Yersinia enterocolitica

The Yersinia genus has 11 species; 4 are pathogenic, but only Y. enterocolitica and Y. pseudotuberculosis cause gastroenteritis. Y. enterocolitica and Y. pseudotuberculosis are small, rod-shaped, Gram-negative bacteria.

Yersinia enterocolitica

Transmission

Both pathogens are transmitted through the fecal-oral route. Both of these gastroenteritis-causing species have been isolated from animals, such as pigs, birds, beavers, cats, and dogs, and, in the case of Y. enterocolitica, frogs, flies, and fleas. Y. enterocolitica has been detected in environmental sources, such as soil and water (e.g., ponds and lakes). Most isolates are not pathogenic.

Pathogenesis

Mortality: Fatalities are extremely rare.

Infective dose: The medium infective dose for humans is not known, but is estimated to be between 104 to 106 organisms.

The infective dose and clinical presentation of symptoms may depend on pathogen (strain-dependent) and host factors. For example, in some cases, in people with gastric hypoacidity, the infective dose may be lower.

Onset: Incubation times from 1 to 11 days have been observed, but occasionally last for several months.

Illness / complications: In some patients, complications arise due to the strain type causing the initial infection and specific human immunologic leukocyte antigen, HLA-B27. These sequelae include reactive arthritis; glomerulonephritis; endocarditis; erythema nodosum (which occurs predominantly in women); uveitis; thyroid disorders, such as Graves’ disease; hyperthyroidism; nontoxic goiter; and Hashimoto’s thyroiditis.

3D computer generated image of Yersinia enterocolita

Reactive arthritis

Y. enterocolitica has been associated with reactive arthritis, which may occur even in the absence of obvious symptoms. The frequency of such postenteritis arthritic conditions is about 2% to 3%. In Japan, Y. pseudotuberculosis was implicated in the etiology of Kawasaki’s disease. Another complication is bacteremia, which raises the possibility of disease dissemination. However, this is rare. Performance of unnecessary appendectomies also may be considered a major complication of yersiniosis, as one of the main symptoms of the disease is abdominal pain in the lower right quadrant.

Treatment

Treatment includes supportive care, since the gastroenteritis is self-limiting. If septicemia or other invasive diseases occur, antibiotic therapy with gentamicin or cefotaxime (doxycycline and ciprofloxacin) typically are administered.

Symptoms

Infection with Y. enterocolitica manifests as nonspecific, self-limiting diarrhea, but may cause a variety of autoimmune complications, as noted above. Most symptomatic infections occur in children younger than 5 years old. Yersiniosis in these children is frequently characterized as gastroenteritis, with diarrhea and/or vomiting; however, fever and abdominal pain are the hallmark symptoms. A small proportion of children (less than 10%) produce bloody stools. Children usually complain of abdominal pain and headache and sore throat at the onset of the illness. Yersinia infections mimic appendicitis and mesenteric lymphadenitis, but the bacteria may also cause infection in other sites, such as wounds, joints, and the urinary tract.

Yersinia enterocolita

Duration: The illness might last from a few days to 3 weeks, unless it becomes chronic enterocolitis, in which case it might continue for several months.  Route of entry: Oral.

Pathway: As zoonotic pathogens, Y. enterocolitica and Y. pseudotuberculosis enter the gastrointestinal tract after ingestion of contaminated food or water. Gastric acid is a significant barrier to infection. Duration:  The illness might last from a few days to 3 weeks, unless it becomes chronic enterocolitis, in which case it might continue for several months.

Route of entry

Oral.

Pathway: As zoonotic pathogens, Y. enterocolitica and Y. pseudotuberculosis enter the gastrointestinal tract after ingestion of contaminated food or water. Gastric acid is a significant barrier to infection. The infective dose might be lower among people with gastric hypoacidity.

Both pathogens harbor plasmid (pYV)-encoded virulence genes that affect pathogenesis. These include an outer-membrane protein, YadA (Yersinia adhesion A), and the genetic suite comprising the type III secretory system. This process usually is facilitated by Yops proteins, which contribute to the ability of Y. enterocolitica cells to resist phagocytosis by causing disruption (cytotoxic changes) of mammalian (human) cells.

Yersinia enterocolitica in SIM Agar1 125

3.  Frequency

Yersiniosis is far more common in Northern Europe, Scandinavia, and Japan than in the United States. It does not occur frequently and tends to be associated with improper food-processing techniques. Y. enterocolitica is a more frequent cause of yersiniosis than is    Y. pseudotuberculosis, and cases have been reported on all continents. Different biotypes of       Y. enterocolitica have been associated with infections around the world, with the most common biotype being 4/O:3. Information on Y. pseudotuberculosis is not as well defined and, as such, is reported less frequently than is Y. enterocolitica.

4.  Sources

Strains of Y. enterocolitica can be found in meats (pork, beef, lamb, etc.), oysters, fish, crabs, and raw milk. However, the prevalence of this organism in soil, water, and animals, such as beavers, pigs, and squirrels, offers many opportunities for Yersinia to enter the food supply. For example, poor sanitation and improper sterilization techniques by food handlers, including improper storage, may be a source of contamination. Raw or undercooked pork products have drawn much attention as a source of Y. enterocolitica, and Y. pseudotuberculosis, particularly since Y. enterocolitica has been associated with pigs.

Yersinia enterocolitica gram stain

5.  Diagnosis

Yersiniosis may be misdiagnosed as Crohn’s disease (regional enteritis) or appendicitis. Diagnosis of yersiniosis begins with isolation of the organism from the human host’s feces, blood, or vomit, and sometimes at the time of appendectomy. Confirmation occurs with the isolation, as well as biochemical and serological identification, of Y. enterocolitica from both the human host and the ingested food. Diarrhea occurs in about 80% of cases; abdominal pain and fever are the most reliable symptoms.

Y. enterocolitica or Y. pseudotuberculosis in patients with acute gastroenteritis can be readily isolated via conventional bacteriological media designed to isolate Yersinia. It is much more challenging to isolate these pathogens in asymptomatic carriers or from foods. Since many Y. enterocolitica isolated from non-human sources are not considered pathogenic, it is imperative to distinguish these isolates from pathogenic Yersinia species. Molecular-based assays, particularly PCR methods, have been developed to target Y. enterocolitica and can be used to rapidly confirm the pathogenicity of the isolate. Several PCR primer sets are directed to either plasmid-borne genes, e.g., virF or yadA, or chromosomally located loci, such as ail.

Serology is used to identify the biotype (based on biochemical analysis) and serogroup (O-antigen). Sera from acute or convalescent patients are titered against the suspect serotype of Yersinia spp.

6.  Target populations

The most susceptible populations for the main disease and potential complications are the very young (< 10 years), the debilitated, the very old, and people undergoing immunosuppressive therapy. Those most susceptible to post-enteritis arthritis are people with the antigen HLA-B27 (or related antigens, such as B7).  

7.  Food Analysis

The isolation method is relatively easy to perform, but in some instances, cold enrichment (25 g sample of the food mixed with 225 ml of Peptone Sorbitol bile broth for 10 days at 10°C) may be required. Y. enterocolitica can be presumptively identified in 36 to 48 hours using biochemical testing or API 20E or Vitek GNI. The genes encoding for invasion of mammalian cells are located on the chromosome, while a 70 kb plasmid, present in almost all pathogenic Yersinia species, encodes most of the other virulence-associated phenotypes. PCR-based assays have been developed to target virulence genes on both the chromosome and plasmid.