Nasal passageway: Difference between revisions

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Scientists researched the "functions of two staphylo9coccal biofilm matrix polymers: poly-N-acetylglucosamine surface polysaccharide (PNAG) and extracellular DNA (ecDNA)" and how the "PNAG-degrading enzyme, dispersin B, and DNase I inhibit biofilm formation, detach preformed biofilms, and sensitize biofilms to killing by the cationic detergent cetylpyridinium chloride (CPC)."  The biofilms will help protect the bacteria from being nullified by antibiotics and host defenses.  The scientists found that both dispersin B and DNase I will inhibit biofilm formation in S. aureus and PNAG-positive S. epidermidis strains.  Dispersin B will efficiently and rapidly detach S. epidermidis biofilms, but not S. aureus.  On the other hand, DNase I will cause separation of the biofilm and the surface in S. aureus, but not S. epidermidis.  PNAG is a major matrix component of only S. epidermidis biofilm cells, but it is produced by both bacteria.  The PNAG performs different functions in the biofilms of the two bacteria.  The PNAG protects the S. epidermidis cells from CPC killing, while the  PNAG works in early stages of S. aureus biofilms, which makes it resistant to the detachment of dispersin B.  Overall, ecDNA and PNAG can be "general diffusion barriers" that stop detergents from killing the bacteria. (7)
Scientists researched the "functions of two staphylo9coccal biofilm matrix polymers: poly-N-acetylglucosamine surface polysaccharide (PNAG) and extracellular DNA (ecDNA)" and how the "PNAG-degrading enzyme, dispersin B, and DNase I inhibit biofilm formation, detach preformed biofilms, and sensitize biofilms to killing by the cationic detergent cetylpyridinium chloride (CPC)."  The biofilms will help protect the bacteria from being nullified by antibiotics and host defenses.  The scientists found that both dispersin B and DNase I will inhibit biofilm formation in S. aureus and PNAG-positive S. epidermidis strains.  Dispersin B will efficiently and rapidly detach S. epidermidis biofilms, but not S. aureus.  On the other hand, DNase I will cause separation of the biofilm and the surface in S. aureus, but not S. epidermidis.  PNAG is a major matrix component of only S. epidermidis biofilm cells, but it is produced by both bacteria.  The PNAG performs different functions in the biofilms of the two bacteria.  The PNAG protects the S. epidermidis cells from CPC killing, while the  PNAG works in early stages of S. aureus biofilms, which makes it resistant to the detachment of dispersin B.  Overall, ecDNA and PNAG can be "general diffusion barriers" that stop detergents from killing the bacteria. (7)


Researchers form Cambridge University have isolated "methicillin-resistant coagulase negative staphylcocci (MRCNS)  from the nasal flora of healthy humans" from three places in Rio de Janeiro City. They obtained swaps from the nares of the adults at two military quarters and students from a public school. Staphylcocci were isolated and "tested for the presence of the mecA gene" by hybridizing the gene with a specific probe. S. epidermidis was the most common MRCNS; it accounted for 38 out of the 45 total. The SmaI-digested DNA was also put through pulsed-field gel electrophoresis in order to study the clonalityof the MRSE S. epidermidis. It appears that the cross-colonization contributed to the spread of the methicillin-resistance. The wide and diverse genome suggests that the spread of the mecA gene among the isolates were probably through horizontal transmission. It was concluded that though it was researched with only three institutions, it reflects how other communities in Rio may have gained methicillin resistance.





Revision as of 22:11, 28 August 2008

Template:Nasal Passageway

Description of Nasal Passageway


Location of the Nasal Passageway

The main entry to the nasal passageway is through the nostrils, inside the nose, which is located on the face. From there, the passageway extends to the throat. The nose is the organ of smell located in the middle of the face. The internal part of the nose lies above the roof of the mouth. It is supported by bone and cartilage. The bony part is formed mainly by the nasal bones on each side and the frontal process of the maxillary bone. The nasal cavity is the air passage starting at the nostril (opening of the nose) and ending at the back of the throat(4). Nasal Obstruction is a partial or complete blockage of one or both of these air passages. Nose is one of the few openings of the body for bacteria and microbes to go inside the body.

