influenzavirus A]]<br />
<br>| species = [[Influenza A virus]]<br />
<br />
{|<br />
| height="10" bgcolor="#FFDF95" |<br />
'''NCBI: [http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=102793&lvl=3&lin=f&keep=1&srchmode=1&unlock] Genome: [[Influenza A Virus H5N1]] <font size="2">[http://www.ncbi.nlm.nih.gov/genome/10290?project_id=15617]</font>'''<br />
|}<br />
<br />
===<i>Description</i>===<br />
<br />
[[Image: H5N1 Flu.jpg |thumb|400px|right| Avian Influenza A (H5N1) virus particles, TEM <br /> From: http://urbantimes.co/magazine/2010/12/artificial-intelligents/h5n1-avian-influenza-virus-particles-tem/]]<br />
<br />
Avian Influenza A (H5N1) is a type of influenza virus responsible for causing severe respiratory disease in birds, generally waterfowl, and humans. However, researchers have yet to definitively document human-to-human transmission and victims of avian-to-human transmission generally spend substantial amounts of time around birds (like poultry farm workers, migratory duck herders, etc.) There is a growing level of concern about the virus because of its high mortality rate and its predisposition to mutation. This renders the human adaptive immune response fairly inadequate against the infection, and the virus has the potential to be devastating to the human population if it were to mutate to a strain capable of human-to-human transmission. Symptoms of H5N1 infection include high fever (>38°C), malaise, cough, sore throat, muscle aches, abdominal or chest pain, and diarrhea. The sequelae of H5N1 infection are often severe respiratory illness including pneumonia and acute respiratory distress syndrome as well as neurological changes like altered mental state and seizures. Treatment often involves implementation of the antiviral medication oseltamivir. At this stage, all vaccinations are still experimental [[#References|[1]]].<br />
<br />
==Pathogenesis==<br />
===<i>Transmission</i>===<br />
Transmission of H5N1 primarily occurs via direct avian-to-human contact. Major risk factors include handling diseased poultry and the consumption of raw or undercooked poultry products. The exact mode and sites of infection in the respiratory tract remain unknown. H5N1 also has several mammalian hosts including cats, dogs, and ferrets. None have been shown to transmit the disease to humans. However, a genetically modified strain of the virus was capable of airborne transmission in ferrets, which gives insight into the possibility of human-to-human transmission [[#References|[2]]]. The mode of transmission remains unclear for about one quarter of infected patients and environment-to-human transmission has not been ruled out. It is still uncertain whether infection can begin in the gastrointestinal tract, but it has been implicated in other mammals and is an open area of research.<br />
<br />
===<i>Infectious Dose, Incubation, and Epidemiology</i>===<br />
====Infectious Dose====<br />
There is not a definitive known infectious dose for H5N1 and it is likely dependent on a number of host factors like age, race, genes, and location. However, it seems clear that a low number of viral particles can proliferate extremely successfully once they have become bound in the respiratory tract.<br />
<br />
====Incubation====<br />
The incubation period for H5N1 infection is generally 7 days or less, many times as little as 2-5 days. In cases where human-to-human transmission likely occurred the average is 3 days. However, some reports estimate as long as 8-9 days.<br />
<br />
====Epidemiology====<br />
The first documented case of H5N1 was in a 3-year-old boy in Hong Kong SAR that promptly died from respiratory failure in 1997. By the end of 1997, 18 people had succumbed to the virus. There have been about 600 reported cases of H5N1 infection since 1997 and the virus reemerges periodically, infecting clustered regions of people who are generally related or in very close proximity. The median age of infected persons is 18 and 90% of patients are under 40 and healthy. Mortality is estimated to be 61% and is highest in the 10-19 year age range. Interestingly, observed cases typically occur in cooler months but are often correlated with outbreaks in poultry. Despite likely widespread human exposure, human infections remain relatively rare [[#References|[3]]].<br />
<br />
===<i>Virulence Factors</i>===<br />
<br />
[[Image: Ha sialic acid.png |thumb|400px|right| A single amino acid change switches avian influenza H5N1 and H7N9 viruses to human receptors <br /> From: http://www.virology.ws/2013/06/11/a-single-amino-acid-change-switches-avian-influenza-h5n1-and-h7n9-viruses-to-human-receptors/]]<br />
<br />
Avian influenza A viruses are enveloped, single stranded negative sense RNA viruses that contain 8 segments of RNA that code for 10 proteins. They have surface antigens called haemagglutinin (HA) and neuraminidase (NA) that are responsible for binding to host tissue. There are 16 subtypes of haemagglutinin and neuraminidase and their genes appear to have a synergistic effect on virulence. Researchers have identified 15 amino acid residues from 4 influenza virus genes from the 1997 Hong Kong strain that seemed to determine high- versos low-pathogenic phenotypes. Furthermore, the absence of glycosylation sites at aa154 in the HA gene result in increased virulence. H5N1 strains isolated from humans have an acquired mutation that permits binding to both ∝2,3-linked sialic acid receptors and ∝2,6-linked sialic acid receptors that also produce increased virulence. However, it seems that the virus will require a mutations in a number of genes in order to confer effective human-to-human transmission.<br />
<br />
==Clinical features==<br />
H5N1 infections typically manifest as severe pneumonia that rapidly progresses in to acute respiratory distress syndrome. The time from on set of infection to death is generally 9 days with fatality percentages ranging from 50-80% depending on the region of the cluster outbreak. Some febrile upper respiratory illness has occurred without pneumonia more frequently since 2005, but this is likely due to increased administration of antivirals. Other commonly related conditions include leucopenia, lymphopenia, mild-to-moderate thrombocytopenia, and elevated levels of aminotransferases as well as elevated levels of lactate dehydrogenase, creatine phosphokinase, hypoalbuminemia, and d-dimer levels. The very non-specific nature of the clinical presentation often results in misdiagnosis [[#References|[4]]]. <br />
<br />
==Diagnosis==<br />
<br />
[[Image: Diagnostic.gif |thumb|400px|right| Viral titers obtained from various regions of red foxes infected with H5N1 <br /> From: http://www.medscape.com/viewarticle/584804_3]]<br />
<br />
Conventional or real-time reverse-transcriptase PCR is the best method under biohazard level 2 conditions. Primers need to be continuously updated, given the high rate at which the virus mutates. Most often primers are engineered to target mutations in the H5 haemagglutinin gene. Diagnostic yields are generally highest from throat specimens rather than nasal swabs because viral loads are usually highest in the throat. A single negative result should not rule out H5N1 infection and multiple samples should be taken. Samples can also be taken from the blood and stool, but they generally have lower diagnostic sensitivity. The detection of anti-H5 antibodies is requisite for diagnosis and microneutralization assays are typically the most reliable method for recognition. However, it should be noted that microneutralization is labor intensive and required biohazard level 3 conditions. Furthermore, haemagglutinin-inhibition assays that use erythrocytes from horses are a promising diagnostic option, but require further investigation.<br />
<br />
==Treatment==<br />
===<i>Antiviral Agents</i>===<br />
Many forms of influenza A virus are susceptible, at least to some extent, to antiviral agents. Oseltamivir, marketed under the tradename Tamiflu, is a neurominidase inhibitor that is most often administered in H5N1 infection cases. However, the dosage is dependent on the strain’s rate of replication, as many oseltamivir-susceptible strains have high rates of replication. The general regimen presecribed for H5N1 infection, when prescribed early (1-3 days after onset of infection), is 75 mg twice daily for 5 days. Other potential treatment involve a combination of oseltamivir and amantadine or zanamivir (in cases where strains are oseltamivirR) depending on the nature of the infecting strain and the stage of the patient’s illness.<br />
<br />
===<i>Other Treatments</i>===<br />
Management of hypoxemia and treatment of nosocomial complications generally supplement antiviral treatments. Furthermore, the use of corticosteroids for any period for the duration of the infection is discouraged, as it may render the patient more susceptible to infection.<br />
<br />
==Prevention==<br />
===<i>General Hygiene</i>===<br />
Avian influenza A viruses can be inactivated by general hygiene measures involving chemical agents and physical conditions like the use of soaps, detergents, and alcohols. <br />
<br />
===<i>Antiviral Chemoprohylaxis</i>===<br />
There are published recommendations for the prophylactic administration of antiviral agents to persons who may have been exposed to the virus [[#References|[5]]]. The WHO has developed mathematical models that indicate that the spread of pandemic strains may be stemmed or contained to manageable regions through prophylactic administration of oseltamivin. <br />
<br />
===<i>Immunization</i>===<br />
Some literature suggests that safe immunogenic inactivated H5 vaccines have been developed [[#References|[6]]]. However, the antibody levels required for protection against H5N1 is unclear and the duration of the antibody response is limited. Additionally, there is serious concern about the cross-reactivity of Avian Influenza A (H5N1) and memory T cells established by seasonal human influenza A infections in healthy individuals, although the risk appears to be lower for children and the elderly[[#References|[7]]]. Various investigational approaches, including conserved antigen vaccines, vectored H5 vaccines, and other adjuvants are currently being investigated. <br />
<br />
==Host Immune Response==<br />
To date, very little is known about the details of the host immune response to H5N1. However, it seems clear that T cell cross-reactivity with conserved portions of H5N1 are responsible for the severity of the disease. Patients typically have exaggerated levels of expression of cytokines and chemokines, which in turn produce a massive inflammatory response, thereby rendering the host more prone to additional infection [[#References|[7]]]. Furthermore, it appears that the serum antibody responses of H5N1 survivors are significantly impaired, suggesting that T cell-based heterosubtypic immunity may be implicated as an important preventative measure [[#References|[8]]].<br />
<br />
<br />
==References==<br />
1. [World Health Organization FAQs: H5N1 influenza. April, 2011. (Accessed July 21, 2013 at http://who.int/influenza/human_animal_interface/avian_influenza/h5n1_research/faqs/en/)]<br />
<br />
2. [Herfst S, Schrauwen JA, Linster M, et al. Airborne Transmission of Influenza A/H5N1 Virus Between Ferrets. Science June 22, 2012; 336 (6088): 1534-41.]<br />
<br />
3. [World Health Organization: Update of Avian Influenza A (H5N1) Virus Infection in Humans. N Engl J Med Jan 17, 2008; 358: 261-273.]<br />
<br />
4. [Yee KS, Carpenter TE, Cardona CJ. Epidemiology of H5N1 avian influenza. J Comp Immun Micro Infec Dis. July 2009; 32(4): 325-340.]<br />
<br />
5. [WHO Rapid Advice Guidelines on pharmacological management of humans infected with avian influenza A (H5N1) virus. May 2006 (Accessed July 22, 2013 at http://www.who.int/influenza/resources/documents/pharmacological_management_h5n1_05_2006/en/)]<br />
<br />
6. Girard MP, Katz J, Pervikov Y, et al. Report of the 6th meeting on the evaluation of pandemic influenza vaccines in clinical trials World Health Organization, Geneva, Switzerland, 17-18 February 2010. Vaccine October 4, 2010; 28(42): 6811-6820.<br />
<br />
7. Yong-Hwa Lee L, Anh Ha DL, Dong T. Memory T cells established by seasonal human influenza A infection cross-react with avian influenza A (H5N1) in healthy individuals. J Clin Invest November 1, 2012; 122(11): 4301.<br />
<br />
8. de Jong MD, Simmons CP, Thanh TT, et al. Fatal outcome of human influenza A (H5N1) is associated with high viral load and hypercytokinemia. Nature Medicine September 10, 2006; 12(2006): 1203-07.<br />
<br />
<br />
Created by Marrett Hild, student of Tyrrell Conway at the University of Oklahoma.</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=H5N1_Influenza_A&diff=91461H5N1 Influenza A2013-07-24T21:31:18Z<p>Magdalene.C.Shaughnessy-1: /* Infectious Dose */</p>
<hr />
<div>{{Curated}}<br />
<br />
[[Image:OULOGOBIANCO.JPEG|thumb|230px|right|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]<br />
<br />
==Etiology/Bacteriology==<br />
===<i>Taxonomy</i>===<br />
<br>| Domain = [[Viruses]] <br />
<br>| Class = [[ssRNA viruses]]<br />
<br>| Order = [[ssRNA negative strand viruses]]<br />
<br>| Family = [[Orthomyxoviridae]]<br />
<br>| Genus = [[Influenzavirus A]]<br />
<br>| species = [[Influenza A virus]]<br />
<br />
{|<br />
| height="10" bgcolor="#FFDF95" |<br />
'''NCBI: [http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=102793&lvl=3&lin=f&keep=1&srchmode=1&unlock] Genome: [[Influenza A Virus H5N1]] <font size="2">[http://www.ncbi.nlm.nih.gov/genome/10290?project_id=15617]</font>'''<br />
|}<br />
<br />
===<i>Description</i>===<br />
<br />
[[Image: H5N1 Flu.jpg |thumb|400px|right| Avian Influenza A (H5N1) virus particles, TEM <br /> From: http://urbantimes.co/magazine/2010/12/artificial-intelligents/h5n1-avian-influenza-virus-particles-tem/]]<br />
<br />
Avian Influenza A (H5N1) is a type of influenza virus responsible for causing severe respiratory disease in birds, generally waterfowl, and humans. However, researchers have yet to definitively document human-to-human transmission and victims of avian-to-human transmission generally spend substantial amounts of time around birds (like poultry farm workers, migratory duck herders, etc.) There is a growing level of concern about the virus because of its high mortality rate and its predisposition to mutation. This renders the human adaptive immune response fairly inadequate against the infection, and the virus has the potential to be devastating to the human population if it were to mutate to a strain capable of human-to-human transmission. Symptoms of H5N1 infection include high fever (>38°C), malaise, cough, sore throat, muscle aches, abdominal or chest pain, and diarrhea. The sequelae of H5N1 infection are often severe respiratory illness including pneumonia and acute respiratory distress syndrome as well as neurological changes like altered mental state and seizures. Treatment often involves implementation of the antiviral medication oseltamivir. At this stage, all vaccinations are still experimental [[#References|[1]]].<br />
