Yersinia enterocolitica infection pathophysiology
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Please help WikiDoc by adding content here. It's easy! Click here to learn about editing. Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Salau, M.B.B.S., FMCPaed [2]
Pathophysiology
- The pathogenesis of Y. enterocolitica is not fully understood.[1][2][3][4][5]
- Y. enterocolitica is transmitted via fecal-oral route, passing from the stools or soiled fingers of one person to the mouth of another person. This may happen when basic hygiene and handwashing habits are inadequate.
- Rarely, the organism is transmitted through contaminated blood during a transfusion.
- Y. enterocolitica is a relatively infrequent cause of diarrhea and abdominal pain.
- Virulent strains of Y. enterocolitica usually have a 70 kilodalton (kd) virulence plasmid known as pYV.
- After transmission, Y. enterocolitica survives the acidic environment in the stomach to get to the gut by producing ammonia to buffer the acid. In the gut it attaches and invades the gut wall through the protein invasin and other surface proteins.
- The organism evades the host immune system, by producing proteins such as, Ail (attachment invasion locus), YadA, and Yersinia outer membrane proteins (Yops). Ail and YadA are adhesins that also confer resistance to complement-mediated opsonization.
- Yersinia virulent strains cross the intestinal epithelium primarily through the FAE (follicle associated epithelial cell), in the Peyer’s patches of the ileum.
- After invasion, Yops are released into host cells via a type III secretion system on contact with the target phagocyte preventing phagocytosis and inflammation.
- Y. enterocolitica strains also have genes for an iron-binding siderophore known as yersiniabactin, which binds iron permitting continued rapid growth of Y. enterocolitica.
Yersinia virulent strains cross the intestinal epithelium primarily through the FAE (follicle associated epithelial cell), in the Peyer’s patches of the ileum
- Yersinia strains therefore remain extracellular in infected Peyer’s patches and mesenteric lymph nodes, and then disseminate to cause local and systemic infection.
References
- ↑ Sabina Y, Rahman A, Ray RC, Montet D (2011). "Yersinia enterocolitica: Mode of Transmission, Molecular Insights of Virulence, and Pathogenesis of Infection". J Pathog. 2011: 429069. doi:10.4061/2011/429069. PMC 3335483. PMID 22567333.
- ↑ Galindo CL, Rosenzweig JA, Kirtley ML, Chopra AK (2011). "Pathogenesis of Y. enterocolitica and Y. pseudotuberculosis in Human Yersiniosis". J Pathog. 2011: 182051. doi:10.4061/2011/182051. PMC 3335670. PMID 22567322.
- ↑ Cornelis GR, Boland A, Boyd AP, Geuijen C, Iriarte M, Neyt C; et al. (1998). "The virulence plasmid of Yersinia, an antihost genome". Microbiol Mol Biol Rev. 62 (4): 1315–52. PMC 98948. PMID 9841674.
- ↑ De Koning-Ward TF, Robins-Browne RM (1995). "Contribution of urease to acid tolerance in Yersinia enterocolitica". Infect Immun. 63 (10): 3790–5. PMC 173532. PMID 7558281.
- ↑ Carniel E (1995). "Chromosomal virulence factors of Yersinia: an update". Contrib Microbiol Immunol. 13: 218–24. PMID 8833839.