Staphylococcus aureus infection pathophysiology: Difference between revisions
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# Staphylococcal enterotoxins cause food poisoning via ingestion of contaminated food. These enterotoxins have a very high stability and they are not easily denatured by heat and low pH (mild cooking or food digestion in the stomach cannot easily eradicate these toxins). | # Staphylococcal enterotoxins cause food poisoning via ingestion of contaminated food. These enterotoxins have a very high stability and they are not easily denatured by heat and low pH (mild cooking or food digestion in the stomach cannot easily eradicate these toxins). | ||
# Unlike most conventional peptides that stimulate roughly 1% of naive T-cells, a staphylococcal superantigen can simultaneously activate a large proportion of T lymphocytes (up to 20%). | # Unlike most conventional peptides that stimulate roughly 1% of naive T-cells, a staphylococcal superantigen can simultaneously activate a large proportion of T lymphocytes (up to 20%). | ||
# Staphylococcal superantigens are also | # Staphylococcal superantigens are also distinct because of their ability to bypass highly specific antigen-driven interaction between T-cells and antigen presenting cells. | ||
# The superantigen toxin have the unique ability to activate T lymphocytes in a TCR Vβ (T cell receptor β-chain variable domain). | |||
==References== | ==References== | ||
Revision as of 14:18, 9 May 2017
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Staphylococcus aureus infection Main page |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Fatimo Biobaku M.B.B.S [2]
Overview
Pathophysiology
Staphylococcus aureus is a highly virulent bacteria that has been recognized as a cause of a wide variety of diseases in humans. Approximately 60% of humans are colonized with Staphylococcus aureus (the nasal membranes and skin are the common habitat).[1][2] Several strains of Staphylococcus aureus bacteria exist. The characteristic attribute of a particular strain such as toxins and extracellular factors, invasive properties (such as adherence, biofilm formation, and resistance to phagocytosis), majorly determine the pathogenesis of Staphylococcus aureus infection.[1] Staphylococcus aureus causes several infections ranging from mild infections to invasive diseases that are life threatening. Some of the infections caused by Staphylococcus aureus include skin and soft tissue infections, osteomyelitis, food poisoning, pneumonia, infective endocarditis and sepsis. The following virulence factors have been recognized in the pathogenesis of Staphylococcus aureus infections:[3][4][2]
- Staphylococcal superantigens (SAgs)
- These have been strongly implicated in a wide range of illnesses such as toxic shock syndrome and staphylococcal food poisoning.
- Several studies also suggest staphylococcal superantigens play a role in diseases such as atopic dermatitis, some forms of psoriasis, Kawasaki disease, and chronic rhinosinusitis.
- Staphylococcal superantigens are exotoxins with more than 20 distinct types, and most staphylococcus aureus strains encode many superantigen gene. Staphylococcus superantigens include staphylococcal enterotoxins, staphylococcal enterotoxin-like proteins, and toxic shock syndrome toxin-1.
- Staphylococcal enterotoxins cause food poisoning via ingestion of contaminated food. These enterotoxins have a very high stability and they are not easily denatured by heat and low pH (mild cooking or food digestion in the stomach cannot easily eradicate these toxins).
- Unlike most conventional peptides that stimulate roughly 1% of naive T-cells, a staphylococcal superantigen can simultaneously activate a large proportion of T lymphocytes (up to 20%).
- Staphylococcal superantigens are also distinct because of their ability to bypass highly specific antigen-driven interaction between T-cells and antigen presenting cells.
- The superantigen toxin have the unique ability to activate T lymphocytes in a TCR Vβ (T cell receptor β-chain variable domain).
References
- ↑ 1.0 1.1 Chessa D, Ganau G, Mazzarello V (2015). "An overview of Staphylococcus epidermidis and Staphylococcus aureus with a focus on developing countries". J Infect Dev Ctries. 9 (6): 547–50. doi:10.3855/jidc.6923. PMID 26142662.
- ↑ 2.0 2.1 Kobayashi SD, Malachowa N, DeLeo FR (2015). "Pathogenesis of Staphylococcus aureus abscesses". Am J Pathol. 185 (6): 1518–27. doi:10.1016/j.ajpath.2014.11.030. PMC 4450319. PMID 25749135.
- ↑ Grumann D, Nübel U, Bröker BM (2014). "Staphylococcus aureus toxins--their functions and genetics". Infect Genet Evol. 21: 583–92. doi:10.1016/j.meegid.2013.03.013. PMID 23541411.
- ↑ Xu SX, McCormick JK (2012). "Staphylococcal superantigens in colonization and disease". Front Cell Infect Microbiol. 2: 52. doi:10.3389/fcimb.2012.00052. PMC 3417409. PMID 22919643.