<br />
==Pathogenesis==<br />
===<i>Transmission</i>===<br />
Transmission of H5N1 primarily occurs via direct avian-to-human contact. Major risk factors include handling diseased poultry and the consumption of raw or undercooked poultry products. The exact mode and sites of infection in the respiratory tract remain unknown. H5N1 also has several mammalian hosts including cats, dogs, and ferrets. None have been shown to transmit the disease to humans. However, a genetically modified strain of the virus was capable of airborne transmission in ferrets, which gives insight into the possibility of human-to-human transmission [[#References|[2]]]. The mode of transmission remains unclear for about one quarter of infected patients and environment-to-human transmission has not been ruled out. It is still uncertain whether infection can begin in the gastrointestinal tract, but it has been implicated in other mammals and is an open area of research.<br />
<br />
===<i>Infectious Dose, Incubation, and Epidemiology</i>===<br />
====Infectious Dose====<br />
There is not a definitive known infectious dose for H5N1 and it is likely dependent on a number of host factors like age, race, genes, and location. However, it seems clear that a low number of viral particles can proliferate extremely successfully once they have become bound in the respiratory tract.<br />
<br />
====Incubation====<br />
The incubation period for H5N1 infection is generally 7 days or less, many times as little as 2-5 days. In cases where human-to-human transmission likely occurred the average is 3 days. However, some reports estimate as long as 8-9 days.<br />
<br />
====Epidemiology====<br />
The first documented case of H5N1 was in a 3-year-old boy in Hong Kong SAR that promptly died from respiratory failure in 1997. By the end of 1997, 18 people had succumbed to the virus. There have been about 600 reported cases of H5N1 infection since 1997 and the virus reemerges periodically infecting clustered regions of people who are generally related or in very close proximity. The median age of infected persons is 18 and 90% of patients are under 40 and healthy. Mortality is estimated to be 61% and is highest in the 10-19 year age range. Interestingly, observed cases typically occur in cooler months but are often correlated with outbreaks in poultry. Despite likely widespread human exposure, human infections remain relatively rare [[#References|[3]]].<br />
<br />
===<i>Virulence Factors</i>===<br />
<br />
[[Image: Ha sialic acid.png |thumb|400px|right| A single amino acid change switches avian influenza H5N1 and H7N9 viruses to human receptors <br /> From: http://www.virology.ws/2013/06/11/a-single-amino-acid-change-switches-avian-influenza-h5n1-and-h7n9-viruses-to-human-receptors/]]<br />
<br />
Avian influenza A viruses are enveloped, single stranded negative sense RNA viruses that contain 8 segments of RNA that code for 10 proteins. They have surface antigens called haemagglutinin (HA) and neuraminidase (NA) that are responsible for binding to host tissue. There are 16 subtypes of haemagglutinin and neuraminidase and their genes appear to have a synergistic effect on virulence. Researchers have identified 15 amino acid residues from 4 influenza virus genes from the 1997 Hong Kong strain that seemed to determine high- versos low-pathogenic phenotypes. Furthermore, the absence of glycosylation sites at aa154 in the HA gene result in increased virulence. H5N1 strains isolated from humans have an acquired mutation that permits binding to both ∝2,3-linked sialic acid receptors and ∝2,6-linked sialic acid receptors that also produce increased virulence. However, it seems that the virus will require a mutations in a number of genes in order to confer effective human-to-human transmission.<br />
<br />
==Clinical features==<br />
H5N1 infections typically manifest as severe pneumonia that rapidly progresses in to acute respiratory distress syndrome. The time from on set of infection to death is generally 9 days with fatality percentages ranging from 50-80% depending on the region of the cluster outbreak. Some febrile upper respiratory illness has occurred without pneumonia more frequently since 2005, but this is likely due to increased administration of antivirals. Other commonly related conditions include leucopenia, lymphopenia, mild-to-moderate thrombocytopenia, and elevated levels of aminotransferases as well as elevated levels of lactate dehydrogenase, creatine phosphokinase, hypoalbuminemia, and d-dimer levels. The very non-specific nature of the clinical presentation often results in misdiagnosis [[#References|[4]]]. <br />
<br />
==Diagnosis==<br />
<br />
[[Image: Diagnostic.gif |thumb|400px|right| Viral titers obtained from various regions of red foxes infected with H5N1 <br /> From: http://www.medscape.com/viewarticle/584804_3]]<br />
<br />
Conventional or real-time reverse-transcriptase PCR is the best method under biohazard level 2 conditions. Primers need to be continuously updated, given the high rate at which the virus mutates. Most often primers are engineered to target mutations in the H5 haemagglutinin gene. Diagnostic yields are generally highest from throat specimens rather than nasal swabs because viral loads are usually highest in the throat. A single negative result should not rule out H5N1 infection and multiple samples should be taken. Samples can also be taken from the blood and stool, but they generally have lower diagnostic sensitivity. The detection of anti-H5 antibodies is requisite for diagnosis and microneutralization assays are typically the most reliable method for recognition. However, it should be noted that microneutralization is labor intensive and required biohazard level 3 conditions. Furthermore, haemagglutinin-inhibition assays that use erythrocytes from horses are a promising diagnostic option, but require further investigation.<br />
<br />
==Treatment==<br />
===<i>Antiviral Agents</i>===<br />
Many forms of influenza A virus are susceptible, at least to some extent, to antiviral agents. Oseltamivir, marketed under the tradename Tamiflu, is a neurominidase inhibitor that is most often administered in H5N1 infection cases. However, the dosage is dependent on the strain’s rate of replication, as many oseltamivir-susceptible strains have high rates of replication. The general regimen presecribed for H5N1 infection, when prescribed early (1-3 days after onset of infection), is 75 mg twice daily for 5 days. Other potential treatment involve a combination of oseltamivir and amantadine or zanamivir (in cases where strains are oseltamivirR) depending on the nature of the infecting strain and the stage of the patient’s illness.<br />
<br />
===<i>Other Treatments</i>===<br />
Management of hypoxemia and treatment of nosocomial complications generally supplement antiviral treatments. Furthermore, the use of corticosteroids for any period for the duration of the infection is discouraged, as it may render the patient more susceptible to infection.<br />
<br />
==Prevention==<br />
===<i>General Hygiene</i>===<br />
Avian influenza A viruses can be inactivated by general hygiene measures involving chemical agents and physical conditions like the use of soaps, detergents, and alcohols. <br />
<br />
===<i>Antiviral Chemoprohylaxis</i>===<br />
There are published recommendations for the prophylactic administration of antiviral agents to persons who may have been exposed to the virus [[#References|[5]]]. The WHO has developed mathematical models that indicate that the spread of pandemic strains may be stemmed or contained to manageable regions through prophylactic administration of oseltamivin. <br />
<br />
===<i>Immunization</i>===<br />
Some literature suggests that safe immunogenic inactivated H5 vaccines have been developed [[#References|[6]]]. However, the antibody levels required for protection against H5N1 is unclear and the duration of the antibody response is limited. Additionally, there is serious concern about the cross-reactivity of Avian Influenza A (H5N1) and memory T cells established by seasonal human influenza A infections in healthy individuals, although the risk appears to be lower for children and the elderly[[#References|[7]]]. Various investigational approaches, including conserved antigen vaccines, vectored H5 vaccines, and other adjuvants are currently being investigated. <br />
<br />
==Host Immune Response==<br />
To date, very little is known about the details of the host immune response to H5N1. However, it seems clear that T cell cross-reactivity with conserved portions of H5N1 are responsible for the severity of the disease. Patients typically have exaggerated levels of expression of cytokines and chemokines, which in turn produce a massive inflammatory response, thereby rendering the host more prone to additional infection [[#References|[7]]]. Furthermore, it appears that the serum antibody responses of H5N1 survivors are significantly impaired, suggesting that T cell-based heterosubtypic immunity may be implicated as an important preventative measure [[#References|[8]]].<br />
<br />
<br />
==References==<br />
1. [World Health Organization FAQs: H5N1 influenza. April, 2011. (Accessed July 21, 2013 at http://who.int/influenza/human_animal_interface/avian_influenza/h5n1_research/faqs/en/)]<br />
<br />
2. [Herfst S, Schrauwen JA, Linster M, et al. Airborne Transmission of Influenza A/H5N1 Virus Between Ferrets. Science June 22, 2012; 336 (6088): 1534-41.]<br />
<br />
3. [World Health Organization: Update of Avian Influenza A (H5N1) Virus Infection in Humans. N Engl J Med Jan 17, 2008; 358: 261-273.]<br />
<br />
4. [Yee KS, Carpenter TE, Cardona CJ. Epidemiology of H5N1 avian influenza. J Comp Immun Micro Infec Dis. July 2009; 32(4): 325-340.]<br />
<br />
5. [WHO Rapid Advice Guidelines on pharmacological management of humans infected with avian influenza A (H5N1) virus. May 2006 (Accessed July 22, 2013 at http://www.who.int/influenza/resources/documents/pharmacological_management_h5n1_05_2006/en/)]<br />
<br />
6. Girard MP, Katz J, Pervikov Y, et al. Report of the 6th meeting on the evaluation of pandemic influenza vaccines in clinical trials World Health Organization, Geneva, Switzerland, 17-18 February 2010. Vaccine October 4, 2010; 28(42): 6811-6820.<br />
<br />
7. Yong-Hwa Lee L, Anh Ha DL, Dong T. Memory T cells established by seasonal human influenza A infection cross-react with avian influenza A (H5N1) in healthy individuals. J Clin Invest November 1, 2012; 122(11): 4301.<br />
<br />
8. de Jong MD, Simmons CP, Thanh TT, et al. Fatal outcome of human influenza A (H5N1) is associated with high viral load and hypercytokinemia. Nature Medicine September 10, 2006; 12(2006): 1203-07.<br />
<br />
<br />
Created by Marrett Hild, student of Tyrrell Conway at the University of Oklahoma.</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=H5N1_Influenza_A&diff=91458H5N1 Influenza A2013-07-24T21:30:05Z<p>Magdalene.C.Shaughnessy-1: /* Description */</p>
<hr />
<div>{{Curated}}<br />
<br />
[[Image:OULOGOBIANCO.JPEG|thumb|230px|right|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]<br />
<br />
==Etiology/Bacteriology==<br />
===<i>Taxonomy</i>===<br />
<br>| Domain = [[Viruses]] <br />
<br>| Class = [[ssRNA viruses]]<br />
<br>| Order = [[ssRNA negative strand viruses]]<br />
<br>| Family = [[Orthomyxoviridae]]<br />
<br>| Genus = [[Influenzavirus A]]<br />
<br>| species = [[Influenza A virus]]<br />
<br />
{|<br />
| height="10" bgcolor="#FFDF95" |<br />
'''NCBI: [http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=102793&lvl=3&lin=f&keep=1&srchmode=1&unlock] Genome: [[Influenza A Virus H5N1]] <font size="2">[http://www.ncbi.nlm.nih.gov/genome/10290?project_id=15617]</font>'''<br />
|}<br />
<br />
===<i>Description</i>===<br />
<br />
[[Image: H5N1 Flu.jpg |thumb|400px|right| Avian Influenza A (H5N1) virus particles, TEM <br /> From: http://urbantimes.co/magazine/2010/12/artificial-intelligents/h5n1-avian-influenza-virus-particles-tem/]]<br />
<br />
Avian Influenza A (H5N1) is a type of influenza virus responsible for causing severe respiratory disease in birds, generally waterfowl, and humans. However, researchers have yet to definitively document human-to-human transmission and victims of avian-to-human transmission generally spend substantial amounts of time around birds (like poultry farm workers, migratory duck herders, etc.) There is a growing level of concern about the virus because of its high mortality rate and its predisposition to mutation. This renders the human adaptive immune response fairly inadequate against the infection, and the virus has the potential to be devastating to the human population if it were to mutate to a strain capable of human-to-human transmission. Symptoms of H5N1 infection include high fever (>38°C), malaise, cough, sore throat, muscle aches, abdominal or chest pain, and diarrhea. The sequelae of H5N1 infection are often severe respiratory illness including pneumonia and acute respiratory distress syndrome as well as neurological changes like altered mental state and seizures. Treatment often involves implementation of the antiviral medication oseltamivir. At this stage, all vaccinations are still experimental [[#References|[1]]].<br />
<br />
==Pathogenesis==<br />
===<i>Transmission</i>===<br />
Transmission of H5N1 primarily occurs via direct avian-to-human contact. Major risk factors include handling diseased poultry and the consumption of raw or undercooked poultry products. The exact mode and sites of infection in the respiratory tract remain unknown. H5N1 also has several mammalian hosts including cats, dogs, and ferrets. None have been shown to transmit the disease to humans. However, a genetically modified strain of the virus was capable of airborne transmission in ferrets, which gives insight into the possibility of human-to-human transmission [[#References|[2]]]. The mode of transmission remains unclear for about one quarter of infected patients and environment-to-human transmission has not been ruled out. It is still uncertain whether infection can begin in the gastrointestinal tract, but it has been implicated in other mammals and is an open area of research.<br />
