Yersinia pseudotuberculosis infection

From MicrobeWiki, the student-edited microbiology resource
Revision as of 14:39, 16 July 2014 by Rachel.garrison (talk | contribs) (Created page with "Category:Pages edited by students of Tyrrell Conway at the University of Oklahoma {{curated}} [[Image:OULOGOBIANCO.JPEG|thumb|230px|left|University of Oklahoma Study Abro...")
(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
This is a curated page. Report corrections to Microbewiki.
University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[1]

Etiology/Bacteriology

Taxonomy

| Domain = Bacteria | Phylum = Firmicutes | Class = Clostridia | Order = Clostridiales | Family = Clostridiaceae | Genus = Clostridium | species = C. difficile

Description


Pathogenesis

Transmission


Infectious Dose and Incubation Period

Characteristic of other Yersinia infections, Yersinia pseudotuberculosis requires a dose of 109 organisms to cause disease. The incubation period of Y. pseudotuberculosis is 5-10 days, however durations of 2-20 days have been reported in occasional outbreaks with the average time being 4 days after exposure to the bacterium.

Epidemiology


Virulence Factors

Yops

Y. pseudotuberculosis contains a 70-kd plasmid that encodes for a type III secretion system that delivers the Yersinia outer proteins (Yops). There are four major Yops proteins which are essential to the pathogenicity of Y. pseudotuberculosis: YopE, YopJ, YopT, and YopH. YopE activates the RhoGTPase of the GTP-binding protein, which plays a role in the actin filament arrangement, promotion of cell rounding, prevention of host cell membrane pores, and inhibition of phagocytosis (MEDSCAPE). YopE also plays a role in decreasing the host cells proinflammatory signals by decreasing the production of interleukin-8. YopJ binds to the protein kinases which blocks phosphorylation in the cell. This will eventually lead to a decrease in the production of interleukin-8, affecting the host cells proinflammatory response. YopT disrupts the actin filament arrangement and prevents phacytosis by the host cell. YopT is not present in the pathogenic strains of Y. pseudotuberculosis. YopH contributes to the disruption of phagocytosis and actin filament arrangement. It also has a role in decreasing the secretion of interleukin-8. The four main Yersinia outer proteins work together to disrupt the host immune response.

Exotoxin-YPM

YPM stimulates T cells, which induce secretion of large amount of inflammatory cytokines.

Adhesion Molecules

The adhesion molecules of Y. pseudotuberculosis bind to the host cell and facilitate its colonization in the host organism. The two major proteins of this group include: invasin and yadA. The invasin binds to the integrins of the M cells of Peyer’s patch in the small intestine. It also plays a role in internalization of bacteria across the M cells. YadA binds to laminin, collage, and fibronectin, which are bound to their receptors on the cell surface.

High Pathogenicity Island (HPI)

High Pathogenicity Island contains the gene that encodes yersiniabactin, which is used for iron uptake.

Twin Arginine Translocation (tat) pathway

The twin arginine translocation pathway is important for the secretion of proteins that function in motility and acid resistance.

Clinical Features


Diagnosis

Yersinia pseudotuberculosis has the potential to be difficult to culture due to the vast presence of healthy microbiota. A fecal sample is needed from the patient and then the microorganism can be isolated. Research has shown that cold-temperature enrichment has been effectively used to culture the microorganism. (1) Polymerase Chain Reaction assay can then be used to identify the bacteria and then can further serotype the organism. (2) The culture can also be isolated and grown on MacConkey agar due to its ability to ferment sorbitol and its ability to produce ornithine decarboxylase. (3) Y. pseudotuberculosis has been serotyped using Enzyme-linked immunosorbent assay along with agglutination tests but the results prove inconclusive due to the possibility of cross-reactions of other pathogenic antibodies. (3) Blood samples can be taken and tested to confirm the presence of the microorganism but a fecal sample is the preferred method of diagnostic testing. (2)

Treatment


Prevention


Host Immune Response


Reference