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Yersiniosis

Diane Williamson, Biomedical Sciences Department, Dstl Porton Down, UK

Yersinia enterocolitica is the etiological agent of a gastroenteritis, known as yersiniosis. Occasionally this can give rise to a pseudoappendicitis, which is more severe than that caused by Y.pseudotuberculosis and can involve an acute terminal ileitis and mesenteric lymphadenitis. Yersiniosis often results in an immune disregulation which is manifest as a reactive arthritis. Unlike the other pathogenic Yersinia, Y.enterocolitica is not thought to be a true zoonosis, being transmitted by the ingestion of infected animal products or by contact. Person-to-person transmission is also possible.

Y.enterocolitica is a small Gram-negative coccobacillus which may be capsulated in vivo and which is classified into 34 different serotypes. However, the majority of human disease is caused by serotypes 03 and 08/09. In common with the other pathogenic Yersinia, Y.enterocolitica possesses a pyV plasmid which encodes a type-three secretion system (T3SS) and the secretion of a virulence (V) antigen and other Yersinia outer proteins (Yops). The V antigen secreted by the Y.enterocolitica 03 serotype is homologous to that of the Y.pestis and Y.pseudotuberculosis V antigens. However the V antigen from the 08 serotype of Y.enterocolitica incorporates an additional hypervariable region, which differs from the V03 sequence. These differences are significant since the V antigen from Y.pestis is an important protective antigen and so some cross-protection between Yersinia strains with homologous V antigens may be possible.

The V antigen regulates T3S and the V antigen is also anti-inflammatory, inducing IL10 secretion and down-regulating the pro-inflammatory cytokines TNFα and IFNγ. There is evidence that the N-terminal region of the V antigen stimulates TLR2 receptors to induce this anti-inflammatory effect in host cells. The T3SS is induced on close contact with a host cell in vivo, when Y.enterocolitica produces a hollow needle-like projection through which effector proteins are translocated directly into the host cell. These effectors are variously cytotoxic, anti-phagocytic or anti-inflammatory and generally promote the apoptosis of host cells and thus the survival of bacteria in the host. By all these means, Y.enterocolitica counters innate immune defences and achieves dissemination in the host to establish a bacteremia. A wide range of antibiotics, except for penicillin, are effective for the therapy of yersiniosis. Y.enterocolitica is susceptible to sulphadiazine, streptomycin, tetracycline, chloramphenicol and cotrimoxazole.

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