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Pediatric Campylobacter Infections

  • Author: Jocelyn Y Ang, MD, FAAP, FIDSA; Chief Editor: Russell W Steele, MD  more...
Updated: Sep 30, 2015


The family Campylobacteraceae includes 2 genera: Campylobacter and Arcobacter. The genus Campylobacter includes 18 species and subspecies; 11 of these are considered pathogenic to humans and cause enteric and extraintestinal illnesses. The major pathogens are Campylobacter jejuni and Campylobacter fetus.

Scanning electron microscope image of Campylobacte Scanning electron microscope image of Campylobacter jejuni, illustrating its corkscrew appearance and bipolar flagella. Source: Virginia-Maryland Regional College of Veterinary Medicine, Blacksburg, Virginia.

The following Campylobacter species and subspecies are pathogenic to humans:

  • Enteric
    • C jejuni subspecies jejuni
    • C jejuni subspecies doylei
    • Campylobacter coli
    • Campylobacter upsaliensis
    • Campylobacter lari
    • C fetus subspecies fetus
    • Campylobacter hyointestinalis
    • Campylobacter concisus
  • Extraintestinal
    • C jejuni subspecies jejuni
    • C upsaliensis
    • C lari
    • C fetus subspecies fetus
    • C concisus
    • Campylobacter sputorum
    • Campylobacter curvus
    • Campylobacter rectus

Campylobacter pylori has been reclassified as Helicobacter pylori and is not addressed in this article (see Helicobacter Pylori Infection).

Campylobacter pathogens are small, curved, motile, microaerophilic, gram-negative rods. They vary in width from 0.2-0.9 mm and vary in length from 0.5-5.0 mm. They exhibit rapid, darting motility in corkscrew fashion using a single flagellum or 2 flagella (monotrichous, amphitrichous). They also possess a lipopolysaccharide endotoxin.

Campylobacteriosis infects humans and animals. The animal reservoir is the gastrointestinal tract of dogs, cats, and other pets that can carry the organism. Transmission of C jejuni to humans occurs by ingestion of contaminated food or water, including unpasteurized milk and undercooked poultry, or by direct contact with fecal material from infected animals or persons. The 2 types of illnesses associated with Campylobacter infections in humans are intestinal infection and extraintestinal infection. The prototype for intestinal infection is C jejuni, and the prototype for extraintestinal infection is C fetus.



Factors responsible for the diseases caused by C jejuni are not well known. Based on clinical illness, researchers have postulated the following mechanisms:[1]

  • Adherence and production of heat-labile enterotoxins, inducing secretory diarrhea
  • Invasion and proliferation within the intestinal epithelium, leading to cell damage and inflammatory response
  • Translocation of the organism into the intestinal mucosa and proliferation in the lamina propria and mesenteric lymph nodes, leading to extraintestinal infections such as meningitis, cholecystitis, urinary tract infection, and mesenteric adenitis

Information on the pathogenesis of Campylobacter infections other than C jejuni is scarce. Bacteremia is more common with C fetus infection. A surface protein in C fetus inhibits the C3b binding responsible for both the serum and phagocytic resistance of the organism, making the organism resistant to the bactericidal effects of human serum. After oral ingestion, C fetus may colonize the intestinal tract, resulting in portal bacteremia. In immunocompetent hosts, the organism is phagocytosed by the reticuloendothelial cells in the liver, preventing further spread. However, in patients that have predisposing factors that might serve as a local site of infection such as a gravid uterus, bacteremia can lead to severe complications. Infants may be affected hematogenously or by ascending infection during amnionitis and premature rupture of membranes.