Physical Conditions of the Nasal Passageway

Normal:

The temperature of the nasal passageway in adults is 34°C. (9) The pressure of the normal passageway should be around 1 atm. There is little known about the pH of the human nasal cavity. The average pH in the anterior of the nose is 6.40. The pH in the posterior of the nasal cavity was 6.27. The overall range in pH was 5.17- 8.13 for the anterior cavity and 5.20 - 8.00 for the posterior cavity. The average baseline human nasal cavity pH is 6.3.(6)

In the nares, the air contains around 21% oxygen and 0.04% carbon dioxide. The oxygen is being absorbed by the epithelial cells which inhibits a gradient in the oxygen content through the mucus. The nares are predominantly an aerobic environment for bacteria to live in. (9)

The nasal passageway walls, and particularly the flap-like middle and inferior nasal conchae, are layered with respiratory mucous membranes secreted by goblet cells. These membranes have many small hair-like cells, known as cilia, that move mucus in waves toward the throat area. Bacteria, along with dust and other particles inhaled from the outside environment are snared by the nasal mucus, carried back out, and dripped into the gastric juices to destroy any possible pathogens. The mucus contains many defensive substances including lysozymes that dissolve and kill the bacteria, lactroferrin, immunoglobulins, and defensins, although some bacteria are not killed by this defensive substance.


Diseased: ????????? Aside from the pH paragraph, I don't really understand how this fits in this section. Actually, I'm having a hard time understanding what the paragraphs below are about. Maybe someone could edit this so that it's more clear? thanks. :) i just thought it would little helpful in this section bcoz its about temperature and wat factors gets affected due to this physical condition. but if u guys dont think its suitable plz fell free to delete it ! thanks Nidhi :)

The nose is the first segment of the upper respiratory tract and is exposed to different climatic conditions of the ambient air. When a microbe is present in the nose, the end-inspiratory intranasal humidity during breathing increases at all locations within the nasal passage and the temperature and humidity of the exposure condition increases. The increase in intranasal temperature has no relation to the different climatic conditions during the short-term exposure. The nasal humidification in ambient air can be influenced by short-term exposure to air of extreme temperature and humidity prior to breathing of ambient air.  ???????????????

As with the normal nasal passageways, little is known about the pH of the diseased niche. But in the infected person, it is known that the pH of the person changes accordingly, due to the presence of the bacterial community.

Nitric oxide (NO) releases into nasal passages by physical characteristics like airflow, temperature, humidity or gases like oxygen, carbon dioxide in nasal air of humans. Increasing airflow through the nose caused incremental increases in NO release and decreased humidity reduces NO release only at the highest airflow rate. Changing temperature has no effect on NO release. Characteristic like Airflow, reduced humidity, carbon dioxide concentration, and oxygen concentration modulate NO release into nasal passages. And this release changes when person is infected or ill with present of the microbe living situation.???????????????????

Influence by Adjacent Communities

The nasal passageway is close to other niches like the lungs, mouth, and throat. The nasal passage is influenced by the bacteria colonies of Staphylococcus aureus. Other pathogens include such as Haemophilus influenzae, S. pneumonia, Nisseria meningitides, Moraxella catarrhalis and S. aureus . Successful colonization depends not only on the ability of S. aureus to survive host factors but also on coexistence with other bacteria.

Sinuses: The diseased maxillary and ethmoid sinuses are most commonly associated with affecting the nasal passages by causing inflammation and congestion. One of the diseases caused by the communities of bacteria is sinusitis. The ability of bacteria to infect the sinuses must first be set up by conditions that create a favorable environment in the sinus cavities. The inflammation in the sinuses is chronic do begin with.(5) The causes for such chronic sinusitis cases are sometimes unclear. The Bacteria that causes the sinusitis are Streptococcus pneumonia, H. influenzae, Moraxella catarrhalis. The sysmptoms of this disease are severe headache, pain or pressure in the areas of the face, cough, and fever. It could also be damaging to the mucous membrane if left untreated.

Throat: The throat is connected to the nasal passageway and contains aerobic, gram-positive bacteria which are characterized by hemolysis. An example of a pathogenic bacteria in the throat is Streptococcus pyogenes, which can infect when the immune system is down and cause diseases such as scarlet fever and pharyngitis (strep throat) among others. An example of nonpathogenic bacteria in the throat is Streptococcus salivarius which may enter the bloodstream and may cause diseases such as septicemia although not very often. These diseases mostly affect the throat, but may move upwards to cause nasal passageway infections.

