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Yersinia Enterocolitica

  • Author: Zartash Zafar Khan, MD, FACP; Chief Editor: Mark R Wallace, MD, FACP, FIDSA  more...
Updated: Oct 20, 2015

Practice Essentials

Yersinia enterocolitica (see the image below) is a bacterial species in the family Enterobacteriaceae that most often causes enterocolitis, acute diarrhea, terminal ileitis, mesenteric lymphadenitis, and pseudoappendicitis but, if it spreads systemically, can also result in fatal sepsis.[1]

Gram stain of Yersinia enterocolitica.
Gram stain of Yersinia enterocolitica.

Signs and symptoms

Symptoms of Y enterocolitica infection typically include the following:

  • Diarrhea - The most common clinical manifestation of this infection; diarrhea may be bloody in severe cases
  • Low-grade fever
  • Abdominal pain - May localize to the right lower quadrant
  • Vomiting - Present in approximately 15-40% of cases

The patient may also develop erythema nodosum, which manifests as painful, raised red or purple lesions, mainly on the patient’s legs and trunk. Lesions appear 2-20 days after the onset of fever and abdominal pain and resolve spontaneously in most cases in about a month.

See Clinical Presentation for more detail.


The following tests can be used in the diagnosis of Y enterocolitica infection:

  • Stool culture - This is the best way to confirm a diagnosis of Y enterocolitica [2, 3] ; the culture result is usually positive within 2 weeks of onset of disease
  • Tube agglutination
  • Enzyme-linked immunosorbent assays
  • Radioimmunoassays
  • Imaging studies - Ultrasonography or computed tomography (CT) scanning may be useful in delineating true appendicitis from pseudoappendicitis
  • Colonoscopy - Findings may vary and are relatively nonspecific
  • Joint aspiration in cases of Yersinia- associated reactive arthropathy

See Workup for more detail.


Care in patients with Y enterocolitica infection is primarily supportive, with good nutrition and hydration being mainstays of treatment.[4]

First-line drugs used against the bacterium include the following agents:

  • Third-generation cephalosporins
  • Trimethoprim-sulfamethoxazole (TMP-SMZ)
  • Tetracyclines
  • Fluoroquinolones - not approved for use in children under 18 years
  • Aminoglycosides

See Treatment and Medication for more detail.



Yersinia enterocolitica is a pleomorphic, gram-negative bacillus that belongs to the family Enterobacteriaceae. As a human pathogen, Y enterocolitica is most frequently associated with enterocolitis, acute diarrhea, terminal ileitis, mesenteric lymphadenitis, and pseudoappendicitis,[1] with the spectrum of disease ranging from asymptomatic to life-threatening sepsis, especially in infants. The bacterium was first reported by Mclver and Picke, in 1934.[5] Schleifstein and Coleman provided the first recognized description of 5 human isolates of Y enterocolitica, in 1939. (See Prognosis and Clinical Presentation.)[6]

In several countries, Y enterocolitica has eclipsed Shigella species and approaches Salmonella and Campylobacter species as the predominant cause of acute bacterial gastroenteritis. Y enterocolitica most commonly affects young individuals (approximately 75% of patients with Y enterocolitica infection are aged 5-15 years), but whether this represents an increased susceptibility or a greater likelihood of developing symptomatic illness is unclear. Most cases of Y enterocolitica infection are sporadic, but reports have documented large outbreaks centered on a single contaminated source. (See Epidemiology.)

Human yersiniosis is attributed to contaminated pork, milk, water, and tofu consumption, as well as to blood transfusion. Infected individuals may shed Y enterocolitica in stools for 90 days after the symptom resolution, suggesting that early detection of Y enterocolitica from diarrheal stool samples is critical in preventing its transmission and an eventual outbreak. (See Pathophysiology, Etiology, Clinical Presentation, and Workup.)[7, 8]


Y enterocolitica is classified according to various distinct biochemical and serologic reactions. Based on biochemical characteristics, 6 biotypes of the bacterium have been described. Biotypes 2, 3, and 4 are most common in humans. The serotyping is based on O and H antigens. More than 60 serotypes of Y enterocolitica have been described. The serotypes most clearly pathogenic to humans include O:3, O:5,27, O:8, O:9, and O:13.

H-antigen typing can be a valuable supplement to O-antigen typing and biochemical characterization in epidemiologic investigations. Accurate identification of pathogenic strains requires consideration of both the biotype and the serotype because some strains can contain multiple cross-reacting O antigens.


