Pseudotuberculosis | Diane Williamson, Biomedical Sciences Department, Dstl Porton Down, UK
Pseudotuberculosis, caused by Yersinia pseudotuberculosis, is a zoonosis which can be transmitted to man through skin contact with infected animals, contaminated water, or by the consumption of contaminated food or vegetables. Y.pseudotuberculosis is a small oval Gram-negative bacillus, and is thought to be the ancestral species from which the other pathogenic Yersinia (Y.pestis and Y.enterocolitica) are thought to have evolved; and like Y.pestis, Gram-staining occurs in a bipolar pattern, at either end of the bacillus. Y.pseudotuberculosis causes an acute mesenteric adenitis (pseudotuberculosis), which can simulate appendicitis. Pseudotuberculosis, as the name implies, can cause TB-like symptoms which can affect the liver, spleen and lymph nodes, causing tissue necrosis and granulomas, accompanied by fever and abdominal pain. Occasionally, Y.pseudotuberculosis can give rise to severe systemic disease which has a high fatality rate.
The strains of Y.pseudotuberculosis can be classified into 6 serotypes, based on a number of heat-stable somatic antigens and thermolabile flagellar antigens which are present in cultures grown at 18–26oC. Like Y.pestis, Y.pseudotuberculosis expresses a truncated form of surface lipopolysaccharide (‘rough’ LPS) which allows it to evade TLR4 recognition in the host, whilst the flagellar antigens deter phagocytosis.
As with the other Yersinia, Y.pseudotuberculosis also harbours the pYV plasmid encoding for type-three secretion (T3S), the V antigen, and other Yersinia outer proteins. The V antigen regulates T3S and is also anti-inflammatory. The T3S enables Y.pseudotuberculosis to produce a hollow needle-like projection on close contact with a host cell in vivo, 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.pseudotuberculosis counters innate immune defences and achieves dissemination in the host to establish a potentially serious bacteremia. The V antigen from Y.pseudotuberculosis has the V03 sequence and is homologous to that secreted by Y.pestis. This is significant because the V antigen is a major protective antigen for vaccination against plague and so some cross-protection with Y.pseudotuberculosis may be possible.
Y.pseudotuberculosis is susceptible to a wide range of antibiotics including penicillin, ampicillin and tetracycline.
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