Conditions under which the environment changes

Do any of the physical conditions change? Are there chemicals, other organisms, nutrients, etc. that might change the community of your niche.

Anything that might irritate a human's nose, like air pollution, allergies, birth control pills, etc., may cause swelling and blockage of the nasal passageways which will lead to bacterial growth and infection. The trapped mucus within the nasal will create a breeding ground for bacteria. (8)

The temperature of the air will also affect the nasal cavity. The cold air will stimulate an increase in mucus production and thicken the mucus.

Sleeping will also affect the nasal cavity by clogging one side of the nasal passageway. When sleeping, one side of the nose is always clogged because of the nasal cycle, which is "normal physiological phenomenon." The nose alternates between phases of congestion and decongestion and it varies between people. The blockage is caused by the swelling and shrinkage of the blood vessels lining inside the nose. (8)

During an infection, inflammation makes the pH of the mucus similar to that of plasma, 7.4. (10) (seems like something we can put. doesn't seem to make sense but after further thought maybe it is to help white blood cells get into the nose to fight off the bacteria? which might mean more interaction with the bacteria. just a thought - Wayne)

Who lives in the Nasal Passageway?

Which microbes are present in the Nasal Passageway?

Even though we cannot see them with our naked eye, microscopic organisms are living inside our nasal passageways. Although most of these bacteria are non-pathogenic, some may induce illness if they successfully break through the bodies defense systems. Some examples of these non-pathogenic bacteria are Streptococcus, Neisseria, Haemophilus, and Micrococcus. Some of the pathogenic examples include Staphylococcus aureus, Corynebacterium diphtheriae, Streptococcus pneumoniae, and Haemophilus influenzae among others. (15)

Normal:

Staphylococcus epidermidis with Corynebacteria predominantly colonizes the upper respiratory tract, especially the nostrils. S. epidermidis covers 90%-100% staphylococci from the nasal cavity when S. aureus is not present. It may form biofilms to attach securely to the epithelial cells in the nasal passageway.

Corynebacterium is a Gram-positive normal flora in the nose. Most species of Corynebacterium will not cause diseases in humans; however, there is a specific species that is highly infectious. The Corynebacterium diptheriae causes infection in the upper respiratory tract, and can be deadly if untreated. (2)

Another Gram-positive bacterium that lives in the human nose is the Staphylococcus aureus, often referred to as staph. It is carried either on the skin or in the nose of healthy people, but 25% - 30% of the population is populated in the nose. Well Staph is growing, it will not cause any infection, until the bacteria can enter a wound.

Micrococcus luteus is an obligate aerobe, Gram positive, spherical, bacterium that also resides in the nose as well as the mouth, skin and upper resipratory tract. M. luteus is normally harmless except for those that have compromised immunities. M. luteus is resistant to reduced water potential that is found in mucus and can tolerate drying and high salt concentrations were the nasal cavity to dry up.


Diseased:

The nasal passages, being as large as it is (from a microbe's standpoint), can be harbor many types of bacteria, viruses, and fungi which can often lead to infection. It is in fact the main site for different organisms to lodge and multiply. One very commonly found gram-positive bacteria is the Staphylococcus epidermidis which colonizes in the anterior naris. (11)It lives naturally on the skin and mucous membranes. Their grape-like appearance when viewed under the microscope only measures approximately 1-micrometer in diameter. This bacteria, if environmental conditions are optimal, will form biofilms to aggregate more securely. A three stage process of the exopolysaccharide casing of the biofilm provides excellent protection against the environment and phagocytosis by their host's immune system as they seek to mature and eventually dissolute from the colony. The slime (biofilm), mainly composed of teichoic acid and typically found on the cell wall of these microbes can also protect them against antibiotics making them very difficult to treat. This unique ability of the Staphylococcus epidermidis to form a biofilm in the nasal passages may be the reason for their strong virulence. A patient's inability to rid of S. epidermis due to its protective biofilm usually leads to infection.(13)

(You guys want to do another microbe instead of S. epidermidis because I already sort of have it and it's part of the normal flora. Didn't you guys find other bacteria to use. It might be better if we don't repeat. Let me know what you guys think. Jacinda) (I don't think it is a problems since you only briefly mentioned its presence in the normal section, but considering S. epidermis is a significant microbe in the nasal passages it seems reasonable to elaborate on it. Also, I spoke to the TA yesterday and she suggested that we emphasize strongly on the more important microbes and briefly mention the less significant ones. Anyone else with thoughts? - Josephe)