Y enterocolitica is non–lactose-fermenting, glucose-fermenting, and oxidase-negative facultative anaerobe that is motile at 25°C and nonmotile at 37°C. Most, but not all, Y enterocolitica isolates reduce nitrates. The presence of bile salts in the medium prevents the organism from fermenting lactose. Colonies of Y enterocolitica do not produce hydrogen sulfide in triple sugar iron medium, but the organism is urease positive.

Patient education

Educate patients and individuals at risk for infection about appropriate hygiene methods and signs or symptoms of infection. Encourage public awareness of outbreaks, modes of transmission, and ways to prevent transmission.



As with other members of the genus Yersinia, Y enterocolitica is an invasive organism that appears to cause disease by tissue destruction. Researchers have elucidated several potential pathogenic properties, including chromosomally mediated effects (eg, attachment to tissue culture, production of enterotoxin) and plasmid-mediated mechanisms (eg, production of Vw antigens, calcium dependency for growth, autoagglutination).

Invasion and colonization

Invasion of human epithelial cells and penetration of the mucosa occurs in the ileum, followed by multiplication in Peyer patches. A 103-kd protein, known as invasin and determined by the INV gene, mediates bacterial invasion. The best-defined pathway is through the action of invasin.[9]

As a foodborne pathogen, Y enterocolitica can efficiently colonize and induce disease in the small intestine. Following ingestion, the bacteria colonize the lumen and invade the epithelial lining of the small intestine, resulting in the colonization of the underlying lymphoid tissues known as Peyer patches. A direct lymphatic link between the Peyer patches and mesenteric lymph nodes may result in bacterial dissemination to these sites, resulting in mesenteric lymphadenitis or systemic infection.

Dissemination to extraintestinal sites, such as the spleen, is hypothesized to occur via 2 main mechanisms: (1) colonization of the Peyer patches, which can then be used as a staging ground for spread into the blood and/or lymph, ultimately resulting in the appearance of bacteria in other tissues, and (2) bypass of the Peyer patches, with Y enterocolitica going straight to systemic colonization. The possibilities of additional avenues for dissemination have yet to be excluded.

Y enterocolitica colonization of the intestinal lymphoid tissues requires transmigration of the bacteria from the intestinal lumen across an epithelial tissue barrier. Antigen-sampling intestinal epithelial cells known as M cells are thought to be critical for this transmigratory process. The epithelium overlying the Peyer patches has a high concentration of M cells (although these cells have also been identified throughout the non–Peyer patch areas of the small intestine).

Y enterocolitica and the related pathogen Y pseudotuberculosis produce at least 3 invasion proteins, Ail, YadA, and the aforementioned invasin, which could potentially promote adherence to and invasion of M cells. Invasin, the principle invasion factor of Y enterocolitica and Y pseudotuberculosis, binds to ß1 -chain integrin receptors with high affinity, promoting internalization. These receptors are found at high levels on the luminal side of M cells but not on the luminal side of enterocytes.[10]


The enterotoxin produced by Y enterocolitica is similar to that produced by the heat-stable Escherichia coli; however, it likely plays a minor role in causing disease, as diarrheal syndromes have been observed in the absence of enterotoxin production. In addition, the toxin does not appear to be produced at temperatures higher than 30°C. The plasmid-mediated outer membrane antigens are associated with bacterial resistance to opsonization and neutrophil phagocytosis.

Iron and pathogenicity

One unique property of Y enterocolitica is its inability to chelate iron, which is an essential growth factor for most bacteria and is obtained through the production of chelators known as siderophores. Y enterocolitica does not produce siderophores but can utilize siderophores produced by other bacteria (eg, desferrioxamine E produced by Streptomyces pilosus).

Iron overload substantially increases the pathogenicity of Y enterocolitica, perhaps through attenuation of the bactericidal activity of the serum. Researchers observe differences in the iron requirements of different serotypes of the organism; such differences may explain, in part, the varying degrees of virulence among serotypes.


After an incubation period of 4-7 days, infection may result in mucosal ulceration (usually in the terminal ileum and rarely in the ascending colon), necrotic lesions in Peyer patches, and mesenteric lymph node enlargement. See the image below.

Yersinia enterocolitis in a 45-year-old white wom Yersinia enterocolitis in a 45-year-old white woman who presented with chronic diarrhea.