<br />
===<i>Infectious Dose, Incubation, and Epidemiology</i>===<br />
====Infectious Dose====<br />
There is not an agreed upon infectious dose for H5N1 and it is likely dependent on a number of host factors like age, race, genes, and location. However, it seems clear that a low number of viral particles can proliferate extremely successfully once they have become bound in the respiratory tract.<br />
<br />
====Incubation====<br />
The incubation period for H5N1 infection is generally 7 days or less, many times as little as 2-5 days. In cases where human-to-human transmission likely occurred the average is 3 days. However, some reports estimate as long as 8-9 days.<br />
<br />
====Epidemiology====<br />
The first documented case of H5N1 was in a 3-year-old boy in Hong Kong SAR that promptly died from respiratory failure in 1997. By the end of 1997, 18 people had succumbed to the virus. There have been about 600 reported cases of H5N1 infection since 1997 and the virus reemerges periodically infecting clustered regions of people who are generally related or in very close proximity. The median age of infected persons is 18 and 90% of patients are under 40 and healthy. Mortality is estimated to be 61% and is highest in the 10-19 year age range. Interestingly, observed cases typically occur in cooler months but are often correlated with outbreaks in poultry. Despite likely widespread human exposure, human infections remain relatively rare [[#References|[3]]].<br />
<br />
===<i>Virulence Factors</i>===<br />
<br />
[[Image: Ha sialic acid.png |thumb|400px|right| A single amino acid change switches avian influenza H5N1 and H7N9 viruses to human receptors <br /> From: http://www.virology.ws/2013/06/11/a-single-amino-acid-change-switches-avian-influenza-h5n1-and-h7n9-viruses-to-human-receptors/]]<br />
<br />
Avian influenza A viruses are enveloped, single stranded negative sense RNA viruses that contain 8 segments of RNA that code for 10 proteins. They have surface antigens called haemagglutinin (HA) and neuraminidase (NA) that are responsible for binding to host tissue. There are 16 subtypes of haemagglutinin and neuraminidase and their genes appear to have a synergistic effect on virulence. Researchers have identified 15 amino acid residues from 4 influenza virus genes from the 1997 Hong Kong strain that seemed to determine high- versos low-pathogenic phenotypes. Furthermore, the absence of glycosylation sites at aa154 in the HA gene result in increased virulence. H5N1 strains isolated from humans have an acquired mutation that permits binding to both ∝2,3-linked sialic acid receptors and ∝2,6-linked sialic acid receptors that also produce increased virulence. However, it seems that the virus will require a mutations in a number of genes in order to confer effective human-to-human transmission.<br />
<br />
==Clinical features==<br />
H5N1 infections typically manifest as severe pneumonia that rapidly progresses in to acute respiratory distress syndrome. The time from on set of infection to death is generally 9 days with fatality percentages ranging from 50-80% depending on the region of the cluster outbreak. Some febrile upper respiratory illness has occurred without pneumonia more frequently since 2005, but this is likely due to increased administration of antivirals. Other commonly related conditions include leucopenia, lymphopenia, mild-to-moderate thrombocytopenia, and elevated levels of aminotransferases as well as elevated levels of lactate dehydrogenase, creatine phosphokinase, hypoalbuminemia, and d-dimer levels. The very non-specific nature of the clinical presentation often results in misdiagnosis [[#References|[4]]]. <br />
<br />
==Diagnosis==<br />
<br />
[[Image: Diagnostic.gif |thumb|400px|right| Viral titers obtained from various regions of red foxes infected with H5N1 <br /> From: http://www.medscape.com/viewarticle/584804_3]]<br />
<br />
Conventional or real-time reverse-transcriptase PCR is the best method under biohazard level 2 conditions. Primers need to be continuously updated, given the high rate at which the virus mutates. Most often primers are engineered to target mutations in the H5 haemagglutinin gene. Diagnostic yields are generally highest from throat specimens rather than nasal swabs because viral loads are usually highest in the throat. A single negative result should not rule out H5N1 infection and multiple samples should be taken. Samples can also be taken from the blood and stool, but they generally have lower diagnostic sensitivity. The detection of anti-H5 antibodies is requisite for diagnosis and microneutralization assays are typically the most reliable method for recognition. However, it should be noted that microneutralization is labor intensive and required biohazard level 3 conditions. Furthermore, haemagglutinin-inhibition assays that use erythrocytes from horses are a promising diagnostic option, but require further investigation.<br />
<br />
==Treatment==<br />
===<i>Antiviral Agents</i>===<br />
Many forms of influenza A virus are susceptible, at least to some extent, to antiviral agents. Oseltamivir, marketed under the tradename Tamiflu, is a neurominidase inhibitor that is most often administered in H5N1 infection cases. However, the dosage is dependent on the strain’s rate of replication, as many oseltamivir-susceptible strains have high rates of replication. The general regimen presecribed for H5N1 infection, when prescribed early (1-3 days after onset of infection), is 75 mg twice daily for 5 days. Other potential treatment involve a combination of oseltamivir and amantadine or zanamivir (in cases where strains are oseltamivirR) depending on the nature of the infecting strain and the stage of the patient’s illness.<br />
<br />
===<i>Other Treatments</i>===<br />
Management of hypoxemia and treatment of nosocomial complications generally supplement antiviral treatments. Furthermore, the use of corticosteroids for any period for the duration of the infection is discouraged, as it may render the patient more susceptible to infection.<br />
<br />
==Prevention==<br />
===<i>General Hygiene</i>===<br />
Avian influenza A viruses can be inactivated by general hygiene measures involving chemical agents and physical conditions like the use of soaps, detergents, and alcohols. <br />
<br />
===<i>Antiviral Chemoprohylaxis</i>===<br />
There are published recommendations for the prophylactic administration of antiviral agents to persons who may have been exposed to the virus [[#References|[5]]]. The WHO has developed mathematical models that indicate that the spread of pandemic strains may be stemmed or contained to manageable regions through prophylactic administration of oseltamivin. <br />
<br />
===<i>Immunization</i>===<br />
Some literature suggests that safe immunogenic inactivated H5 vaccines have been developed [[#References|[6]]]. However, the antibody levels required for protection against H5N1 is unclear and the duration of the antibody response is limited. Additionally, there is serious concern about the cross-reactivity of Avian Influenza A (H5N1) and memory T cells established by seasonal human influenza A infections in healthy individuals, although the risk appears to be lower for children and the elderly[[#References|[7]]]. Various investigational approaches, including conserved antigen vaccines, vectored H5 vaccines, and other adjuvants are currently being investigated. <br />
<br />
==Host Immune Response==<br />
To date, very little is known about the details of the host immune response to H5N1. However, it seems clear that T cell cross-reactivity with conserved portions of H5N1 are responsible for the severity of the disease. Patients typically have exaggerated levels of expression of cytokines and chemokines, which in turn produce a massive inflammatory response, thereby rendering the host more prone to additional infection [[#References|[7]]]. Furthermore, it appears that the serum antibody responses of H5N1 survivors are significantly impaired, suggesting that T cell-based heterosubtypic immunity may be implicated as an important preventative measure [[#References|[8]]].<br />
<br />
<br />
==References==<br />
1. [World Health Organization FAQs: H5N1 influenza. April, 2011. (Accessed July 21, 2013 at http://who.int/influenza/human_animal_interface/avian_influenza/h5n1_research/faqs/en/)]<br />
<br />
2. [Herfst S, Schrauwen JA, Linster M, et al. Airborne Transmission of Influenza A/H5N1 Virus Between Ferrets. Science June 22, 2012; 336 (6088): 1534-41.]<br />
<br />
3. [World Health Organization: Update of Avian Influenza A (H5N1) Virus Infection in Humans. N Engl J Med Jan 17, 2008; 358: 261-273.]<br />
<br />
4. [Yee KS, Carpenter TE, Cardona CJ. Epidemiology of H5N1 avian influenza. J Comp Immun Micro Infec Dis. July 2009; 32(4): 325-340.]<br />
<br />
5. [WHO Rapid Advice Guidelines on pharmacological management of humans infected with avian influenza A (H5N1) virus. May 2006 (Accessed July 22, 2013 at http://www.who.int/influenza/resources/documents/pharmacological_management_h5n1_05_2006/en/)]<br />
<br />
6. Girard MP, Katz J, Pervikov Y, et al. Report of the 6th meeting on the evaluation of pandemic influenza vaccines in clinical trials World Health Organization, Geneva, Switzerland, 17-18 February 2010. Vaccine October 4, 2010; 28(42): 6811-6820.<br />
<br />
7. Yong-Hwa Lee L, Anh Ha DL, Dong T. Memory T cells established by seasonal human influenza A infection cross-react with avian influenza A (H5N1) in healthy individuals. J Clin Invest November 1, 2012; 122(11): 4301.<br />
<br />
8. de Jong MD, Simmons CP, Thanh TT, et al. Fatal outcome of human influenza A (H5N1) is associated with high viral load and hypercytokinemia. Nature Medicine September 10, 2006; 12(2006): 1203-07.<br />
<br />
<br />
Created by Marrett Hild, student of Tyrrell Conway at the University of Oklahoma.</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=91304Toxoplasmosis2013-07-24T11:36:07Z<p>Magdalene.C.Shaughnessy-1: </p>
<hr />
<div>{{curated}}[[Image:OULOGOBIANCO.JPEG|thumb|130px|right|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans and asexually reproduce within them, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks after infection. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection in other hosts. Intermediate hosts, commonly birds and rodents (typical prey of felines), may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals (including many of those bred for food) may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), and infection of a fetus transplacentally from the mother. A less likely method of infection is receiving a blood transfusion or organ transplant from individuals harboring tissue cysts. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease within a host, although it has been suggested that the number is very low due to high rates of infection. [[#References|[2]]] There are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br /><font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, that's fairly typical, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle and reproduce sexually to further diversify the species. <br />
<br />
<font size="3.5"><br/><i>Modifying intermediate host behavior</i></font><br />
<br />Logically, it may be inferred that the best way to enter a new feline host would be to be eaten by a feline host, so <i>T. gondii</i> has developed a mechanism by which it may alter its intermediate host's behavior to ensure it ends up in the stomach of a cat. Generally, mice and rats (common intermediate hosts for Toxoplasmosis) have a strong aversion to the smell of cat urine, as it is indicative of the presence of a cat (or to a mouse, a predator) in the immediate vicinity. <i>T.gondii</i> has developed a mechanism by which it changes rodent's innate aversion to feline odors and instead produces an attraction to these smells, thus increasing the likelihood that the intermediate rodent host will be eaten by the feline definitive host. This adaptation by <i>T. gondii</i>aids in its transmission to a definitive host, and ensure its ability to reproduce sexually. The mechanisms by which <i>T.gondii</i> is able to make such behavior modifications are still unknown. [[#References|[7]]]<br />
<br />
<font size="3.5"><br/><i>Toxoplasma influence on human behavior</i></font><br />
<br />While the symptoms of Toxoplasma infection seem to be fairly mild, recent research regarding this parasite has revealed an abundance of information pertaining to the psychological effects that Toxoplasmosis infection can induce in a human host. Indeed, Toxoplasma infection has been linked to increased risk of developing schizophrenia in infants whose mothers were infected by Toxoplasmosis,correlated to differences in behaviors between cultures, linked to increased neuroticism, and an alarmingly high correlation between infection and suicide rates. [[#References|[8]]] In one specific study, scientists were able to measure antibody levels for <i>T. gondii</i> from children to determine both the mother's infection status (because children's antibodies reflect those of their mothers until about three months after birth), and use a cause of death register later to passively screen the relationship between Toxoplasmosis infection and self-directed violence and suicide. [[#References|[9]]] The correlation between Toxoplasmosis infection and suicide was alarmingly high, women (the mothers of the children that had been screened) with Toxoplasmosis were 54% more likely to have attempted suicide, and two times as likely to have succeeded in that endeavor. Specifically, women infected with Toxoplasmosis were more likely to have attempted (or succeeded in) committing suicide violently (with a knife, gun, etc.). Additionally, it was determined that those with the highest levels of antibody serum were even more likely to commit a violent suicide (91%) than women with lower levels of antibody serum or uninfected women. [[#References|[9]]] This new information regarding Toxoplasmosis infection is alarming, and especially so because scientists do not fully understand the mechanism by which <i>T. gondii</i> is able to hijack the brain's neurochemical pathways to significantly alter human behavior.<br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu-like symptoms, swollen lymph nodes, muscle aches/pain, etc. for a few weeks that eventually disappear. [[#References|[1]]] <br />
