Theresa J. Ochoa
Thomas G. Cleary
Yersinia enterocolitica produces acute gastroenteritis in younger children and mesenteric adenitis in older children. It also has been associated with a variety of extraintestinal manifestations. Although initially reported in the cooler regions of Europe and North America, the organism has been recognized worldwide as a cause of human infection.
ETIOLOGY AND EPIDEMIOLOGY
The genus Yersinia belongs to the family Enterobacteriaceae. Three of the eleven species are pathogenic to humans: Y. pestis, Y. enterocolitica, and Y. pseudotuberculosis.
Y. enterocolitica is an oxidase-negative, nonlactose-fermenting, aerobic, gram-negative coccobacillus. It ferments glucose, galactose, and mannose; reduces nitrates; and does not produce hydrogen peroxide. The organism is motile at 22°C to 25°C but not at 37°C. These properties help to differentiate it from Y. pestis and other Enterobacteriaceae. Y. enterocolitica grows well on ordinary media, such as blood, MacConkey medium, heart infusion, and Salmonella-Shigella agars, although a selective agar medium has been developed specifically for its isolation. Y. enterocolitica strains have been differentiated into approximately 70 serogroups (based on somatic O antigens) and six biotypes. Eleven of the serogroups of Y. enterocolitica commonly cause human disease. Most animal and environmental isolates are avirulent for humans. Biogroups 1B, 2, 3, 4, and 5 are associated with human infection. Biogroup 1A includes nonpathogenic environmental isolates. Serologically, the most frequent serogroups associated with human infection are 0:3, 0:5, 27, 0:8, and 0:9.
Y. enterocolitica is widespread in nature. It is present in the gastrointestinal tract of wild and domestic mammals, in the environment (surface water, sewage), and in certain foods (meats, dairy products, seafood, and vegetables). Most of the known pathogenic biogroups are associated with definitive animal hosts, especially the pig. In case-control studies, a correlation has been demonstrated between infection and the consumption or handling of raw or undercooked pork products such as chitterlings.
Gastrointestinal infection with Y. enterocolitica appears to be most common in developed countries within the temperate zones. Most cases occur during the winter. The organism is cold-adapted and capable of multiplication at low temperatures. Water- and food-borne infections have been documented, as has person-to-person transmission in family and community outbreaks. The significance of food-product contamination during processing is underscored by the organism’s ability to grow in properly refrigerated food, including raw and cooked meat and milk. Y. enterocolitica has emerged as a significant cause of transfusion-associated sepsis. Factors contributing to this are the ability of the bacterium to multiply at 4°C and to utilize iron liberated from aging erythrocytes.
The incubation period for intestinal infection is typically 4 to 6 days, varying from 1 to 14 days. The excretion of the bacteria in stools continues for a few weeks after cessation of the symptoms.
Y. enterocolitica usually causes diffuse inflammation of the ileum and colon, with infiltrates in the lamina propria and superficial ulcerations in the terminal ileum and colon. Mesenteric lymphadenitis, with reactive germinal centers and sometimes microabscess formation, often is associated. In most cases, the appendix is grossly and histologically normal or shows only mild inflammation.
The usual route of acquisition of Y. enterocolitica is through the ingestion of food or water contaminated with the bacteria. Prior to the initiation of an infectious process, this microorganism undergoes a temperature adaptation in the human host, making use of both chromosomal and plasmid-associated virulence determinants that are temperature regulated. Once attached to M cells (overlaying Peyer patches), the bacteria penetrate these cells to gain access to and multiply in adjacent tissue. The pathogenic strains carry a plasmid for Yersinia virulence (pYV) coding for virulence proteins such as the Yersinia outer proteins (Yops) and the Yersinia adhesion A (YadA). These strains also express chromosomally encoded virulence factors including enterotoxins and those proteins related to invasion and serum resistance. Pathogenic Yersinia species share the Yop virulon, which is the core of the Yersinia pathogenicity machinery. The Yop virulon is an archetype of the Type III Secretion System, which enables bacteria to secrete and inject bacterial proteins into the cytosol of eukaryotic host cells. The Yops perturb the cytoskeleton, disrupting phagocytosis and blocking the production of proinflammatory cytokines, thus favoring the survival of the invading Yersinia. In addition, pathogenic Yersinia species produce antiinflammatory proteins.