Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

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.

Diagnosis

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.

Management

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.

Next

Background

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]

Classification

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.

Metabolism

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.

Previous
Next

Pathophysiology

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]

Enterotoxicity

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.

Complications

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]

Previous
Next

Etiology

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]

Previous
Next

Epidemiology

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.

Previous
Next

Prognosis

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.

Previous
 
 
Contributor Information and Disclosures
Author

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.

Coauthor(s)

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.

Acknowledgements

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.

References
  1. Bercovier H, Brenner DJ, Ursing J, Steigerwalt AG, Fanning GR, Alonso JM, et al. Characterization of Yersinia enterocolitica sensu stricto. Current Microbiology. 1980. 4:201-6.

  2. Zheng H, Wang J, Sun Y, Jiang B. Clinical isolation and characterization of Yersinia enterocolitica in China using real-time PCR and culture method. Digestion. 2007. 75(4):199-204. [Medline].

  3. Zheng HX, Sun Y, Jiang B. [Evaluation of 4 culture methods of Yersinia enterocolitica]. Nan Fang Yi Ke Da Xue Xue Bao. 2007 Sep. 27(9):1438-40. [Medline].

  4. Centers for Disease Control and Prevention. Diagnosis and management of foodborne illnesses: a primer for physicians and other health care professionals. MMWR Recomm Rep. 2004 Apr 16. 53:1-33. [Medline].

  5. Bottone EJ. Yersinia enterocolitica: a panoramic view of a charismatic microorganism. CRC Crit Rev Microbiol. 1977. 5(2):211-41. [Medline].

  6. Schleifstein J, Coleman, MB. An unidentified microorganism resembling B. lignieresi and Pasteurella pseudotuberculosis, pathogenic for man. New York State Journal of Medicine. 1939. 39:1749-53.

  7. Zheng H, Sun Y, Lin S, Mao Z, Jiang B. Yersinia enterocolitica infection in diarrheal patients. Eur J Clin Microbiol Infect Dis. 2008 Aug. 27(8):741-52. [Medline].

  8. Huovinen E, Sihvonen LM, Virtanen MJ, Haukka K, Siitonen A, Kuusi M. Symptoms and sources of Yersinia enterocolitica-infection: a case-control study. BMC Infect Dis. 2010 May 20. 10:122. [Medline]. [Full Text].

  9. Young VB, Falkow S, Schoolnik GK. The invasin protein of Yersinia enterocolitica: internalization of invasin-bearing bacteria by eukaryotic cells is associated with reorganization of the cytoskeleton. J Cell Biol. 1992 Jan. 116(1):197-207. [Medline].

  10. Handley SA, Newberry RD, Miller VL. Yersinia enterocolitica invasin-dependent and invasin-independent mechanisms of systemic dissemination. Infect Immun. 2005 Dec. 73(12):8453-5. [Medline].

  11. Bradford WD, Noce PS, Gutman LT. Pathologic features of enteric infection with Yersinia enterocolitica. Arch Pathol. 1974 Jul. 98(1):17-22. [Medline].

  12. Aho K, Ahvonen P, Lassus A, Sievers K, Tiilikainen A. HL-A 27 in reactive arthritis. A study of Yersinia arthritis and Reiter's disease. Arthritis Rheum. 1974 Sep-Oct. 17(5):521-6. [Medline].

  13. Välimäki E, Aittomäki S, Karenko L, Kantonen J, Pettersson T, Turunen U, et al. Normal inflammasome activation and low production of IL-23 by monocyte-derived macrophages from subjects with a history of reactive arthritis. Scand J Rheumatol. 2013 Feb 20. [Medline].

  14. Stoddard JJ, Wechsler DS, Nataro JP, Casella JF. Yersinia enterocolitica infection in a patient with sickle cell disease after exposure to chitterlings. Am J Pediatr Hematol Oncol. 1994 May. 16(2):153-5. [Medline].

  15. Centers for Disease Control and Prevention. Yersinia enterocolitica gastroenteritis among infants exposed to chitterlings--Chicago, Illinois, 2002. MMWR Morb Mortal Wkly Rep. 2003 Oct 10. 52(40):956-8. [Medline].

  16. Notes from the field: Yersinia enterocolitica infections associated with pasteurized milk --- southwestern Pennsylvania, March-August, 2011. MMWR Morb Mortal Wkly Rep. 2011 Oct 21. 60(41):1428. [Medline].

  17. Tacket CO, Narain JP, Sattin R, Lofgren JP, Konigsberg C Jr, Rendtorff RC, et al. A multistate outbreak of infections caused by Yersinia enterocolitica transmitted by pasteurized milk. JAMA. 1984 Jan 27. 251(4):483-6. [Medline].

  18. Cortes PR, Contreras Funes V, Huerta VG, Dichiara DM. [Yersinia enterocolitica in the fecal material from 6 pediatric patients in the city of Córdoba]. Rev Argent Microbiol. 2010 Jan-Feb. 42(1):79. [Medline].