<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including severe inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and is generally around 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]] Treatments for behavior modification's that result from Toxoplasmosis infection in humans have not yet been discovered because the specific cause of psychological disturbance in individuals infected with <i>T. gondii</i> has not yet been identified. [[#References|[8]]]<br />
<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduces the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and diminishes approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will commence and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen. Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2.]<br />
<br />8 [http://blogs.scientificamerican.com/science-sushi/2012/07/04/toxoplasmas-dark-side-the-link-between-parasite-and-suicide/ Christie Wilcox. Toxoplasma’s Dark Side: The Link Between Parasite and Suicide. Scientific American. Published online July 4, 2012.]<br />
<br />9 [http://www.ncbi.nlm.nih.gov/pubmed/10359408 Lebech M, Andersen O, Christensen NC, Hertel J, Nielsen HE, Peitersen B, Rechnitzer C, Larsen SO, Nørgaard-Pedersen B, Petersen E.Feasibility of neonatal screening for toxoplasma infection in the absence of prenatal treatment. Danish Congenital Toxoplasmosis Study Group. Lancet. 1999 May 29;353(9167):1834-7.]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=91302Toxoplasmosis2013-07-24T11:35:11Z<p>Magdalene.C.Shaughnessy-1: </p>
<hr />
<div>{{curated}}[[Image:OULOGOBIANCO.JPEG|thumb|230px|right|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans and asexually reproduce within them, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks after infection. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection in other hosts. Intermediate hosts, commonly birds and rodents (typical prey of felines), may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals (including many of those bred for food) may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), and infection of a fetus transplacentally from the mother. A less likely method of infection is receiving a blood transfusion or organ transplant from individuals harboring tissue cysts. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease within a host, although it has been suggested that the number is very low due to high rates of infection. [[#References|[2]]] There are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br /><font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, that's fairly typical, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle and reproduce sexually to further diversify the species. <br />
<br />
<font size="3.5"><br/><i>Modifying intermediate host behavior</i></font><br />
<br />Logically, it may be inferred that the best way to enter a new feline host would be to be eaten by a feline host, so <i>T. gondii</i> has developed a mechanism by which it may alter its intermediate host's behavior to ensure it ends up in the stomach of a cat. Generally, mice and rats (common intermediate hosts for Toxoplasmosis) have a strong aversion to the smell of cat urine, as it is indicative of the presence of a cat (or to a mouse, a predator) in the immediate vicinity. <i>T.gondii</i> has developed a mechanism by which it changes rodent's innate aversion to feline odors and instead produces an attraction to these smells, thus increasing the likelihood that the intermediate rodent host will be eaten by the feline definitive host. This adaptation by <i>T. gondii</i>aids in its transmission to a definitive host, and ensure its ability to reproduce sexually. The mechanisms by which <i>T.gondii</i> is able to make such behavior modifications are still unknown. [[#References|[7]]]<br />
<br />
<font size="3.5"><br/><i>Toxoplasma influence on human behavior</i></font><br />
<br />While the symptoms of Toxoplasma infection seem to be fairly mild, recent research regarding this parasite has revealed an abundance of information pertaining to the psychological effects that Toxoplasmosis infection can induce in a human host. Indeed, Toxoplasma infection has been linked to increased risk of developing schizophrenia in infants whose mothers were infected by Toxoplasmosis,correlated to differences in behaviors between cultures, linked to increased neuroticism, and an alarmingly high correlation between infection and suicide rates. [[#References|[8]]] In one specific study, scientists were able to measure antibody levels for <i>T. gondii</i> from children to determine both the mother's infection status (because children's antibodies reflect those of their mothers until about three months after birth), and use a cause of death register later to passively screen the relationship between Toxoplasmosis infection and self-directed violence and suicide. [[#References|[9]]] The correlation between Toxoplasmosis infection and suicide was alarmingly high, women (the mothers of the children that had been screened) with Toxoplasmosis were 54% more likely to have attempted suicide, and two times as likely to have succeeded in that endeavor. Specifically, women infected with Toxoplasmosis were more likely to have attempted (or succeeded in) committing suicide violently (with a knife, gun, etc.). Additionally, it was determined that those with the highest levels of antibody serum were even more likely to commit a violent suicide (91%) than women with lower levels of antibody serum or uninfected women. [[#References|[9]]] This new information regarding Toxoplasmosis infection is alarming, and especially so because scientists do not fully understand the mechanism by which <i>T. gondii</i> is able to hijack the brain's neurochemical pathways to significantly alter human behavior.<br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu-like symptoms, swollen lymph nodes, muscle aches/pain, etc. for a few weeks that eventually disappear. [[#References|[1]]] <br />
<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including severe inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and is generally around 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]] Treatments for behavior modification's that result from Toxoplasmosis infection in humans have not yet been discovered because the specific cause of psychological disturbance in individuals infected with <i>T. gondii</i> has not yet been identified. [[#References|[8]]]<br />
<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduces the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and diminishes approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will commence and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen. Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2.]<br />
<br />8 [http://blogs.scientificamerican.com/science-sushi/2012/07/04/toxoplasmas-dark-side-the-link-between-parasite-and-suicide/ Christie Wilcox. Toxoplasma’s Dark Side: The Link Between Parasite and Suicide. Scientific American. Published online July 4, 2012.]<br />
<br />9 [http://www.ncbi.nlm.nih.gov/pubmed/10359408 Lebech M, Andersen O, Christensen NC, Hertel J, Nielsen HE, Peitersen B, Rechnitzer C, Larsen SO, Nørgaard-Pedersen B, Petersen E.Feasibility of neonatal screening for toxoplasma infection in the absence of prenatal treatment. Danish Congenital Toxoplasmosis Study Group. Lancet. 1999 May 29;353(9167):1834-7.]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=91063Toxoplasmosis2013-07-23T17:37:53Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans and asexually reproduce within them, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks after infection. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection in other hosts. Intermediate hosts, commonly birds and rodents (typical prey of felines), may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals (including many of those bred for food) may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), and infection of a fetus transplacentally from the mother. A less likely method of infection is receiving a blood transfusion or organ transplant from individuals harboring tissue cysts. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease within a host, although it has been suggested that the number is very low due to high rates of infection. [[#References|[2]]] There are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br /><font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, that's fairly typical, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle and reproduce sexually to further diversify the species. <br />
<br />
<font size="3.5"><br/><i>Modifying intermediate host behavior</i></font><br />
<br />Logically, it may be inferred that the best way to enter a new feline host would be to be eaten by a feline host, so <i>T. gondii</i> has developed a mechanism by which it may alter its intermediate host's behavior to ensure it ends up in the stomach of a cat. Generally, mice and rats (common intermediate hosts for Toxoplasmosis) have a strong aversion to the smell of cat urine, as it is indicative of the presence of a cat (or to a mouse, a predator) in the immediate vicinity. <i>T.gondii</i> has developed a mechanism by which it changes rodent's innate aversion to feline odors and instead produces an attraction to these smells, thus increasing the likelihood that the intermediate rodent host will be eaten by the feline definitive host. This adaptation by <i>T. gondii</i>aids in its transmission to a definitive host, and ensure its ability to reproduce sexually. The mechanisms by which <i>T.gondii</i> is able to make such behavior modifications are still unknown. [[#References|[7]]]<br />
<br />
<font size="3.5"><br/><i>Toxoplasma influence on human behavior</i></font><br />
<br />While the symptoms of Toxoplasma infection seem to be fairly mild, recent research regarding this parasite has revealed an abundance of information pertaining to the psychological effects that Toxoplasmosis infection can induce in a human host. Indeed, Toxoplasma infection has been linked to increased risk of developing schizophrenia in infants whose mothers were infected by Toxoplasmosis,correlated to differences in behaviors between cultures, linked to increased neuroticism, and an alarmingly high correlation between infection and suicide rates. [[#References|[8]]] In one specific study, scientists were able to measure antibody levels for <i>T. gondii</i> from children to determine both the mother's infection status (because children's antibodies reflect those of their mothers until about three months after birth), and use a cause of death register later to passively screen the relationship between Toxoplasmosis infection and self-directed violence and suicide. [[#References|[9]]] The correlation between Toxoplasmosis infection and suicide was alarmingly high, women (the mothers of the children that had been screened) with Toxoplasmosis were 54% more likely to have attempted suicide, and two times as likely to have succeeded in that endeavor. Specifically, women infected with Toxoplasmosis were more likely to have attempted (or succeeded in) committing suicide violently (with a knife, gun, etc.). Additionally, it was determined that those with the highest levels of antibody serum were even more likely to commit a violent suicide (91%) than women with lower levels of antibody serum or uninfected women. [[#References|[9]]] This new information regarding Toxoplasmosis infection is alarming, and especially so because scientists do not fully understand the mechanism by which <i>T. gondii</i> is able to hijack the brain's neurochemical pathways to significantly alter human behavior.<br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu-like symptoms, swollen lymph nodes, muscle aches/pain, etc. for a few weeks that eventually disappear. [[#References|[1]]] <br />
<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including severe inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and is generally around 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]] Treatments for behavior modification's that result from Toxoplasmosis infection in humans have not yet been discovered because the specific cause of psychological disturbance in individuals infected with <i>T. gondii</i> has not yet been identified. [[#References|[8]]]<br />
<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduces the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and diminishes approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will commence and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen. Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2.]<br />
<br />8 [http://blogs.scientificamerican.com/science-sushi/2012/07/04/toxoplasmas-dark-side-the-link-between-parasite-and-suicide/ Christie Wilcox. Toxoplasma’s Dark Side: The Link Between Parasite and Suicide. Scientific American. Published online July 4, 2012.]<br />
<br />9 [http://www.ncbi.nlm.nih.gov/pubmed/10359408 Lebech M, Andersen O, Christensen NC, Hertel J, Nielsen HE, Peitersen B, Rechnitzer C, Larsen SO, Nørgaard-Pedersen B, Petersen E.Feasibility of neonatal screening for toxoplasma infection in the absence of prenatal treatment. Danish Congenital Toxoplasmosis Study Group. Lancet. 1999 May 29;353(9167):1834-7.]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=91040Toxoplasmosis2013-07-23T16:57:16Z<p>Magdalene.C.Shaughnessy-1: /* Treatment */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans and asexually reproduce within them, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks after infection. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection in other hosts. Intermediate hosts, commonly birds and rodents (typical prey of felines), may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals (including many of those bred for food) may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), and infection of a fetus transplacentally from the mother. A less likely method of infection is receiving a blood transfusion or organ transplant from individuals harboring tissue cysts. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease within a host, although it has been suggested that the number is very low due to high rates of infection. [[#References|[2]]] There are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br /><font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, that's fairly typical, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle and reproduce sexually to further diversify the species. <br />
