eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Campylobacter Infections

Author: Jocelyn Y Ang, MD, Assistant Professor, Department of Pediatrics, Division of Infectious Diseases, Children's Hospital of Michigan and Wayne State University
Coauthor(s): Sharon Nachman, MD, Chief of Pediatric Infectious Diseases, Associate Professor, Department of Pediatrics, Division of Infectious Diseases, State University of New York at Stony Brook
Contributor Information and Disclosures

Updated: Sep 7, 2007

Introduction

Background

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. 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.

Pathophysiology

Factors responsible for the diseases caused by C jejuni are not well known. Based on clinical illness, researchers have postulated 3 mechanisms, as follows:

  • 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.

Frequency

United States

In the United States, 2 million symptomatic enteric Campylobacter infections are estimated per year (1% of the US population per year). Incidence in the rural population is 5-6 times higher because of increased consumption of raw milk. In 2005, the overall incidence rate of laboratory-confirmed Campylobacter infections in the United States was 12.7 cases per 100,000 population.1 However, the incidence rate of symptomatic Campylobacter infections has been estimated to be 760-1100 cases per 100,000 population.2

International

In developing countries, C jejuni is often isolated from stools of healthy individuals and is especially common during the first 5 years of life. Isolation rates in children who are asymptomatic or in children with diarrhea range from 8-45%, with an annual incidence rate as high as 2.1 episodes of Campylobacter -associated diarrhea per child.

In developed countries, the average incidence rate of Campylobacter bacteremia is estimated to be 1.5 per 1000 patients with enteritis.

Mortality/Morbidity

  • 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. The symptomatic Campylobacter infection–associated mortality rate in the United States is estimated to be 24 deaths per 10,000 culture-confirmed cases (200 deaths per year).
  • Infection with C fetus is a concern in immunocompromised patients, pregnant women, and neonates.
  • Previously healthy patients usually recover without complications.

Race

  • Campylobacter infection has no race predilection.

Sex

  • In individuals aged 45 years or younger, the C jejuni isolation rate is higher in males than in females. In individuals older than 45 years, no sexual predilection is reported.
  • In the adult population, the male-to-female C fetus infection ratio is 3:1.
  • No sex predilection is noted in children.

Age

  • 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 15-30 years. In developing countries, symptomatic infection chiefly affects children younger than 5 years and declines with age. 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 65 years and older. In this age group, the incidence rate of Campylobacter bacteremia is 1 case per 170 intestinal infections; in children younger than 14 years, the incidence rate is 1 case per 3000 intestinal infections. Roughly 60-90% of isolates are C jejuni or C coli; 8-15% are C fetus. In children from developing countries, bacteremia appears common, occurring in 45 per 1000 cases of intestinal infection. C jejuni subspecies jejuni accounts for 41% of these infections, C jejuni subspecies doylei accounts for 24%, and C upsaliensis accounts for 5.6%.

Clinical

History

Clinical manifestations of all Campylobacter species infections that cause enteric illness overlap and appear identical. These manifestations include the following:

  • Diarrhea
    • Mild episodes of diarrhea subside within 7 days in 60-70% of cases, last for 2 weeks in 20-30%, and persist longer than 2 weeks in 5-10% of cases. In one third to one half of patients, initial symptoms include periumbilical cramping, intense abdominal pain that mimics appendicitis, malaise, myalgias, headache, and vomiting.
    • Watery secretory diarrhea consists of more than 10 stools per day and is frequently seen in younger children. