Yersinia enterocolitica is a Gram-negative, rod-shapedbacterium, belonging to the family Yersiniaceae. It is motile at temperatures of 22–29°C (72–84°F), but becomes nonmotile at normal human body temperature.[1][2]Y. enterocolitica infection causes the disease yersiniosis, which is an animal-borne disease occurring in humans, as well as in a wide array of animals such as cattle, deer, pigs, and birds. Many of these animals recover from the disease and become carriers; these are potential sources of contagion despite showing no signs of disease.[3] The bacterium infects the host by sticking to its cells using trimeric autotransporter adhesins.
Y. enterocolitica is widespread in nature, occurring in reservoirs ranging from the intestinal tracts of numerous mammals, avian species, cold-blooded species, and even from terrestrial and aquatic niches. Most environmental isolates are avirulent; however, isolates recovered from porcine sources contain human pathogenic serogroups. In addition, dogs, sheep, wild rodents, and environmental water may also be a reservoir of pathogenic Y. enterocolitica strains. Human pathogenic
strains are usually confined to the intestinal tract and lead to enteritis/diarrhea.[4]
Within the genus Yersinia, only Y. pestis, Y. pseudotuberculosis, and certain strains of Y. enterocolitica are pathogenic for humans and certain animals. The other species are environmental in origin.[5]
Y. enterocolitica strains can be identified through the use of stool samples being grown on MacConkey plates and Yersinia Selective Agar. The MacConkey plates employ the fact that Y. enterocolitica is non-lactose fermenting, and therefore show up on the plates as 2mm translucent pale colonies. On Yersinia Selective Agar plates Y. enterocolitica produces 1.5mm colonies with a dark pink center and translucent border.[6][5]
Y. enterocolitica is a heterogeneous group of strains, which are traditionally classified by biotyping into six biogroups on the basis of phenotypic characteristics, and by serotyping into more than 57 O serogroups, on the basis of their O (lipopolysaccharide or LPS) surface antigen. Five of the six biogroups (1B and 2–5) are regarded as pathogens. However, only a few of these serogroups have been associated with disease in either humans or animals. Strains that belong to serogroups O:3 (biogroup 4), O:5,27 (biogroups 2 and 3), O:8 (biogroup 1B), and O:9 (biogroup 2) are most frequently isolated worldwide from human samples. However, the most important Y. enterocolitica serogroup in many European countries is serogroup O:3 followed by O:9, whereas the serogroup O:8 is mainly detected in the United States.
There have been six identified pathways of transmission of Yersinia enterocolitica.[7]
Foodborne Transmission: Yersinia enterocolitica has been isolated from various food items, including beef, oysters, fish, chocolate milk, but the main food transmission is through exposure to undercooked or raw pork.
Human-to-Human Transmission: Whilst very rare, cases of human-to-human transmission of Yersinia enterocolitica via diarrheal disease has been isolated and reported.
Animal-to-Human Transmission: Yersinia enterocolitica has been reported to spread through indirect and direct contactwith infected animals and their feces, most notably pig.
Waterborne Transmission: Yersinia enterocolitica is able to grow in cool aquatic environments, meaning that indirectly contaminated water can cause the spread of the bacterium.
Direct Transmission: Whilst also very rare, there have been reported cases of direct inoculation of Yersinia enterocolitica resulting from traumatic punctures, suggesting environmental infection of Y. enterocolitica.
Blood Transfusion: Y. enterocolitica can be transmitted through contaminated blood, and can cause posttransfusion sepsis.
The portal of entry is the gastrointestinal tract. The organism is acquired usually by insufficiently cooked pork or contaminated water, meat, or milk. In recent years Y. enterocolitica has increasingly been causing smaller outbreaks via ready-to-eat (RTE) vegetables.[8] Acute Y. enterocolitica infections usually lead to mild, self-limiting enterocolitis or terminal ileitis and adenitis in humans. Yersiniosis symptoms may include watery or bloody diarrhea and fever, resembling appendicitis, salmonellosis, or shigellosis. After oral uptake, Yersinia species replicate in the terminal ileum and invade Peyer's patches. From here, they can disseminate further to mesenteric lymph nodes causing lymphadenopathy. This condition can be confused with appendicitis, so is called pseudoappendicitis. In immunosuppressed individuals, they can disseminate from the gut to the liver and spleen and form abscesses. Because Yersinia species are siderophilic (iron-loving) bacteria, people with hereditary hemochromatosis (a disease resulting in high body iron levels) are more susceptible to infection with Yersinia (and other siderophilic bacteria). In fact, the most common contaminant of stored blood is Y. enterocolitica.[9]
Y. enterocolitica seems to be associated with autoimmune Graves-Basedowthyroiditis.[14]
Whilst indirect evidence exists, direct causative evidence is limited.[15]Y. enterocolitica is probably not a major cause of this disease, but may contribute to the development of thyroid autoimmunity arising for other reasons in genetically susceptible individuals.[16]Y. enterocolitica infection has also been suggested to be not the cause of autoimmune thyroid disease, but rather an associated condition, with both sharing a common inherited susceptibility.[17]
More recently, the role for Y. enterocolitica has been disputed.[18]
^Ryan KJ; Ray CG, eds. (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN978-0-8385-8529-0.
^Hill Gaston JS, Lillicrap MS (2003). "Arthritis associated with enteric infection". Best Practice & Research Clinical Rheumatology. 17 (2): 219–39. doi:10.1016/S1521-6942(02)00104-3. PMID12787523.
^Benvenga S, Santarpia L, Trimarchi F, Guarneri F (2006). "Human Thyroid Autoantigens and Proteins of Yersinia and Borrelia Share Amino Acid Sequence Homology That Includes Binding Motifs to HLA-DR Molecules and T-Cell Receptor". Thyroid. 16 (3): 225–236. doi:10.1089/thy.2006.16.225. PMID16571084.
^Toivanen P, Toivanen A (1994). "Does Yersinia induce autoimmunity?". International Archives of Allergy and Immunology. 104 (2): 107–11. doi:10.1159/000236717. PMID8199453.
