ABSTRACT
During the course of systemic disease promoted by enteropathogenic Yersinia, the bacteria appear to be largely extracellular after they translocate out of an intestinal locale and enter deep tissue sites (Heesemann et al., 1993). This is consistent with the fact that many of the known translocated protein substrates of the Yersinia Type III secretion system (TTSS) are highly effective at antagonizing phagocytosis by virtue of inactivating key cytoskeletal signaling cascade components (Cornelis, 2000). In this regard, the enteropathogens are probably similar to Yersinia pestis during growth within lymphoid tissue. Yersinia enterocolitica and Yersinia pseudotuberculosis, however, are not transmitted by the flea, and disease by these organisms does not initiate after an insect bite. Instead, disease is initiated after oral ingestion of contaminated foodstuffs, which is followed shortly afterward by the entry of the bacteria into M cells overlying the gut-
associated lymphoid tissue (GALT) (Kraehenbuhl and Neutra, 2000). This is the only stage in the disease process on which there is general agreement that enteropathogenic Yersinia species are found in an intracellular locale. Therefore, the enteropathogens must encode proteins that allow initiation of disease after oral ingestion of the microorganisms, and have strategies that allow their dissemination to other hosts after colonization is initiated within the gastrointestinal tract.