The Streptococcus pneumoniae bacteria is another Gram-positive bacteria that is commonly found in the nasal passages, primarily in a patient with acute sinusitis. This lancet-shaped bacteria, approximately 0.5 - 1.25 micrometers in diameter, is one of the primary causes of pneumonia. Although they are also found in the upper respiratory tract of healthy individuals, they are usually the cause of sinus infection when a small amount of this bacteria is lodged in the sinus cavities such as the ethmoid or maxillary sinuses, typically by the force of a sneeze or the blowing of the nose. They are mostly found in pairs (diplococci), but can sometimes be seen alone or in short chains. (12) The S. pneumoniae has an extremely thick cell wall, approximately six layers compose of peptidoglycan with teichoic acid. This teichoic acid has two choline residues that bind specifically to choline-binding receptors on human cells. Its capsule, composed of polysaccharides prevents phagocytosis of the bacteria. The pili structures on some strains of S. pneumoniae have been identified in the involvement of colonization in the nasal passages. (12) This allows them to gain a strong attachment to epithelial cells and sometimes leads to a challenging problem if left untreated.

Haemophilus influenzae is a Gram-negative, rod-shaped bacterium that resides in the nasopharnyx region of the human nasal passage. They lack motility due to the absence of a flagella or pili. Its dimensions are about 1.0 x 0.3 um. There are 6 strains of encapsulated H. influenzae, which are categorized based on the type of polysaccharide capsule. The differences are denoted a through f, with H. influenzae serotype b (Hib), as the most commonly vaccinated strain. This vaccination helps in the prevention of invasive H. influenzae disease in young children. However, there also exists a non-encapsulated strain referred to as non-typeable H. influenzae (NTHi) which is unaffected by the vaccine due to lacking an antigenic capsule. (14) Virulance of this bacterial strain is based in large part to the lipopolysaccharide (LPS) component of its outer membrane. The LPS is an endotoxin and is composed of varying elements of monosaccharides, such as L-glycero-D-manno heptose, D-Glc, D-Gal, and sialic acid (Neu5Ac), which provide added protection against chemical attack and an increase the ability to cause disease. NThi usually infects the upper and lower respiratory tracts leading to pneumonia, sinusitis, and otitis media, which is an infection of the middle ear. Its encapsulated counterpart, specifically Hib and Hif, can cause meningitis and bacteremia, usually occurring in 3rd world countries where children are unvaccinated. (14)

The collaborate effect of these microbes can cause some major and minor symptoms of disease including facial pain, fever, nasal congestion, purulent nasal discharge, facial fullness, headaches, fatigue, cough, ear pressure and dental pain. A number of these symptoms may last up to four weeks or even twelve weeks in patients with chronic sinusitis.

Are there any other non-microbes present?

Normal: No plants, animals, or fungi live in the normal nasal passageway, although there is the presence of dust and other small particles which are inhaled from the outside environment.

Diseased: Fungal infection are not very common in the nasal passages, however, there have been cases in which patients that are immune-suppressed have experienced mycosis. Patients with uncontrolled diabetes or those with acquired immunodeficiency syndrome (AIDS) are typically a target for either Phycomycetes or Aspergillus. Other types of mycotic pathogens also infect humans, but are more uncommon. The fungal pathogens that usually invade the nasal passages are saprophytes which are found in soils and on plants, thriving in high glucose and acidic environments. As aspergillosis originates in the nose and paranasal sinuses it can invade the brain and vascular structures via arterial wall invasion causing tissue necrosis and arterial thrombosis. The aspergillus and bipolaris species can illicit an allergic response in the sinuses leading to chronic progressive inflammatory response which causes bone expansion and even bone destruction. Aeration and irrigation of the sinuses with a topical antifungal agent are treatments that may speed up the recovery process. (11)

Do the microbes that are present interact with each other?

