Yersinia species: Yersinia pestis is transmitted from rats to humans by a flea bite, but Yersinia pseudotuberculosis and Yersinia enterocolitica are foodborne pathogens. Y pseudotuberculosis gives rise to mesenteric adenitis and septicemia, and Y enterocolitica causes a broad range of gastrointestinal syndromes. From an enteric point of view, Y enterocolitica appears to cross the intestinal epithelium via M cells, destroying Peyer’s patches in the process. This ability is mediated by an outer membrane protein, invasin. However, it is important to point out that Y enterocolitica is not, as has been generally assumed in the past, an intracellular pathogen — an assumption that rested mainly on the ability of Yersinia species to invade cultured cells.
Yersinia is in fact an extracellular, potent antiphagocytic pathogen, particularly when present in lymph nodes. Much less is known about the mechanisms responsible for gas-troenteritic syndromes caused by Yersinia species than those involved in resisting phagocytosis; the latter is an extremely important virulence attribute for an organism that, if phagocytosed, is readily killed! Strictly, the antiphagocytic property of Yersinia species is something outside the scope of this review. Nevertheless, brief allusion is made to this aspect because a great deal is known about the molecular basis of the antiphagocytic capability of Yersinia species, due largely to the work of Cornelis and colleagues. It has been shown that the capacity to resist host defence mechanisms depends on the Yop virulon, which is a sophisticated system encoded by more than 50 genes on a 70 kb plasmid (pYV) in Y enterocolitica. Upon contact with host cell membrane, expression of a type III secretion occurs. Effector proteins are delivered to the target eukaryotic cell, which disrupt cytoskeletal dynamics, which in the case of a phagocyte would render it powerless; eventually the phagocyte dies.