  19. Leclercq A, Martin L, Vergnes ML, Ounnoughene N, Laran JF, Giraud P, et al. Fatal Yersinia enterocolitica biotype 4 serovar O:3 sepsis after red blood cell transfusion. Transfusion. 2005 May. 45(5):814-8. [Medline].

  20. Centers for Disease Control and Prevention. Yersinia enterocolitica. CDC. Available at http://www.cdc.gov/ncidod/dbmd/diseaseinfo/yersinia_g.htm. Accessed: Feb 22 2013.

  21. Centers for Disease Control and Prevention. Vital signs: incidence and trends of infection with pathogens transmitted commonly through food--foodborne diseases active surveillance network, 10 U.S. sites, 1996-2010. MMWR Morb Mortal Wkly Rep. 2011 Jun 10. 60(22):749-55. [Medline]. [Full Text].

  22. Scallan E, Mahon BE, Hoekstra RM, Griffin PM. Estimates of Illnesses, Hospitalizations, and Deaths Caused By Major Bacterial Enteric Pathogens in Young Children in the United States. Pediatr Infect Dis J. 2012 Dec 17. [Medline].

  23. Abdel-Haq NM, Asmar BI, Abuhammour WM, Brown WJ. Yersinia enterocolitica infection in children. Pediatr Infect Dis J. 2000 Oct. 19(10):954-8. [Medline].

  24. Rosner BM, Stark K, Werber D. Epidemiology of reported Yersinia enterocolitica infections in Germany, 2001-2008. BMC Public Health. 2010 Jun 14. 10:337. [Medline]. [Full Text].

  25. Saebo A, Vik E, Lange OJ, Matuszkiewicz L. Inflammatory bowel disease associated with Yersinia enterocolitica O:3 infection. Eur J Intern Med. 2005 Jun. 16(3):176-182. [Medline].

  26. Ray SM, Ahuja SD, Blake PA, Farley MM, Samuel M, Fiorentino T, et al. Population-based surveillance for Yersinia enterocolitica infections in FoodNet sites, 1996-1999: higher risk of disease in infants and minority populations. Clin Infect Dis. 2004 Apr 15. 38 Suppl 3:S181-9. [Medline].

  27. Metchock B, Lonsway DR, Carter GP, Lee LA, McGowan JE Jr. Yersinia enterocolitica: a frequent seasonal stool isolate from children at an urban hospital in the southeast United States. J Clin Microbiol. 1991 Dec. 29(12):2868-9. [Medline].

  28. Koehler KM, Lasky T, Fein SB, Delong SM, Hawkins MA, Rabatsky-Ehr T, et al. Population-based incidence of infection with selected bacterial enteric pathogens in children younger than five years of age, 1996-1998. Pediatr Infect Dis J. 2006 Feb. 25(2):129-34. [Medline].

  29. Helms M, Simonsen J, Mølbak K. Foodborne bacterial infection and hospitalization: a registry-based study. Clin Infect Dis. 2006 Feb 15. 42(4):498-506. [Medline].

  30. Girszyn N, Kerleau JM, Robaday S, Lefebvre S, Marie I, Levesque H. [Pneumonia with bacteremia due to Yersinia enterocolitica in a diabetic patient carrying HLA-B27]. Rev Med Interne. 2007 Dec. 28(12):882-4. [Medline].

  31. Hoelen DW, Tjan DH, Schouten MA, Dujardin BC, van Zanten AR. Severe Yersinia enterocolitica sepsis after blood transfusion. Neth J Med. 2007 Sep. 65(8):301-3. [Medline].

  32. Pulvirenti D, Aikaterini T, Neri S. Septicemia, hepatic abscess, and encephalitis due to Yersinia enterocolitica. J Clin Gastroenterol. 2007 Mar. 41(3):333-4. [Medline].

  33. Jess T, Jess P. Acute terminal ileitis, yersiniosis, and Crohn's disease: a long-term follow-up study of the relationships. Eur J Intern Med. 2001 Apr. 12(2):98-100. [Medline].

  34. Navarro-Llavat M, Domènech E, Masnou H, Ojanguren I, Mañosa M, Lorenzo-Zúñiga V, et al. Collagenous duodeno-ileo-colitis with transient IgG deficiency preceded by Yersinia enterocolitica intestinal infection: case report and review of literature. Gastroenterol Hepatol. 2007 Apr. 30(4):219-21. [Medline].

  35. Berner R, Kist M, Sauer M. Encephalopathy associated with Yersinia enterocolitica O:3. Lancet. 1998 Feb 7. 351(9100):418. [Medline].

  36. von Eckardstein K, Spuler A, Brauer C, Mehl M, Kiwit J. Spontaneous cervical osteomyelitis due to Yersinia enterocolitica in a non-immunocompromised host. Eur J Clin Microbiol Infect Dis. 2004 Jan. 23(1):66-8. [Medline].

  37. Krajinovic V, Tambic Andrasevic A, Barsic B. Tricuspidal valve endocarditis due to Yersinia enterocolitica. Infection. 2007 Jun. 35(3):203-5. [Medline].