Describe any negative (competition) or positive (symbiosis) behavior

The reason only 25% - 30% of the nasal passageway is populated by the Staph. aureus is beacuse Staph. epidermidis and Corynebacterium have a negative symbiosis behavior with the Staph. aureus. Some possible reasons for the decrease in Staph. aureus may be the synthesis of bactericidal exoprotiens by the Staph. epidermidis or the competition of specific attachment to epithelial cells, which Corynebacterium has a higher affinity for mucus than Staph. aureus. Although Stap. epidermidis has a negative impact on Staph. aureus, Staph. aureus has a higher affinity for mucus than does Staph. epidermidis. (1)

Competition for mucosal surface in the nasopharyngeal region exists between Streptococcus pneumoniae and Haemophilus influenza. These bacterial species compete for limited space in order to form stable colonies and propagate. Both will employ forms of microbial interference to exert their dominance over the opposition. S. pneumoniae, through neuramindase, has the ability to cleave terminal sialic acid residues. It will utilize this strategy to strip off sialic acid from the lipopolysaccharide component of H. infuenzae’s outer membrane thereby compromising its ability to withstand chemical attack. During the weakened state of its rival, S. pneumoniae will deliver the final blow by generating high levels of hydrogen peroxide via aerobic metabolism, which on contact, is lethal to H. influenza. However, even in the face of such awesome firepower, it is H. influenzae that wins out. H. influenza relies on the inflammatory response of the local host to get rid the competition. Although exact details are still being researched, H. influenzae has the ability to recruit the host responder, neutrophils. Neutrophils are a type of white blood cell that is capable of getting rid of S. pneumoniae and other microorganisms via phagocytosis. Due to its capsule, H. influenzae is able to avoid suffering the same fate as its rival. Once the competition is eliminated, H. influenzae is free to proliferate and infect the upper respiratory tract of its host. Conversely, when taking into consideration the application of vaccines and antimicrobials, these factors can also influence bacterial interspecies behavior and the outcome of the competition between them. (8)

Do the microbes change their environment?

Do they alter pH, attach to surfaces, secrete anything, etc. etc.

Do the microbes carry out any metabolism that affects their environment?

Do they ferment sugars to produce acid, break down large molecules, fix nitrogen, etc. etc.

Current Research

Enter summaries of the most recent research. You may find it more appropriate to include this as a subsection under several of your other sections rather than separately here at the end. You should include at least FOUR topics of research and summarize each in terms of the question being asked, the results so far, and the topics for future study. (more will be expected from larger groups than from smaller groups)

As previously mentioned, Staphylococcus aureus is found in the nose of about 25% - 30% of the human population. Researchers from the University of Washington were interested in finding out why this bacterium is able to survive the human's natural production of nitric oxide in the nasal passages. This production of nitric oxide in the nose and nasal passages usually protects against disease causing bacteria by preventing their respiration process. These researchers found out that Staph aureus produces lactic acid in the presence of nitric oxide,making a chemical balance, allowing it to continue to grow in this type of environment. The researchers then found a way to remove the lactic acid production by Staphylococcus aureus and found that it was then not able to survive in the presence of nitric oxide. This was tested in mice and the researchers also found that there were no diseases caused by the modified bacterium. The researchers hope to use this type of modification to find new ways to prevent the survival of such bacteria without the use of antibiotics.

Scientists researched the "functions of two staphylo9coccal biofilm matrix polymers: poly-N-acetylglucosamine surface polysaccharide (PNAG) and extracellular DNA (ecDNA)" and how the "PNAG-degrading enzyme, dispersin B, and DNase I inhibit biofilm formation, detach preformed biofilms, and sensitize biofilms to killing by the cationic detergent cetylpyridinium chloride (CPC)." The biofilms will help protect the bacteria from being nullified by antibiotics and host defenses. The scientists found that both dispersin B and DNase I will inhibit biofilm formation in S. aureus and PNAG-positive S. epidermidis strains. Dispersin B will efficiently and rapidly detach S. epidermidis biofilms, but not S. aureus. On the other hand, DNase I will cause separation of the biofilm and the surface in S. aureus, but not S. epidermidis. PNAG is a major matrix component of only S. epidermidis biofilm cells, but it is produced by both bacteria. The PNAG performs different functions in the biofilms of the two bacteria. The PNAG protects the S. epidermidis cells from CPC killing, while the PNAG works in early stages of S. aureus biofilms, which makes it resistant to the detachment of dispersin B. Overall, ecDNA and PNAG can be "general diffusion barriers" that stop detergents from killing the bacteria. (7)

Researchers form Cambridge University have isolated "methicillin-resistant coagulase negative staphylcocci (MRCNS) from the nasal flora of healthy humans" from three places in Rio de Janeiro City. They obtained swaps from the nares of the adults at two military quarters and students from a public school. Staphylcocci were isolated and "tested for the presence of the mecA gene" by hybridizing the gene with a specific probe. S. epidermidis was the most common MRCNS; it accounted for 38 out of the 45 total. The SmaI-digested DNA was also put through pulsed-field gel electrophoresis in order to study the clonalityof the MRSE S. epidermidis. It appears that the cross-colonization contributed to the spread of the methicillin-resistance. The wide and diverse genome suggests that the spread of the mecA gene among the isolates were probably through horizontal transmission. It was concluded that though it was researched with only three institutions, it reflects how other communities in Rio may have gained methicillin resistance.