In severe cases, bowel necrosis may occur, as a result of mesenteric vessel thrombosis.[11] Focal abscesses may occur. In persons with human leukocyte antigen (HLA)–B27, reactive arthritis is not uncommon, possibly because of the molecular similarity between HLA-B27 antigen and Yersinia antigens. The pathogenesis of Yersinia -associated erythema nodosum is unknown.[12, 13]



Human clinical Y enterocolitica infections ensue after ingestion of the microorganisms in contaminated food or water or by direct inoculation through blood transfusion.

Y enterocolitica is potentially transmitted by contaminated unpasteurized milk and milk products, raw pork, tofu, meats, oysters, and fish.[14, 15] Outbreaks have been associated with raw vegetables; the surface of vegetables can become contaminated with pathogenic microorganisms through contact with soil, irrigation water, fertilizers, equipment, humans, and animals.

Pasteurized milk and dairy products can also cause outbreaks because Yersinia can proliferate at refrigerated temperatures.[16, 17]

Animal reservoirs of Y enterocolitica include swine (principle reservoir), dogs, cats, cows, sheep, goats, rodents, foxes, porcupines, and birds.

Reports of person-to-person spread are conflicting and are generally not observed in large outbreaks. Transmission via blood products has occurred, however, and infection can be transmitted from mother to newborn infant. Fecal-oral transmission among humans has not been proven.[18, 19]



Occurrence in the United States

Yersiniosis is rare in the absence of a breakdown in food-processing techniques. The Centers for Disease Control and Prevention (CDC) estimates that 1 culture-confirmed Y enterocolitica infection per 100,000 persons is found annually.[20] The bacterium has been isolated in 1.4-2.8% of stools of children with diarrhea.

For 2010, the CDC’s Foodborne Diseases Active Surveillance Network (FoodNet), using surveillance data from 10 US sites, preliminarily identified a total of 19,089 laboratory-confirmed cases of infection caused by bacterial pathogens that are commonly transmitted through food. The number of cases and incidence per 100,000 population were reported as follows[21] :

  • Salmonella (8256; 17.6)
  • Campylobacter (6365; 13.6)
  • Shigella (1780; 3.8)
  • Shiga toxin-producing E coli (STEC) non-O157 (451; 1.0)
  • STEC O157 (442; 0.9)
  • Vibrio (193; 0.4)
  • Yersinia (159; 0.3)
  • Listeria (125; 0.3)

In the United States, Yersinia enterocolitica accounts for approximately 5% of bacterial enteric infections among children younger than 5 years, according to a 2012 study by Scallan et al. The investigators found this to be a greater incidence than that for the enterohemorrhagic E coli strain O157 (3%), but a lower incidence than those for nontyphoidal Salmonella (42%), Campylobacter (28%), and Shigella (21%).[22]

Scallan et al estimated that the 5 pathogens together cause more than 290,000 illnesses annually in children under 5 years.

Y enterocolitica infection is more common in cooler climates, and its prevalence peaks from November to January.[23]

International statistics

Y enterocolitica has been isolated in patients in many countries worldwide, but the infection appears to occur predominantly in cooler climates, being much more common in northern Europe, Scandinavia, and Japan. Most isolates reported from Canada and Europe are O:3 and O:9 serotypes.[24] The O:3 serotype is also common in Japan. Isolation of Y enterocolitica in developing countries is uncommon.[25]

Race- and age-related demographics

Higher incidence of Y enterocolitica infection has been observed among black infants in the United States.[26]

Reports document symptomatic Y enterocolitica infection most commonly in younger age groups. A sample collection from 1988-1991 showed that 77.6% of infections occurred in children aged 12 months and younger, making Y enterocolitica the second most common cause of bacterial gastrointestinal infection in children.[22, 27, 28]

Clinical manifestations of Y enterocolitica infection exhibit some age-dependent predilections, with reactive arthritis and erythema nodosum being more common in older patients. Older patients with more debility are more likely to develop bacteremia than are younger, healthier patients.



Yersiniosis is usually either self-limited or is responsive to therapy; however, reinfection is possible. Most patients with Y enterocolitica infection are symptomatic; however, asymptomatic carriage may occur. Death is uncommon, but patients with significant comorbidities are at risk for Y enterocolitica bacteremia, which carries a case fatality rate of 34-50%.