<br />
<font size="3.5"><br/><i>Modifying intermediate host behavior</i></font><br />
<br />Logically, it may be inferred that the best way to enter a new feline host would be to be eaten by a feline host, so <i>T. gondii</i> has developed a mechanism by which it may alter its intermediate host's behavior to ensure it ends up in the stomach of a cat. Generally, mice and rats (common intermediate hosts for Toxoplasmosis) have a strong aversion to the smell of cat urine, as it is indicative of the presence of a cat (or to a mouse, a predator) in the immediate vicinity. <i>T.gondii</i> has developed a mechanism by which it changes rodent's innate aversion to feline odors and instead produces an attraction to these smells, thus increasing the likelihood that the intermediate rodent host will be eaten by the feline definitive host. This adaptation by <i>T. gondii</i>aids in its transmission to a definitive host, and ensure its ability to reproduce sexually. The mechanisms by which <i>T.gondii</i> is able to make such behavior modifications are still unknown. [[#References|[7]]]<br />
<br />
<font size="3.5"><br/><i>Toxoplasma influence on human behavior</i></font><br />
<br />While the symptoms of Toxoplasma infection seem to be fairly mild, recent research regarding this parasite has revealed an abundance of information pertaining to the psychological effects that Toxoplasmosis infection can induce in a human host. Indeed, Toxoplasma infection has been linked to increased risk of developing schizophrenia in infants whose mothers were infected by Toxoplasmosis,correlated to differences in behaviors between cultures, linked to increased neuroticism, and an alarmingly high correlation between infection and suicide rates. [[#References|[8]]] In one specific study, scientists were able to measure antibody levels for <i>T. gondii</i> from children to determine both the mother's infection status (because children's antibodies reflect those of their mothers until about three moths after birth), and use a cause of death register later to passively screen the relationship between Toxoplasmosis infection and self-directed violence and suicide. [[#References|[9]]] The correlation between Toxoplasmosis infection and suicide was alarmingly high, women (the mothers of the children that had been screened) with Toxoplasmosis were 54% more likely to have attempted suicide, and two times as likely to have succeeded in that endeavor. Specifically, women infected with Toxoplasmosis were more likely to have attempted (or succeeded in) committing suicide violently (with a knife, gun, etc.). Additionally, it was determined that those with the highest levels of antibody serum were even more likely to commit a violent suicide (91%) than women with lower levels of antibody serum or uninfected women. [[#References|[9]]] This new information regarding Toxoplasmosis infection is alarming, and especially so because scientists do not fully understand the mechanism by which <i>T. gondii</i> is able to hijack the brain's neurochemical pathways to significantly alter human behavior.<br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu-like symptoms, swollen lymph nodes, muscle aches/pain, etc. for a few weeks that eventually disappear. [[#References|[1]]] <br />
<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including severe inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and is generally around 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]] Treatments for behavior modification's that result from Toxoplasmosis infection in humans have not yet been discovered because the specific cause of psychological disturbance in individuals infected with <i>T. gondii</i> has not yet been identified. [[#References|[8]]]<br />
<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduces the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and diminishes approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will commence and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen. Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2.]<br />
<br />8 [http://blogs.scientificamerican.com/science-sushi/2012/07/04/toxoplasmas-dark-side-the-link-between-parasite-and-suicide/ Christie Wilcox. Toxoplasma’s Dark Side: The Link Between Parasite and Suicide. Scientific American. Published online July 4, 2012.]<br />
<br />9 [http://www.ncbi.nlm.nih.gov/pubmed/10359408 Lebech M, Andersen O, Christensen NC, Hertel J, Nielsen HE, Peitersen B, Rechnitzer C, Larsen SO, Nørgaard-Pedersen B, Petersen E.Feasibility of neonatal screening for toxoplasma infection in the absence of prenatal treatment. Danish Congenital Toxoplasmosis Study Group. Lancet. 1999 May 29;353(9167):1834-7.]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=91039Toxoplasmosis2013-07-23T16:57:02Z<p>Magdalene.C.Shaughnessy-1: /* Treatment */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans and asexually reproduce within them, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks after infection. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection in other hosts. Intermediate hosts, commonly birds and rodents (typical prey of felines), may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals (including many of those bred for food) may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), and infection of a fetus transplacentally from the mother. A less likely method of infection is receiving a blood transfusion or organ transplant from individuals harboring tissue cysts. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease within a host, although it has been suggested that the number is very low due to high rates of infection. [[#References|[2]]] There are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br /><font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, that's fairly typical, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle and reproduce sexually to further diversify the species. <br />
<br />
<font size="3.5"><br/><i>Modifying intermediate host behavior</i></font><br />
<br />Logically, it may be inferred that the best way to enter a new feline host would be to be eaten by a feline host, so <i>T. gondii</i> has developed a mechanism by which it may alter its intermediate host's behavior to ensure it ends up in the stomach of a cat. Generally, mice and rats (common intermediate hosts for Toxoplasmosis) have a strong aversion to the smell of cat urine, as it is indicative of the presence of a cat (or to a mouse, a predator) in the immediate vicinity. <i>T.gondii</i> has developed a mechanism by which it changes rodent's innate aversion to feline odors and instead produces an attraction to these smells, thus increasing the likelihood that the intermediate rodent host will be eaten by the feline definitive host. This adaptation by <i>T. gondii</i>aids in its transmission to a definitive host, and ensure its ability to reproduce sexually. The mechanisms by which <i>T.gondii</i> is able to make such behavior modifications are still unknown. [[#References|[7]]]<br />
<br />
<font size="3.5"><br/><i>Toxoplasma influence on human behavior</i></font><br />
<br />While the symptoms of Toxoplasma infection seem to be fairly mild, recent research regarding this parasite has revealed an abundance of information pertaining to the psychological effects that Toxoplasmosis infection can induce in a human host. Indeed, Toxoplasma infection has been linked to increased risk of developing schizophrenia in infants whose mothers were infected by Toxoplasmosis,correlated to differences in behaviors between cultures, linked to increased neuroticism, and an alarmingly high correlation between infection and suicide rates. [[#References|[8]]] In one specific study, scientists were able to measure antibody levels for <i>T. gondii</i> from children to determine both the mother's infection status (because children's antibodies reflect those of their mothers until about three moths after birth), and use a cause of death register later to passively screen the relationship between Toxoplasmosis infection and self-directed violence and suicide. [[#References|[9]]] The correlation between Toxoplasmosis infection and suicide was alarmingly high, women (the mothers of the children that had been screened) with Toxoplasmosis were 54% more likely to have attempted suicide, and two times as likely to have succeeded in that endeavor. Specifically, women infected with Toxoplasmosis were more likely to have attempted (or succeeded in) committing suicide violently (with a knife, gun, etc.). Additionally, it was determined that those with the highest levels of antibody serum were even more likely to commit a violent suicide (91%) than women with lower levels of antibody serum or uninfected women. [[#References|[9]]] This new information regarding Toxoplasmosis infection is alarming, and especially so because scientists do not fully understand the mechanism by which <i>T. gondii</i> is able to hijack the brain's neurochemical pathways to significantly alter human behavior.<br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu-like symptoms, swollen lymph nodes, muscle aches/pain, etc. for a few weeks that eventually disappear. [[#References|[1]]] <br />
<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including severe inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and is generally around 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]] Treatments for behavior modification's that result from Toxoplasmosis infection in humans have not yet been discovered because the specific cause of psychological disturbance in individuals infected with <i>T. gondii</i> has not yet been identified. [[#References|[8]]]<br />
<br />
<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduces the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and diminishes approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will commence and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen. Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2.]<br />
<br />8 [http://blogs.scientificamerican.com/science-sushi/2012/07/04/toxoplasmas-dark-side-the-link-between-parasite-and-suicide/ Christie Wilcox. Toxoplasma’s Dark Side: The Link Between Parasite and Suicide. Scientific American. Published online July 4, 2012.]<br />
<br />9 [http://www.ncbi.nlm.nih.gov/pubmed/10359408 Lebech M, Andersen O, Christensen NC, Hertel J, Nielsen HE, Peitersen B, Rechnitzer C, Larsen SO, Nørgaard-Pedersen B, Petersen E.Feasibility of neonatal screening for toxoplasma infection in the absence of prenatal treatment. Danish Congenital Toxoplasmosis Study Group. Lancet. 1999 May 29;353(9167):1834-7.]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=91037Toxoplasmosis2013-07-23T16:49:23Z<p>Magdalene.C.Shaughnessy-1: </p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans and asexually reproduce within them, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks after infection. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection in other hosts. Intermediate hosts, commonly birds and rodents (typical prey of felines), may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals (including many of those bred for food) may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), and infection of a fetus transplacentally from the mother. A less likely method of infection is receiving a blood transfusion or organ transplant from individuals harboring tissue cysts. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease within a host, although it has been suggested that the number is very low due to high rates of infection. [[#References|[2]]] There are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br /><font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, that's fairly typical, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle and reproduce sexually to further diversify the species. <br />
<br />
<font size="3.5"><br/><i>Modifying intermediate host behavior</i></font><br />
<br />Logically, it may be inferred that the best way to enter a new feline host would be to be eaten by a feline host, so <i>T. gondii</i> has developed a mechanism by which it may alter its intermediate host's behavior to ensure it ends up in the stomach of a cat. Generally, mice and rats (common intermediate hosts for Toxoplasmosis) have a strong aversion to the smell of cat urine, as it is indicative of the presence of a cat (or to a mouse, a predator) in the immediate vicinity. <i>T.gondii</i> has developed a mechanism by which it changes rodent's innate aversion to feline odors and instead produces an attraction to these smells, thus increasing the likelihood that the intermediate rodent host will be eaten by the feline definitive host. This adaptation by <i>T. gondii</i>aids in its transmission to a definitive host, and ensure its ability to reproduce sexually. The mechanisms by which <i>T.gondii</i> is able to make such behavior modifications are still unknown. [[#References|[7]]]<br />
<br />
<font size="3.5"><br/><i>Toxoplasma influence on human behavior</i></font><br />
<br />While the symptoms of Toxoplasma infection seem to be fairly mild, recent research regarding this parasite has revealed an abundance of information pertaining to the psychological effects that Toxoplasmosis infection can induce in a human host. Indeed, Toxoplasma infection has been linked to increased risk of developing schizophrenia in infants whose mothers were infected by Toxoplasmosis,correlated to differences in behaviors between cultures, linked to increased neuroticism, and an alarmingly high correlation between infection and suicide rates. [[#References|[8]]] In one specific study, scientists were able to measure antibody levels for <i>T. gondii</i> from children to determine both the mother's infection status (because children's antibodies reflect those of their mothers until about three moths after birth), and use a cause of death register later to passively screen the relationship between Toxoplasmosis infection and self-directed violence and suicide. [[#References|[9]]] The correlation between Toxoplasmosis infection and suicide was alarmingly high, women (the mothers of the children that had been screened) with Toxoplasmosis were 54% more likely to have attempted suicide, and two times as likely to have succeeded in that endeavor. Specifically, women infected with Toxoplasmosis were more likely to have attempted (or succeeded in) committing suicide violently (with a knife, gun, etc.). Additionally, it was determined that those with the highest levels of antibody serum were even more likely to commit a violent suicide (91%) than women with lower levels of antibody serum or uninfected women. [[#References|[9]]] This new information regarding Toxoplasmosis infection is alarming, and especially so because scientists do not fully understand the mechanism by which <i>T. gondii</i> is able to hijack the brain's neurochemical pathways to significantly alter human behavior.<br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu-like symptoms, swollen lymph nodes, muscle aches/pain, etc. for a few weeks that eventually disappear. [[#References|[1]]] <br />