Cadavers have also been used to study nasal airflow patterns and have been measured at an average of 2-3 m/sec in the horizontal meatus . It then increases to 3-4 m/sec as they join in the nasopharynx, and decreases to 1 m/sec as it goes down the bronchi. (10) (might seem a bit out of place, need help on the flow - Wayne)???

References

[Sample reference] Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "Palaeococcus ferrophilus gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". International Journal of Systematic and Evolutionary Microbiology. 2000. Volume 50. p. 489-500.

1. Lina, G., Boutite, F., Tristan, A., Bes, M., Etienne, J., Vandenesch, F., "Bacterial Competition for Human Nasal Cavity Colonization: Role of Staphylococcal agr Alleles". "Applied and Environmental Microbiology". 2003. Vol. 69. No. 1. p. 18-23.

2. Santo-Pietro, Karen. "Microorganism of the Month: Corynebacterium species'". 'The Environmental Reporter: EMLAB'. 2007. Volume 5. Issue 5

3. Richardson, A., Libby,S., Fang,F."A nitric oxide Inducible Lactate Dehydrogenase Enables Staphylococcus aureus to Resist Innate Immunity". Science. 2008. Vol. 319. p. 1672-1676.

4. Hall, Colman’s. Diseases of the Ear, .Nose and Throat. Harcourt Brace and Company, 2000.

5. Gest, Howard. Microbes an invisible Universe. Washington, D.C, 2003.

6. Washington N, Steeler, Jackson. “Determination of baseline human nasal PH and effect of intranasal administrative buffer.” Journal of Pharmaceutical 198 (2000): 139-146.

7. Izano, E., Amarante, M., Kher, W., Kaplan, J. "Differential Roles of Poly-N-Acetylglucosamine Surface Polysaccharide and Extracellular DNA in Staphylococcus aureus and Staphylococcus epidermidis Biofilms." "Applied and Environmental Microbiology". 2008. Vol. 74, No. 2, p. 470-476.

8. Rosin, Deborah. "Nasal Obstruction." "WebMD:'The Sinus Sourcebook.'" 1998.

9. Wilson, Michael. Microbial Inhabitants of Humans. Cambridge University Press. 2005. p. 140

10. Proctor, Donald F. The Nose: Upper Airway Physiology and the Atmospheric Environment. Elsevier Biomedical Press. 1982.

11. Lysenko, Elena S, et al. "The Role of Innate Immune Responses in the Outcome of Interspecies Competition for Colonization of Mucosal Surfaces". "PLoS Pathogens". 2005. VOL.1 is.1 p.e1

11. Donald, Paul J., Jack L. Gluckman, Dale H. Rice. The Sinuses. New York. 1995. pgs 57-60.

12. Todar's Online Textbook of Microbiology. Kenneth Todar. 2008. University of Wisconsin-Madison Department of Bacteriology. 24 August 2008. <http://www.textbookofbacteriology.net/S.pneumoniae.html>

13. M.U. Rasheed, Mohammed Awole: Staphylococcus epidermidis : A Commensal Emerging As A Pathogen With Increasing Clinical Significance Especially In Nosocomial Infections. The Internet Journal of Microbiology. 2007. Volume 3 Number 2.

14. Elke K.H. Schweda, Brigitte Twelkmeyer, and Jianjun Li. Invited review: “Profiling structural elements of short-chain lipopolysaccharide of non-typeable Haemophilus influenzae”. Innate Immunity, August 2008; 14: 199 - 211.

15. Kerr, McHale. "Flora of the Nose and Throat". Applications in General Microbiology. 2003. Edition 6. p.331-335.

Edited by Jacinda Chen , Wayne Chen , Josephe Dalidi , Jennifer Hao , Rutu Kothari , Nidhi Patel , Natividad Rodriguez , Prudencio Sy, students of Rachel Larsen