United States

In the United States, 2 million symptomatic enteric Campylobacter infections are estimated per year (1% of the US population per year).[2] Incidence in the rural population is 5-6 times higher because of increased consumption of raw milk. According to the Foodborne Diseases Active Surveillance Network (FoodNet) of the Centers for Diseases Control and Prevention (CDC), which collects data on the incidence of infection with foodborne pathogens. In 2010, 6,365 cases of laboratory-confirmed Campylobacter infections were reported in the United States with an overall incidence rate of 13.6 cases per 100,000 population; this was not a significant change when compared with the previous 2 years.[3] Among all age groups, the highest incidence occurred among children younger than 5 years; hospitalization occurred in 927 of cases (4.6%), and 8 individuals died. In 2011, the incidence of Campylobacter infections increased by 11% compared with 2006-2008.[4]


In developing and developed countries, continuous increases in the number of C jejuni infections has been seen, with incidence rates as high as 73 cases per 100,000 population reported.[5]

In England and Wales, an increase of laboratory confirmed Campylobacter cases was noted, from 44,544 per year in 2004 to 64,582 per year in 2011 (provisional data 2011). Between 2004 and 2011, a 36% increase of cases occurred among children younter than 10 years, a 25% increase occurred among persons aged 10-45 years, and an 81% increase occurred among those aged 50 years and older.[6]

Overall, Campylobacter gastroenteritis is still common during the first 5 years of life.[7, 8, 9] Isolation rates in children with acute diarrhea range from 10-46%.[7, 9, 10]


The vast majority of patients fully recover from C jejuni infection within 5 days (range, 2-10 d), either spontaneously or after appropriate antimicrobial therapy. Infection with C fetus is a concern in immunocompromised patients, pregnant women, and neonates. Previously healthy patients usually recover without complications.


Campylobacter infection has no race predilection.


In England and Wales, incidence was higher in males from birth until age 17 years and in females aged 20-36 years.[11]


Individuals of any age can be infected with C jejuni enteritis. The rate of infection differs between developed and developing countries. In developed countries, the peak attack rates are in infants younger than 1 year; a second, broader peak attack rate occurs in persons aged 20-29 years.[12] In developing countries, symptomatic infection chiefly affects children younger than 5 years and declines with age.[13, 14] This is likely due to the development of protective immunity secondary to a high level of exposure to the organism early in life.

In contrast to the age-specific distribution of Campylobacter enteritis, the highest rate of bacteremia occurs in patients aged 69 years and older.[15] Roughly 30% of isolates are C jejuni, 9% are C coli, and 53% are C fetus.

Contributor Information and Disclosures

Jocelyn Y Ang, MD, FAAP, FIDSA Associate Professor, Department of Pediatrics, Wayne State University School of Medicine; Consulting Staff, Division of Infectious Diseases, Children's Hospital of Michigan

Jocelyn Y Ang, MD, FAAP, FIDSA is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.


Sharon Nachman, MD Professor of Pediatrics, Associate Dean for Research, Stony Brook University School of Medicine

Sharon Nachman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

Mark R Schleiss, MD Minnesota American Legion and Auxiliary Heart Research Foundation Chair of Pediatrics, Professor of Pediatrics, Division Director, Division of Infectious Diseases and Immunology, Department of Pediatrics, University of Minnesota Medical School

Mark R Schleiss, MD is a member of the following medical societies: American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

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, Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Itzhak Brook, MD, MSc Professor, Department of Pediatrics, Georgetown University School of Medicine

Itzhak Brook, MD, MSc is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Immunocompromised Host Society, International Society for Infectious Diseases, Medical Society of the District of Columbia, New York Academy of Sciences, Pediatric Infectious Diseases Society, Society for Experimental Biology and Medicine, Society for Pediatric Research, Southern Medical Association, Society for Ear, Nose and Throat Advances in Children, American Federation for Clinical Research, Surgical Infection Society, Armed Forces Infectious Diseases Society

Disclosure: Nothing to disclose.

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Scanning electron microscope image of Campylobacter jejuni, illustrating its corkscrew appearance and bipolar flagella. Source: Virginia-Maryland Regional College of Veterinary Medicine, Blacksburg, Virginia.
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