<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including severe inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and is generally around 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]] <br />
<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduces the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and diminishes approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will commence and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen. Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2.]<br />
<br />8 [http://blogs.scientificamerican.com/science-sushi/2012/07/04/toxoplasmas-dark-side-the-link-between-parasite-and-suicide/ Christie Wilcox. Toxoplasma’s Dark Side: The Link Between Parasite and Suicide. Scientific American. Published online July 4, 2012.]<br />
<br />9 [http://www.ncbi.nlm.nih.gov/pubmed/10359408 Lebech M, Andersen O, Christensen NC, Hertel J, Nielsen HE, Peitersen B, Rechnitzer C, Larsen SO, Nørgaard-Pedersen B, Petersen E.Feasibility of neonatal screening for toxoplasma infection in the absence of prenatal treatment. Danish Congenital Toxoplasmosis Study Group. Lancet. 1999 May 29;353(9167):1834-7.]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90915Toxoplasmosis2013-07-23T11:15:04Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br /><font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, that's fairly typical, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle. <br />
<font size="3.5"><br/><i>Modifying intermediate host behavior</i></font><br />
<br />Logically, it may be inferred that the best way to enter a new feline host would be to be eaten by a feline host, so <i>T. gondii</i> has developed a mechanism by which it may alter its intermediate host's behavior to ensure it ends up in the stomach of a cat. Generally, mice and rats (common intermediate hosts for Toxoplasmosis) have a strong aversion to the smell of cat urine, as it is indicative of the presence of a cat (or to a mouse, a predator) in the immediate vicinity. <i>T.gondii</i> has developed a mechanism by which it changes rodent's innate aversion to feline odors and instead produces an attraction to these smells, thus increasing the likelihood that the intermediate rodent host will be eaten up by the feline definitive host. This adaptation by <i>T. gondii</i>aids in its transmission to a definitive host, and ensure its ability to reproduce sexually. The mechanisms by which <i>T.gondii</i> is able to make such behavior modifications are still unknown. [[#References|[7]]]<br />
<font size="3.5"><br/><i>Toxoplasma influence on human behavior</i></font><br />
<br />While the symptoms of Toxoplasma infection seem to be fairly mild, recent research regarding this parasite has revealed an abundance of information pertaining to the psychological effects that Toxoplasmosis infection can induce in a human host. Indeed, Toxoplasma infection has been linked to increased risk of developing schizophrenia in infants with mothers infected by Toxoplasmosis, behavior differences between cultures, neuroticism, and an alarmingly high correlation between infection and suicide rates. [[#References|[8]]] In one specific study, scientists were able to measure antibody levels for <i>T. gondii</i> from children to determine both the mother's infection status (because children's antibodies reflect those of their mothers until about three moths after birth), and use a cause of death register later to passively screen the relationship between Toxoplasmosis infection and self-directed violence and suicide. [[#References|[9]]] The correlation between infection and suicide was alarmingly high, women (the mothers of the children that had been screened) with Toxoplasmosis were 54% more likely to have attempted suicide, and two times as likely to have succeeded in that endeavor. Specifically, women infected with Toxoplasmosis were more likely to have attempted (or succeeded in) committing suicide via a violent mechanism. Additionally, it was determined that those with the highest levels of antibody serum were even more likely to commit a violent suicide (91%) than women with lower levels of antibody serum or uninfected women. [[#References|[9]]] This new information regarding Toxoplasmosis infection is alarming, and especially so because scientists do not fully understand the mechanism by which <i>T. gondii</i> is able to hijack our neurochemical pathways to significantly alter human behavior.<br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2.]<br />
<br />8 [http://blogs.scientificamerican.com/science-sushi/2012/07/04/toxoplasmas-dark-side-the-link-between-parasite-and-suicide/ Christie Wilcox. Toxoplasma’s Dark Side: The Link Between Parasite and Suicide. Scientific American. Published online July 4, 2012.]<br />
<br />9 [http://www.ncbi.nlm.nih.gov/pubmed/10359408 Lebech M, Andersen O, Christensen NC, Hertel J, Nielsen HE, Peitersen B, Rechnitzer C, Larsen SO, Nørgaard-Pedersen B, Petersen E.Feasibility of neonatal screening for toxoplasma infection in the absence of prenatal treatment. Danish Congenital Toxoplasmosis Study Group. Lancet. 1999 May 29;353(9167):1834-7.]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90825Toxoplasmosis2013-07-23T09:49:00Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br /><font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, that's fairly typical, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle. <br />
<font size="3.5"><br/><i>Modifying intermediate host behavior</i></font><br />
<br />Logically, it may be inferred that the best way to enter a new feline host would be to be eaten by a feline host, so <i>T. gondii</i> has developed a mechanism by which it may alter its intermediate host's behavior to ensure it ends up in the stomach of a cat. Generally, mice and rats (common intermediate hosts for Toxoplasmosis) have a strong aversion to the smell of cat urine, as it is indicative of the presence of a cat (or to a mouse, a predator) in the immediate vicinity. <i>T.gondii</i> has developed a mechanism by which it changes rodent's innate aversion to feline odors and instead produces an attraction to these smells, thus increasing the likelihood that the intermediate rodent host will be eaten up by the feline definitive host. This adaptation by <i>T. gondii</i>aids in its transmission to a definitive host, and ensure its ability to reproduce sexually. The mechanisms by which <i>T.gondii</i> is able to make such behavior modifications are still unknown. [[#References|[7]]]<br />
<font size="3.5"><br/><i>Toxoplasma influence on human behavior</i></font><br />
While the symptoms of Toxoplasma infection seem to be fairly mild, recent research regarding this parasite has revealed an abundance of information pertaining to the psychological effects that Toxoplasmosis infection can induce in a human host. Indeed, Toxoplasma infection has been linked to increased risk of developing schizophrenia in infants with mothers infected by Toxoplasmosis, behavior differences between cultures, neuroticism, and an alarmingly high correlation between infection and suicide rates. [[#References|[8]]] In one specific study, scientists were able to measure antibody levels for <i>T. gondii</i> from children to determine both the mother's infection status (because children's antibodies reflect those of their mothers until about three moths after birth), and use a cause of death register later to passively screen the relationship between Toxoplasmosis infection and self-directed violence and suicide. [[#References|[9]]] The correlation between infection and suicide was alarmingly high, women (the mothers of the children that had been screened) with Toxoplasmosis were 54% more likely to have attempted suicide, and two times as likely to have succeeded in that endeavor. Specifically, women infected with Toxoplasmosis were more likely to have attempted (or succeeded in) committing suicide via a violent mechanism. Additionally, it was determined that those with the highest levels of antibody serum were even more likely to commit a violent suicide (91%) than women with lower levels of antibody serum or uninfected women. [[#References|[9]]] This new information regarding Toxoplasmosis infection is alarming, and especially so because scientists do not fully understand the mechanism by which <i>T. gondii</i> is able to hijack our neurochemical pathways to significantly alter human behavior.<br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2.]<br />
<br />8 [http://blogs.scientificamerican.com/science-sushi/2012/07/04/toxoplasmas-dark-side-the-link-between-parasite-and-suicide/ Christie Wilcox. Toxoplasma’s Dark Side: The Link Between Parasite and Suicide. Scientific American. Published online July 4, 2012.]<br />
<br />9 [http://www.ncbi.nlm.nih.gov/pubmed/10359408 Lebech M, Andersen O, Christensen NC, Hertel J, Nielsen HE, Peitersen B, Rechnitzer C, Larsen SO, Nørgaard-Pedersen B, Petersen E.Feasibility of neonatal screening for toxoplasma infection in the absence of prenatal treatment. Danish Congenital Toxoplasmosis Study Group. Lancet. 1999 May 29;353(9167):1834-7.]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90821Toxoplasmosis2013-07-23T09:48:29Z<p>Magdalene.C.Shaughnessy-1: </p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br /><font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, that's fairly typical, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle. <br />
<font size="3.5"><br/><i>Modifying intermediate host behavior</i></font><br />
<br />Logically, it may be inferred that the best way to enter a new feline host would be to be eaten by a feline host, so <i>T. gondii</i> has developed a mechanism by which it may alter its intermediate host's behavior to ensure it ends up in the stomach of a cat. Generally, mice and rats (common intermediate hosts for Toxoplasmosis) have a strong aversion to the smell of cat urine, as it is indicative of the presence of a cat (or to a mouse, a predator) in the immediate vicinity. <i>T.gondii</i> has developed a mechanism by which it changes rodent's innate aversion to feline odors and instead produces an attraction to these smells, thus increasing the likelihood that the intermediate rodent host will be eaten up by the feline definitive host. This adaptation by <i>T. gondii</i>aids in its transmission to a definitive host, and ensure its ability to reproduce sexually. The mechanisms by which <i>T.gondii</i> is able to make such behavior modifications are still unknown. [[#References|[7]]]<br />
<font size="3.5"><br/><i>Toxoplasma influence on human behavior</i></font><br />
While the symptoms of Toxoplasma infection seem to be fairly mild, recent research regarding this parasite has revealed an abundance of information pertaining to the psychological effects that Toxoplasmosis infection can induce in a human host. Indeed, Toxoplasma infection has been linked to increased risk of developing schizophrenia in infants with mothers infected by Toxoplasmosis, behavior differences between cultures, neuroticism, and an alarmingly high correlation between infection and suicide rates. [[#References|[8]]] In one specific study, scientists were able to measure antibody levels for <i>T. gondii</i> from children to determine both the mother's infection status (because children's antibodies reflect those of their mothers until about three moths after birth), and use a cause of death register later to passively screen the relationship between Toxoplasmosis infection and self-directed violence and suicide. [[#References|[9]]] The correlation between infection and suicide was alarmingly high, women (the mothers of the children that had been screened) with Toxoplasmosis were 54% more likely to have attempted suicide, and two times as likely to have succeeded in that endeavor. Specifically, women infected with Toxoplasmosis were more likely to have attempted (or succeeded in) committing suicide via a violent mechanism. Additionally, it was determined that those with the highest levels of antibody serum were even more likely to commit a violent suicide (91%) than women with lower levels of antibody serum or uninfected women. [[#References|[9]]] This new information regarding Toxoplasmosis infection is alarming, and especially so because scientists do not fully understand the mechanism by which <i>T. gondii</i> is able to hijack our neurochemical pathways to significantly alter our behavior.<br />
<br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2.]<br />
<br />8 [http://blogs.scientificamerican.com/science-sushi/2012/07/04/toxoplasmas-dark-side-the-link-between-parasite-and-suicide/ Christie Wilcox. Toxoplasma’s Dark Side: The Link Between Parasite and Suicide. Scientific American. Published online July 4, 2012.]<br />
<br />9 [http://www.ncbi.nlm.nih.gov/pubmed/10359408 Lebech M, Andersen O, Christensen NC, Hertel J, Nielsen HE, Peitersen B, Rechnitzer C, Larsen SO, Nørgaard-Pedersen B, Petersen E.Feasibility of neonatal screening for toxoplasma infection in the absence of prenatal treatment. Danish Congenital Toxoplasmosis Study Group. Lancet. 1999 May 29;353(9167):1834-7.]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90799Toxoplasmosis2013-07-23T09:24:49Z<p>Magdalene.C.Shaughnessy-1: /* References */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br /><font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, that's fairly typical, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle. <br />
<font size="3.5"><br/><i>Modifying intermediate host behavior</i></font><br />
