Yersinia enterocolitica

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

Yersinia enterocolitica is a species of gram-negative coccobacillus-shaped bacterium, belonging to the family Enterobacteriaceae. Yersinia enterocolitica infection causes the disease yersiniosis, which is a zoonotic disease occurring in humans as well as a wide array of animals such as cattle, deer, pigs, and birds. Many of these animals recover from the disease and become asymptomatic carriers.[1] It infects the host by sticking to the cells of the host using Trimeric Autotransporter Adhesins (TAA). At present, the genus Yersinia includes 11 established 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 and therefore have to be identified at the species level. Y. enterocolitica is a heterogeneous group of strains, which are traditionally classified by biotyping into 6 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 6 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.5 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, other studies have suggested that 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 [2]enteritis/diarrhea.[3]

Signs and symptoms[edit]

Acute Y. enterocolitica infections usually lead to mild self-limiting entero-colitis or terminal ileitis in humans. Symptoms may include watery or bloody diarrhea and fever. After oral uptake yersiniae replicate in the terminal ileum and invade Peyer's patches. From here yersiniae can disseminate further to mesenteric lymph nodes causing lymphadenopathy. This condition can be confused with appendicitis and is therefore called pseudoappendicitis. In immunosuppressed individuals, yersiniae can disseminate from the gut to liver and spleen and form abscesses. Because Yersinia is a 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.[4] See yersiniosis for further details. Yersiniae are usually transmitted to humans by insufficiently cooked pork or contaminated water.

Treatment[edit]

Yersiniosis is usually self-limiting and does not require treatment. Severe infections (septicemia, focal infection, immunosuppression) can be treated with doxycycline in combination with an aminoglycoside. Other antibiotics that are 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.[5]

Prognosis[edit]

Y. enterocolitica infections are sometimes followed by chronic inflammatory diseases such as arthritis.[6]

Y. enterocolitica seems to be associated with autoimmune Graves-Basedow thyroiditis.[7] Whilst indirect evidence exists, direct causative evidence is limited,[8] 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.[9] It has also been suggested that Y. enterocolitica infection is not the cause of auto-immune thyroid disease, but rather is only an associated condition; with both having a shared inherited susceptibility.[10] More recently the role for Y. enterocolitica has been disputed.[11]

References[edit]

  1. ^ Collins FM (1996). Pasteurella, and Francisella. In: Barron's Medical Microbiology (Barron S et al., eds.) (4th ed.). Univ of Texas Medical Branch. ISBN 0-9631172-1-1. (via NCBI Bookshelf). 
  2. ^ Yersinia enterocolitica: Pathogenesis, virulence and antimicrobial resistance
  3. ^ Yersinia enterocolitica: Pathogenesis, virulence and antimicrobial resistance
  4. ^ Goljan, Edward F. Rapid Review Pathology. Second Edition. Page 279, Table 15-1.
  5. ^ Bottone, Edward (April 1997). "Yersinia enterocolitica: the charisma continues". Clinical Microbiology Reviews (American Society for Microbiology) 10 (2): 257–276. PMC 172919. PMID 9105754. 
  6. ^ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 0-8385-8529-9. 
  7. ^ 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. 
  8. ^ 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. 
  9. ^ Toivanen P, Toivanen A (1994). "Does Yersinia induce autoimmunity?". Int Arch Allergy Immunol 104 (2): 107–11. doi:10.1159/000236717. PMID 8199453. 
  10. ^ 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 1808711. PMID 12699417. 
  11. ^ 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 1809723. PMID 16968395. 

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