Yersinia enterocolitica

Yersinia enterocolitica
Yersinia enterocolitica colonies growing on XLD agar plates
Scientific classification
Domain: Bacteria
Phylum: Proteobacteria
Class: Gammaproteobacteria
Order: Enterobacteriales
Family: Enterobacteriaceae
Genus: Yersinia
Species: Y. enterocolitica
Binomial name
Yersinia enterocolitica
(Schleifstein & Coleman 1939)

Yersinia enterocolitica is a Gram-negative bacillus-shaped bacterium, belonging to the family Enterobacteriaceae. It is motile at temperatures between 22–29°C, but becomes non-motile 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 (TAAs).

The genus Yersinia includes 11 species: Y. pestis, Y. pseudotuberculosis, Y. enterocolitica, Y. frederiksenii, Y. intermedia, Y. kristensenii, Y. bercovieri, Y. mollaretii, Y. rohdei, Y. aldovae and Y. ruckeri. Among them, only Y. pestis, Y. pseudotuberculosis, and certain strains of Y. enterocolitica are of pathogenic importance for humans and certain warm-blooded animals, whereas the other species are of environmental origin and may, at best, act as opportunists. However, Yersinia strains can be isolated from clinical materials, so have to be identified at the species level.

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.

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]

Signs and symptoms

The portal of entry is the gastrointestinal tract. The organism is acquired usually by insufficiently cooked pork or contaminated water, meat, or milk. Acute Y. enterocolitica infections usually lead to mild self-limiting enterocolitis or terminal ileitis and adenitis in humans. Symptoms may include watery or bloody diarrhea and fever, resembling appendicitis or 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 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.[5] See yersiniosis for further details.

Treatment

Yersiniosis is usually self-limiting and does not require treatment. For severe infections (sepsis, focal infection) especially if associated with immunosuppression, the recommended regimen includes doxycycline in combination with an aminoglycoside. Other antibiotics active against Y. enterocolitica include trimethoprim-sulfamethoxasole, fluoroquinolones, ceftriaxone, and chloramphenicol. Y. enterocolitica is usually resistant to penicillin G, ampicillin, and cephalotin due to beta-lactamase production.[6]

Prognosis

Y. enterocolitica infections are sometimes followed by chronic inflammatory diseases such as arthritis,[7] erythema nodosum, and reactive arthritis. This is most likely because of some immune-mediated mechanism.[8]

Y. enterocolitica seems to be associated with autoimmune Graves-Basedow thyroiditis.[9] Whilst indirect evidence exists, direct causative evidence is limited,[10] and 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.[11] Y. enterocolitica infection has also been suggested to not be the cause of autoimmune thyroid disease, but rather is only an associated condition, with both having a shared inherited susceptibility.[12] More recently, the role for Y. enterocolitica has been disputed.[13]

References

  1. ↑ Kapatral, V.; Olson, J. W.; Pepe, J. C.; Miller, V. L.; Minnich, S. A. (1996-03-01). "Temperature-dependent regulation of Yersinia enterocolitica Class III flagellar genes". Molecular Microbiology. 19 (5): 1061–1071. doi:10.1046/j.1365-2958.1996.452978.x. ISSN 0950-382X. PMID 8830263.
  2. ↑ "Yersinia spp. | MicrobLog: Microbiology Training Log". microblog.me.uk. Retrieved 2016-02-10.
  3. ↑ Collins FM (1996). "Pasteurella, and Francisella". In Barron S; et al. Barron's Medical Microbiology (4th ed.). University of Texas. ISBN 0-9631172-1-1. NBK7798.
  4. ↑ Fàbrega A, Vila J (2012). "Yersinia enterocolitica: pathogenesis, virulence and antimicrobial resistance". Enferm. Infecc. Microbiol. Clin. 30 (1): 24–32. doi:10.1016/j.eimc.2011.07.017. PMID 22019131.
  5. ↑ Goljan, Edward F. Rapid Review Pathology. Second Edition. Page 279, Table 15-1.
  6. ↑ Bottone, Edward (April 1997). "Yersinia enterocolitica: the charisma continues". Clinical Microbiology Reviews. American Society for Microbiology. 10 (2): 257–276. PMC 172919Freely accessible. PMID 9105754.
  7. ↑ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 0-8385-8529-9.
  8. ↑ Hill Gaston JS, Lillicrap MS (2003). "Arthritis associated with enteric infection". Best Pract Res Clin Rheumatol. 17 (2): 219–39. doi:10.1016/S1521-6942(02)00104-3. PMID 12787523.
  9. ↑ 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. PMID 16571084.
  10. ↑ Tomer Y, Davies T (1993). "Infection, thyroid disease, and autoimmunity" (PDF). Endocr Rev. 14 (1): 107–20. doi:10.1210/er.14.1.107. PMID 8491150.
  11. ↑ Toivanen P, Toivanen A (1994). "Does Yersinia induce autoimmunity?". Int Arch Allergy Immunol. 104 (2): 107–11. doi:10.1159/000236717. PMID 8199453.
  12. ↑ Strieder T, Wenzel B, Prummel M, Tijssen J, Wiersinga W (2003). "Increased prevalence of antibodies to enteropathogenic Yersinia enterocolitica virulence proteins in relatives of patients with autoimmune thyroid disease". Clin Exp Immunol. 132 (2): 278–82. doi:10.1046/j.1365-2249.2003.02139.x. PMC 1808711Freely accessible. PMID 12699417.
  13. ↑ Hansen P, Wenzel B, Brix T, Hegedüs L (2006). "Yersinia enterocolitica infection does not confer an increased risk of thyroid antibodies: evidence from a Danish twin study". Clin Exp Immunol. 146 (1): 32–8. doi:10.1111/j.1365-2249.2006.03183.x. PMC 1809723Freely accessible. PMID 16968395.
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