<br />Logically, it may be inferred that the best way to enter a new feline host would be to be eaten by a feline host, so <i>T. gondii</i> has developed a mechanism by which it may alter its intermediate host's behavior to ensure it ends up in the stomach of a cat. Generally, mice and rats (common intermediate hosts for Toxoplasmosis) have a strong aversion to the smell of cat urine, as it is indicative of the presence of a cat (or to a mouse, a predator) in the immediate vicinity. <i>T.gondii</i> has developed a mechanism by which it changes rodent's innate aversion to feline odors and instead produces an attraction to these smells, thus increasing the likelihood that the intermediate rodent host will be eaten up by the feline definitive host. This adaptation by <i>T. gondii</i>aids in its transmission to a definitive host, and ensure its ability to reproduce sexually. The mechanisms by which <i>T.gondii</i> is able to make such behavior modifications are still unknown. [[#References|[7]]]<br />
<font size="3.5"><br/><i>Potential link between Toxoplasmosis infection and suicide in human hosts</i></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2.]<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90793Toxoplasmosis2013-07-23T09:19:32Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br /><font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, that's fairly typical, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle. <br />
<font size="3.5"><br/><i>Modifying intermediate host behavior</i></font><br />
<br />Logically, it may be inferred that the best way to enter a new feline host would be to be eaten by a feline host, so <i>T. gondii</i> has developed a mechanism by which it may alter its intermediate host's behavior to ensure it ends up in the stomach of a cat. Generally, mice and rats (common intermediate hosts for Toxoplasmosis) have a strong aversion to the smell of cat urine, as it is indicative of the presence of a cat (or to a mouse, a predator) in the immediate vicinity. <i>T.gondii</i> has developed a mechanism by which it changes rodent's innate aversion to feline odors and instead produces an attraction to these smells, thus increasing the likelihood that the intermediate rodent host will be eaten up by the feline definitive host. This adaptation by <i>T. gondii</i>aids in its transmission to a definitive host, and ensure its ability to reproduce sexually. The mechanisms by which <i>T.gondii</i> is able to make such behavior modifications are still unknown. [[#References|[7]]]<br />
<font size="3.5"><br/><i>Potential link between Toxoplasmosis infection and suicide in human hosts</i></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2.]<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90787Toxoplasmosis2013-07-23T09:13:06Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br /><font size="4"><b>Virulence factors</b></font><br />
<font size="3.5"><br/><i>Modifying intermediate host behavior</i></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, that's fairly typical, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle. Logically, it may be inferred that the best way to enter a new feline host would be to be eaten by a feline host, so <i>T. gondii</i> has developed a mechanism by which it may alter its intermediate host's behavior to ensure it ends up in the stomach of a cat. Generally, mice and rats (common intermediate hosts for Toxoplasmosis) have a strong aversion to the smell of cat urine, as it is indicative of the presence of a cat (or to a mouse, a predator) in the immediate vicinity. <i>T.gondii</i> has developed a mechanism by which it changes rodent's innate aversion to feline odors and instead produces an attraction to these smells, thus increasing the likelihood that the intermediate rodent host will be eaten up by the feline definitive host. This adaptation by <i>T. gondii</i>aids in its transmission to a definitive host, and ensure its ability to reproduce sexually. The mechanisms by which <i>T.gondii</i> is able to make such behavior modifications are still unknown. [[#References|[7]]]<br />
<font size="3.5"><br/><i>Potential link between Toxoplasmosis infection and suicide in human hosts</i></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2.]<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90778Toxoplasmosis2013-07-23T09:01:31Z<p>Magdalene.C.Shaughnessy-1: /* References */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle.<br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2.]<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90776Toxoplasmosis2013-07-23T09:00:57Z<p>Magdalene.C.Shaughnessy-1: /* References */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle.<br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />7 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851063/#__ffn_sectitle Ajai Vyas, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. Proc Natl Acad Sci U S A. 2007 April 10; 104(15): 6442–6447. Published online 2007 April 2. doi: 10.1073/pnas.0608310104]<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90774Toxoplasmosis2013-07-23T08:58:57Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />Arguably the most interesting aspect of the protozoan parasite <i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle.<br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90773Toxoplasmosis2013-07-23T08:56:12Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
Arguably the most interesting aspect of the protozoan parasite<i>Toxoplasmosis gondii</i> are its virulence factors. Not so much in the way it colonizes and causes disease within a host, but the mechanisms it has developed in order to ensure it is able to find the "right" host, a cat, in which it may complete its lifecycle.<br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90767Toxoplasmosis2013-07-23T08:34:17Z<p>Magdalene.C.Shaughnessy-1: /* Clinical features */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are vary drastically from around 30-95% of persons being infected within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90766Toxoplasmosis2013-07-23T08:32:33Z<p>Magdalene.C.Shaughnessy-1: /* Host Immune Response */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
<br />After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90765Toxoplasmosis2013-07-23T08:32:15Z<p>Magdalene.C.Shaughnessy-1: /* Host Immune Response */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection by <i>T. gondii</i>. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90764Toxoplasmosis2013-07-23T08:31:54Z<p>Magdalene.C.Shaughnessy-1: /* Host Immune Response */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection. [[#References|[6]]]<br />
<br /><i><font size="3.5">Adaptive immune response</font></i><br />
After the initiation of the non-specific innate immune response, the adaptive immune response will initiate and begin to develop and produce specific antibodies and effector cells to eliminate <i>T. gondii</i>. The innate immune response signals the necessity for the differentiation of macrophages, B cells, and dendritic cells to differentiate into antigen presenting cells. Antigen presenting cells may then present the antigen to T cells, stimulating the differentiation of T cells into effector cells, including CD8 cytotoxic T cells, to directly kill<i>T. gondii</i>. Specifically in humans, the infection of dendritic cells by <i>T. gondii</i> leads to the activation of CD40, which induces the production of effector cells which can directly kill, or secrete cytokines to recruit other cells to eliminate the pathogen.<br />
Eventually, immunological memory will be developed in response to the Toxoplasmosis infection. This immunological memory can protect the host from re-infection. It is hypothesized that this immunological memory is responsible for the rupturing of intracellular cysts caused by <i>T. gondii</i>. [[#References|[6]]] Unfortunately, because infants in utero do not have a strong adaptive immune response, they are much more susceptible to disease as a result of Toxoplasmosis infection.<br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90744Toxoplasmosis2013-07-23T08:07:50Z<p>Magdalene.C.Shaughnessy-1: </p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
Directly after ingestion/infection of <i>Toxoplasma gondii</i> the host innate immune response recognizes and responds to the protozoan as a foreign antigen. <i>T. gondii</i> triggers the activation of macrophages in the tissues along with NK cells which begin an attempt to eliminate the invader. The intent of the innate immune response is not to entirely eliminate the invader, but to limit the proliferation of the parasite and to signal for the activation of the adaptive immune response. The innate immune response begins directly after infection and ends approximately two weeks after the initial infection. [[#References|[6]]]<br />
<i><font size="3.5">Adaptive immune response</font></i><br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90738Toxoplasmosis2013-07-23T08:00:36Z<p>Magdalene.C.Shaughnessy-1: /* Host Immune Response */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
<i><font size="3.5">Innate immune response</font></i><br />
<br />
<br />
<i><font size="3.5">Adaptive immune response</font></i><br />
<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90735Toxoplasmosis2013-07-23T07:58:30Z<p>Magdalene.C.Shaughnessy-1: /* References */</p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />6 [http://www.iss.it/publ/anna/2004/1/40171.pdf Denis Filisetti and Ermanno Candolfi. Institut de Parasitologie et de Pathologie Tropicale, Strasbourg, France. Ann Ist Super Sanità 2004;40(1):71-80]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90504Toxoplasmosis2013-07-22T18:08:40Z<p>Magdalene.C.Shaughnessy-1: </p>
<hr />
<div>{{curated}}<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90500Toxoplasmosis2013-07-22T18:05:35Z<p>Magdalene.C.Shaughnessy-1: /* Prevention */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90499Toxoplasmosis2013-07-22T18:04:59Z<p>Magdalene.C.Shaughnessy-1: </p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
[[Image: Toxoplasmosis5.jpeg |thumb|400px|right| Pregnant women should not clean cat litter boxes <br /> From: http://www.cat-lovers-only.com/toxoplasmosis-pregnancy.html]]<br />
<br />
<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=File:Toxoplasmosis5.jpeg&diff=90496File:Toxoplasmosis5.jpeg2013-07-22T18:03:11Z<p>Magdalene.C.Shaughnessy-1: toxoplasmosis5</p>
<hr />
<div>toxoplasmosis5</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90489Toxoplasmosis2013-07-22T18:01:04Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90487Toxoplasmosis2013-07-22T18:00:40Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90485Toxoplasmosis2013-07-22T18:00:11Z<p>Magdalene.C.Shaughnessy-1: /* Prevention */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand, or after cleaning a cat's litter box. Outdoor sandboxes should be kept covered so that cats are not tempted to use them instead of a litter box. Children should be instructed as to the importance of proper hand washing to prevent infections. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat) for the duration of their pregnancy. Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90480Toxoplasmosis2013-07-22T17:58:33Z<p>Magdalene.C.Shaughnessy-1: /* Prevention */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. Additionally, untreated water should not be consumed. [[#References|[1]]]<br />
<br /><font size="3.5"><i>Reduce risk of infection from the environment</i></font><br />
<br />To reduce the risk of becoming infected Toxoplasmosis from the environment, gloves should be worn when in contact with any soil or sand that could contain cat feces. Proper hand washing techniques should be employed after contact with any soil or sand. Outdoor sandboxes should be kept covered so that cats are not tempted to use them as a litter box. And finally, pregnant women should have someone else clean the cat's litter box (if they have a cat). Cats that are kept indoors and are fed only well cooked or commercially purchased foods are unlikely to become infected with <i>T. gondii</i> unless there is a rodent infestation in their environment. [[#References|[1]]]<br />
<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90468Toxoplasmosis2013-07-22T17:52:52Z<p>Magdalene.C.Shaughnessy-1: /* Prevention */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. [[#References|[1]]]<br />
<br /><font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90466Toxoplasmosis2013-07-22T17:52:26Z<p>Magdalene.C.Shaughnessy-1: /* Prevention */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
<font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
In order to reduce the risk of Toxoplasmosis infection from meat sources, foods should be cooked to standard "safe" temperatures. The internal temperature of cooked meats should be taken using a food thermometer. The USDA recommends whole cuts of meat be cooked to at least 145° F, ground meat be cooked to at least 160° F, and all poultry products should be cooked to at least 165° F before consumption. Additionally, foods may be frozen at at least 0° F for a few days before cooking to greatly decrease the risk of infection. To reduce the risk of Toxoplasma infection from contaminated fruits and vegetables, the foods should be washed thoroughly and/or peeled before eating. Other sanitation techniques may be used in order to further reduce the risk of infection, ensuring all utensils that were in contact with raw or unwashed food products should be thoroughly cleaned before reuse. [[#References|[1]]]<br />
< br/><font size="3.5"><i>Reduce risk of infection via contaminated food sources</i></font><br />
<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90441Toxoplasmosis2013-07-22T17:36:53Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission and Colonization</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90438Toxoplasmosis2013-07-22T17:34:28Z<p>Magdalene.C.Shaughnessy-1: /* Diagnosis */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Colonization</b></font><br />
<br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.[[#References|[4]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90435Toxoplasmosis2013-07-22T17:30:41Z<p>Magdalene.C.Shaughnessy-1: /* Diagnosis */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Colonization</b></font><br />
<br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. In addition, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. In some cases, immunohistochemical staining and electron microscopy are used to enable the technician to observe Toxoplasmosis parasites in tissue samples obtained from the infected individual. [[#References|[4]]] <br />