  38. Kelesidis T, Balba G, Worthington M. Axillary abscess in a patient with Yersinia enterocolitica infection as a result of exposure to pork. Am J Med. 2008 Mar. 121(3):e1. [Medline].

  39. Mills DM, Meyer DR. Posttraumatic cellulitis and ulcerative conjunctivitis caused by Yersinia enterocolitica O:8. Ophthal Plast Reconstr Surg. 2008 Sep-Oct. 24(5):425-6. [Medline].

  40. Tennant SM, Hartland EL, Phumoonna T, Lyras D, Rood JI, Robins-Browne RM, et al. Influence of gastric acid on susceptibility to infection with ingested bacterial pathogens. Infect Immun. 2008 Feb. 76(2):639-45. [Medline]. [Full Text].

  41. Lamps LW, Madhusudhan KT, Greenson JK, Pierce RH, Massoll NA, Chiles MC, et al. The role of Yersinia enterocolitica and Yersinia pseudotuberculosis in granulomatous appendicitis: a histologic and molecular study. Am J Surg Pathol. 2001 Apr. 25(4):508-15. [Medline].

  42. Taccetti G, Trapani S, Ermini M, Falcini F. Reactive arthritis triggered by Yersinia enterocolitica: a review of 18 pediatric cases. Clin Exp Rheumatol. 1994 Nov-Dec. 12(6):681-4. [Medline].

  43. De Berardis B, Torresini G, Brucchi M, Marinelli S, Mattucci S, Schietroma M, et al. Yersinia enterocolitica intestinal infection with ileum perforation: report of a clinical observation. Acta Biomed. 2004 Apr. 75(1):77-81. [Medline].

  44. Reed RP, Robins-Browne RM, Williams ML. Yersinia enterocolitica peritonitis. Clin Infect Dis. 1997 Dec. 25(6):1468-9. [Medline].

  45. Hervás JA, Albertí P, Bregante JI, Boya E, Reina J, Gil J. Chronic intussusception associated with Yersinia enterocolitica mesenteric adenitis. J Pediatr Surg. 1992 Dec. 27(12):1591-2. [Medline].

  46. Chandler ND, Parisi MT. Radiological case of the month. Yersinia enterocolitica masquerading as appendicitis. Arch Pediatr Adolesc Med. 1994 May. 148(5):527-8. [Medline].

  47. Bottone EJ. Yersinia enterocolitica: the charisma continues. Clin Microbiol Rev. 1997 Apr. 10(2):257-76. [Medline].

  48. Vento S, Cainelli F, Cesario F. Infections and thalassaemia. Lancet Infect Dis. 2006 Apr. 6(4):226-33. [Medline].

  49. Bergmann TK, Vinding K, Hey H. Multiple hepatic abscesses due to Yersinia enterocolitica infection secondary to primary haemochromatosis. Scand J Gastroenterol. 2001 Aug. 36(8):891-5. [Medline].

  50. Antonopoulos P, Constantinidis F, Charalampopoulos G, Dalamarinis K, Karanicas I, Kokkini G. An emergency diagnostic dilemma: a case of Yersinia enterocolitica colitis mimicking acute appendicitis in a beta-thalassemia major patient: the role of CT and literature review. Emerg Radiol. 2008 Mar. 15(2):123-6. [Medline].

  51. Renaud N, Lecci L, Courcol RJ, Simonet M, Gaillot O. CHROMagar Yersinia: a new chromogenic agar for the screening of potentially pathogenic Yersinia enterocolitica in stools. J Clin Microbiol. 2013 Jan 30. [Medline].

  52. You Y, Fu C, Zeng X, Fang D, Yan X, Sun B, et al. A novel DNA microarray for rapid diagnosis of enteropathogenic bacteria in stool specimens of patients with diarrhea. J Microbiol Methods. 2008 Dec. 75(3):566-71. [Medline].

  53. Kojima M, Morita Y, Shimizu K, Yoshida T, Yamada I, Togo T, et al. Immunohistological findings of suppurative granulomas of Yersinia enterocolitica appendicitis: a report of two cases. Pathol Res Pract. 2007. 203(2):115-9. [Medline].

  54. Noble RC. Failure of cefotaxime in the treatment of Yersinia enterocolitica sepsis despite in vitro susceptibility. Current Therapeutic Research, Clinical and Experimental. 1989. 46(4):692-4.

  55. Lal M, Kaur H, Gupta LK. Y.enterocolitica gastroenteritis - A prospective study. Indian J Med Microbiol. 2003 Jul-Sep. 21(3):186-8. [Medline].

  56. Chan J, Gandhi RT. A Case of Septic Arthritis of the Shoulder Due to Yersinia enterocolitica with Review of the Literature. Open Forum Infect Dis. 2014 Sep. 1 (2):ofu054. [Medline].

 
Previous
Next
 
Yersinia enterocolitis in a 45-year-old white woman who presented with chronic diarrhea.
Gram stain of Yersinia enterocolitica.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.