Pediatric Yersinia Enterocolitica 

  • Author: Swetha G Pinninti, MD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Jun 5, 2009
 

Background

Yersinia enterocolitica is a well-described enteric pathogen with distinctive clinical manifestations, a range of outcomes, and a predilection for children. In 1939, Schleifstein and Coleman first described Y enterocolitica. Approximately 75% of patients with Y enterocolitica infection are children aged 5-15 years. The spectrum of disease ranges from asymptomatic to life-threatening sepsis, especially in infants.

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

This organism belongs to the family Enterobacteriaceae, genus Yersinia, which includes 11 species. Among them, only 3 species are pathogenic to humans: Yersinia pestis (bubonic plague), Yersinia pseudotuberculosis (mesenteric adenitis), and Y enterocolitica. Humans are accidental hosts. Yersinia species are gram-negative, oxidase-negative, and non–lactose-fermenting bacilli.

Species are differentiated based on traits, such as urease positivity (Y enterocolitica is urease negative), motility (Y enterocolitica is motile at 22 o C), and sugar fermentation reactions. Biotyping and serotyping can be performed. Of the 34 serotypes of O antigen of Y enterocolitica, types 0:3 (sporadic cases in the United States);[1] 0:5,27; 0:8 (food-borne outbreaks in the United States); and 0:9 are the most common and represent the most virulent worldwide causes of human yersiniosis. Virulence factors can be chromosomal or plasmid-encoded.

Y enterocolitica grows most efficiently in environments with a pH of 5-9, hence the increased incidence of the disease in patients who take antacids and histamine 2 blockers.[2] The organism requires iron to survive, and Yersinia sepsis has been reported in clinical states of iron overload[3] , such as hemochromatosis[4] , and in children following accidental iron overdose. Y enterocolitica grows on basic enteric media, producing subtle pinpoint colonies after 24 hours of incubation. Optimally, if Y enterocolitica is suspected, cefsulodin-irgasan-novobiocin (CIN) agar should be used.

After ingestion of the organism, the terminal ileum is the site of mucosal adherence and penetration, followed by reproduction of the organism in Peyers patches. Nonspecific ileocolitis is often noted, with an inflammatory infiltrate in the lamina propria. The bacteria may then spread to the mesenteric lymph nodes; this spread may lead to bacteremia[5] or to the development of abscesses and pain in the right lower quadrant that mimic the pain of appendicitis.[6]

Although Y enterocolitica does produce a heat-stable enterotoxin similar to that of Escherichia coli, the enterotoxin does not contribute to the pathogenicity of the organism. Plasmid-encoded proteins of the outer membrane represent a major determinant in the pathogenicity of Y enterocolitica by contributing to adherence and invasion of the organism; antibodies directed against these proteins are present in patients convalescing from disease.

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Epidemiology

Frequency

United States

Y enterocolitica infection is more common in cooler climates and its prevalence peaks from November to January.[5]Y enterocolitica has been isolated in 1.4-2.8% of stools of children with diarrhea. Disease occurs in 1 person per 100,000 population per year in the United States.

International

Most frequently recognized in Northern Europe.

Mortality/Morbidity

The incubation period is 1-14 days and the duration of stool excretion is 14-97 days. Symptoms typically persist for 5-14 days.

Race

Higher incidence is observed among black infants.[7]

Sex

The male-to-female ratio is 1.7:1.

Age

Most infections occur in children younger than 7 years, with more severe infections in children less than 1 year of age.[8]

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Contributor Information and Disclosures
Author

Swetha G Pinninti, MD  Resident Physician, Department of Pediatrics, St Peter's University Hospital

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

Disclosure: Nothing to disclose.

Coauthor(s)

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Sanofi Pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

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.

Specialty Editor Board

Leonard R Krilov, MD  Chief of Pediatric Infectious Diseases, 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

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

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.

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Sanofi Pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

Chief Editor

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.

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Gram stain of Yersinia enterocolitica.
 
 
 
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