<br />Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]] PCR techniques are especially helpful for detecting congenital infections. Additionally, computed tomography techniques can be used in identifying cerebral Toxoplasmosis infection, and ultrasounds may be used to identify Toxoplasmosis infection in a fetus.<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90431Toxoplasmosis2013-07-22T17:21:34Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce sexually are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Colonization</b></font><br />
<br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. Additionally, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90427Toxoplasmosis2013-07-22T17:17:18Z<p>Magdalene.C.Shaughnessy-1: /* References */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Colonization</b></font><br />
<br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. Additionally, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />5 [http://www.mayoclinic.com/health/toxoplasmosis/DS00510/DSECTION=treatments-and-drugs The Mayo Clinic Staff. Toxoplasmosis: Treatment and Drugs. Last Updated: June 24, 2011]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90425Toxoplasmosis2013-07-22T17:15:52Z<p>Magdalene.C.Shaughnessy-1: /* Treatment */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Colonization</b></font><br />
<br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. Additionally, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]]<br />
<br />
==Treatment==<br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Since 80-90% of Toxoplasmosis infections in healthy individuals are asymptomatic, the majority of infections go unnoticed and do not require treatment. When the rare occasion arises that an otherwise healthy individual presents with symptoms of acute Toxoplasmosis, a combination of pyrimethamine, an anti-malaria medication, and sulfadiazine, an antibiotic, may be prescribed. Folic acid is often prescribed along with pyrimethamine to avoid potentially harmful side effects of this drug. [[#References|[5]]]<br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />The treatment for an immunocompromised individual (i.e. one with HIV/AIDS) is also a combination of pyrimethamine and sulfadiazine. In some cases clindamycin may be prescribed as an alternative to sulfadiazine. Unlike immunocompetent patients, immunosuppressed patients may have to remain on these medications for life in order to keep the infection at bay. [[#References|[5]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />Pregnant women infected with toxoplasmosis whose fetus remain unaffected by Toxoplasmosis may be given the antibiotic spiramycin. This drug reduced the likelihood that the infant will become infected and suffer severe disease symptoms later on in life. Pyrimethamine and sulfadiazine are typically not prescribed to pregnant women whose babies are already infected as the drug will not repair any damage that has already been done, and the drugs come with serious risk of side effects for the unborn child. [[#References|[5]]]<br />
<br />
==Prevention==<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90415Toxoplasmosis2013-07-22T16:53:46Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Colonization</b></font><br />
<br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose, or approximate number, of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br /><font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. Additionally, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]]<br />
<br />
==Treatment==<br />
==Prevention==<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90414Toxoplasmosis2013-07-22T16:52:21Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Colonization</b></font><br />
<br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. Additionally, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]]<br />
<br />
==Treatment==<br />
==Prevention==<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90413Toxoplasmosis2013-07-22T16:51:38Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Colonization</b></font><br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. Additionally, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]]<br />
<br />
==Treatment==<br />
==Prevention==<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90412Toxoplasmosis2013-07-22T16:49:43Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br /><font size="4"><b>Colonization</b></font><br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br />
<font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. Additionally, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]]<br />
<br />
==Treatment==<br />
==Prevention==<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90411Toxoplasmosis2013-07-22T16:49:01Z<p>Magdalene.C.Shaughnessy-1: /* Pathogenesis */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission</b></font><br />
<font size="3.5"><br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<font size="3.5"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<font size="4"><b>Colonization</b></font><br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br />
<font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. Additionally, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]]<br />
<br />
==Treatment==<br />
==Prevention==<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1https://microbewiki.kenyon.edu/index.php?title=Toxoplasmosis&diff=90410Toxoplasmosis2013-07-22T16:48:09Z<p>Magdalene.C.Shaughnessy-1: /* Clinical features */</p>
<hr />
<div>{{curated}}<br />
[[Image:OUA.png|thumb|400px|center|Microbiology in Italy, July 2013 [http://cas.ou.edu/study-abroad/]]]<br />
[[Image: Toxoplasmosis2.jpeg |thumb|400px|right| <i>Toxoplasmosis gondii</i> <br /> From: http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v4/v4c046.html]]<br />
[[Image: Toxoplasmosis3.jpeg |thumb|400px|right| The only definitive hosts for <i>Toxoplasmosis gondii</i> are cats. <br /> From: http://www.economist.com/node/16271339]]<br />
<br />
==Description/Etiology/Taxonomy==<br />
<i>Toxoplasma gondii</i> is an obligate, intracellular parasitic protozoan that infects most species of warm blooded animals, including humans, and is the causative agent of the disease Toxoplasmosis. While <i>T. gondii</i> may infect humans to asexually reproduce and cause disease, the only host in which the protozoa may complete its life cycle and sexually reproduce are family Felidae, more commonly referred to as domestic cats and their relatives. [[#References|[1]]] <br />
<br />
<b>Taxonomy of <i>Toxoplasma gondii</i></b><br />
<br />Domain: Eukaryota<br />
<br />Kingdom: Chromalveolata<br />
<br /> Superphylum: Alveolata<br />
<br />Phylum: Apicomplexa<br />
<br />Class: Conoidasida<br />
<br /> Subclass: Coccidiasina<br />
<br /> Order: Eucoccidiorida<br />
<br /> Family: Sarcocystidae<br />
<br /> Subfamily: Toxoplasmatinae<br />
<br />Genus: <i>Toxoplasma</i><br />
<br />Species: <i> Toxoplasma gondii</i><br />
<br />
==Pathogenesis==<br />
[[Image: Toxoplasmosis4.gif |thumb|400px|right| <i>Toxoplasma gondii</i> life cycle. From: http://www.cdc.gov/parasites/toxoplasmosis/biology.html]]<br />
<font size="4"><br /><b>Transmission</b><br />
<br /><i>Lifecycle</i></font><br />
<br />The only hosts in which <i>Toxoplasma gondii</i> can mature and reproduce are members of the family Felidae. Infected domestic cats (and those related to them) will shed large numbers of unsporulated oocysts in their feces for approximately one to two weeks. Oocysts released into the environment take from one to five days to form spores and become capable of causing infection. Intermediate hosts, commonly birds and rodents as they are typical prey of felines, may then become infected by consuming materials contaminated with <i>T. gondii</i> spores. After ingestion, oocysts develop into tachyzoites which localize in neural and muscle tissues to develop into cyst bradyzoites. Members of the family Felidae become infected after consuming intermediate hosts that have these cysts in their tissues. Additionally, other animals may become infected with cysts after ingesting <i>T. gondii</i> spores from the environment. [[#References|[1]]]<br />
<br />
<font size="4"><br/><i>Infecting humans</i></font><br />
<br />Humans may become infected with <i>Toxoplasma gondii</i> by a variety of routes. The most common methods of infection include: consuming undercooked meat of animals that had tissue cysts, consuming food or water contaminated with infected cat feces, consuming food or water contaminated by infected environmental samples (e.g. soil, cat litter), receiving a blood transfusion or organ transplant from individuals harboring tissue cysts, and infection of a fetus transplacentally from the mother. Unlike its lifecycle in felines and intermediate hosts, <i>T. gondii</i> commonly forms cysts in the skeletal muscle, brain, eyes, and myocardium of the human host. Additionally, rather than being shed in feces like the feline host, the cysts in a human host may remain for the entire life of the human host. [[#References|[1]]]<br />
<br />
<font size="4"><b>Colonization</b></font><br />
<br />
<font size="4"><b>Infectious dose</b></font><br />
<br />There is no known specific infectious dose of <i>Toxoplasma gondii</i> organisms required to cause disease, however it has been suggested that the number is very low. [[#References|[2]]] However, there are three stages of the <i>T. gondii</i> lifecycle in which it is infectious. The first infectious phase of the <i>T. gondii</i> lifecycle is during the oocyst stage; <i>T. gondii</i> oocysts may be found in soil or water and can survive in the environment for several months. The second infectious phase is the tachysoite stage, a phase of rapid replication in the tissues of the host; this is the stage responsible for the onset of acute toxoplasmosis. Finally, the third infectious stage of the <i>T.gondii</i> lifecycle is the bradyzoite stage in which the parasite slowly replicates in the muscle and brain tissue of the infected host. [[#References|[3]]] <br />
<br />
<font size="4"><b>Incubation period</b></font><br />
<br /> The incubation period, or the time between exposure to the organism and the onset of symptoms, of <i>Toxoplasma gondii</i> in a human host is 10 to 23 days after consuming contaminated food or water, and 5 to 20 days after exposure to infected cat feces. [[#References|[4]]]<br />
<br />
<br />
<font size="4"><b>Virulence factors</b></font><br />
<br />
==Clinical features==<br />
<font size="4"><b>Epidemiology</b></font><br />
<br />It is estimated that 22.5% of the United States population over age 12 is infected with <i>Toxoplasma gondii</i>. In other countries, the infection rates are close to 95% of infected persons within a population. <i>Toxoplamsa gondii</i> infects a greater percentage of people in areas of the world that lower in altitude and have hot, moist environments. [[#References|[1]]] <br />
<font size="4"><br /><b>Symptoms</b></font><br />
<br /><font size="3.5"><i>In healthy Individuals</i></font><br />
<br />Healthy individuals who become infected with <i>Toxoplasma gondii</i> are often asymptomatic. Occasionally, a non-immunosuppressed individual will develop flu like symptoms for a few weeks that eventually fade. [[#References|[1]]] <br />
<font size="3.5"><br /><i>In immunocompromised individuals</i></font><br />
<br />Immunocompromised individuals, for example individuals who have HIV/AIDS, suffer a wide range of symptoms from <i>Toxoplasma gondii</i> infection including inflammation of the lung tissue, myocarditis, and acute inflammation of the brain. [[#References|[2]]]<br />
<font size="3.5"><br /><i>Pregnancy-associated infection</i></font><br />
<br />If a woman becomes infected with <i>Toxoplasma gondii</i> while pregnant, especially in the early stages of pregnancy, the parasite may be congenitally transmitted to the unborn child. Results of a congenital infection often result in a miscarriage or still birth. Some children may be born asymptomatically and develop symptoms such as vision loss, mental disability, and seizures later in life. [[#References|[1]]]<br />
<font size="4"><br /><b>Morbidity/mortality</b></font><br />
<br />Toxoplasmosis infection is asymptomatic is 80-90% of infected healthy individuals and immunity typically remains consistent throughout the life of the host unless they become immunocompromised. However, in immunosuppressed patients, the mortality rate from infection is very high. For example, Toxoplasma-related encephalitis occurs in 25% of AIDS patients and was 84% fatal in this particularly immunosuppressed group. Additionally, the earlier on in a pregnancy that a fetus becomes congenitally infected, the higher the likelihood is that they would develop severe disease. [[#References|[4]]]<br />
<br />
==Diagnosis==<br />
Diagnosis of Toxoplasmosis is generally achieved via serology, or the examination of plasma or other bodily fluids to determine whether the body has produced antibodies in response to a specific antigen. Additionally, Toxoplasmosis may be diagnosed via the identification of <i>T.gondii</i> cysts in a tissue sample taken from a suspected infected individual. Diagnosis of Toxoplasmosis infection before birth may be determined by confirming the presence of <i>T. gondii</i> DNA in amniotic fluid. [[#References|[1]]]<br />
<br />
==Treatment==<br />
==Prevention==<br />
==Host Immune Response==<br />
==References==<br />
1 [http://www.cdc.gov/parasites/toxoplasmosis/biology.html Centers for Disease Control (CDC). General Information Toxoplasmosis. Page last updated: January 10, 2013]<br />
<br />2 [http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/msds153e-eng.php Public Health Agency of Canada. Toxoplasma gondii - Material Safety Data Sheets (MSDS). Date Modified: 2011-02-18]<br />
<br />3 [http://www.waterbornepathogens.org/index.php?option=com_content&view=article&id=65&Itemid=73 Sarah Staggs and Eric Villegas. Waterborne Pathogens: Toxoplasma. Last Updated: 04 April 2012]<br />
<br />4 [http://www.cfsph.iastate.edu/Factsheets/pdfs/toxoplasmosis.pdf Iowa State University. The Center for Food Security and Public Health. Toxoplasmosis: Toxoplasma Infection. Last Updated: May 2005]<br />
<br />
<br />
Created by Magdalene C. Shaughnessy, student of Tyrrell Conway at the University of Oklahoma</div>Magdalene.C.Shaughnessy-1