A national, registry-based study of 52,121 patients in Denmark reported estimates for the risk of developing severe, hospitalization-requiring complications and long-term sequelae up to 1 year after infection with 5 common bacterial gastrointestinal pathogens. Of the 3922 cases of Y enterocolitica infection reported, 368 required hospitalization.[29]

A report from the CDC stated that in 2010 (preliminary data), of 159 Yersinia infections in the United States, 52 required hospitalization and 1 resulted in death.[21]

Various manifestations of Y enterocolitica infection have been reported, including the following[30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42] :

  • Enterocolitis
  • Pseudoappendicitis
  • Mesenteric adenitis
  • Reactive arthritis - Can last 1-4 months
  • Erythema nodosum
  • Septicemia
  • Pharyngitis
  • Dermatitis
  • Myocarditis
  • Glomerulonephritis

Iron is an essential growth factor for the organism, and iron overload (eg, chronic hemolysis, hereditary hemochromatosis) is associated with an increased risk of systemic disease. Deferoxamine therapy also increases susceptibility to Y enterocolitica disease.

Contributor Information and Disclosures

Zartash Zafar Khan, MD, FACP Infectious Disease Consultant

Zartash Zafar Khan, MD, FACP is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America, International Society for Infectious Diseases

Disclosure: Nothing to disclose.


Daniel R Bronfin, MD Clinical Professor of Pediatrics, Tulane University School of Medicine; Vice Chairman of Pediatrics, Ochsner Children's Health Center

Daniel R Bronfin, MD is a member of the following medical societies: American Academy of Pediatrics, American Cleft Palate-Craniofacial Association

Disclosure: Nothing to disclose.

Michelle R Salvaggio, MD, FACP Assistant Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine; Medical Director of Infectious Diseases Institute, Director, Clinical Trials Unit, Director, Ryan White Programs, Department of Medicine, University of Oklahoma Health Sciences Center; Attending Physician, Infectious Diseases Consultation Service, Infectious Diseases Institute, OU Medical Center

Michelle R Salvaggio, MD, FACP is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

Disclosure: Received honoraria from Merck for speaking and teaching.

Chief Editor

Mark R Wallace, MD, FACP, FIDSA Clinical Professor of Medicine, Florida State University College of Medicine; Clinical Professor of Medicine, University of Central Florida College of Medicine

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society, Florida Infectious Diseases Society

Disclosure: Nothing to disclose.


Daniel R Bronfin, MD Head, General Academic Pediatrics, Ochsner Children's Health Center

Daniel R Bronfin, MD is a member of the following medical societies: American Academy of Pediatrics and American Cleft Palate/Craniofacial Association

Disclosure: Nothing to disclose.

Richard B Brown, MD, FACP Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal Medicine, Tufts University School of Medicine

Richard B Brown, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Brooks D Cash, MD, FACP Director of Clinical Research, Assistant Professor of Medicine, Gastroenterology, National Naval Medical Center

Disclosure: Nothing to disclose.

Joseph Domachowske, MD Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York Upstate Medical University

Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Thomas E Herchline, MD Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio

Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, Infectious Diseases Society of America, and Infectious Diseases Society of Ohio

Disclosure: Nothing to disclose.

Mark H Johnston, MD Associate Professor of Medicine, Uniformed Services University of the Health Sciences; Consulting Staff, Lancaster Gastroenterology, Inc

Mark H Johnston, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Leonard R Krilov, MD Chief of Pediatric Infectious Diseases and International Adoption, Vice Chair, Department of Pediatrics, Professor of Pediatrics, Winthrop University Hospital

Leonard R Krilov, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Society for Pediatric Research

Disclosure: Medimmune Grant/research funds Cliinical trials; Medimmune Honoraria Speaking and teaching; Medimmune Consulting fee Consulting

Gregory J Martin, MD Director, Infectious Diseases Clinical Research Program (IDCRP) Associate Professor of Medicine, Uniformed Services University, Bethesda, MD

Gregory J Martin, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Tropical Medicine and Hygiene, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Swetha G Pinninti, MD Fellow in Pediatric Infectious Diseases, Department of Pediatrics, University of Alabama at Birmingham School of Medicine

Swetha G Pinninti, MD is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Yersinia enterocolitis in a 45-year-old white woman who presented with chronic diarrhea.
Gram stain of Yersinia enterocolitica.
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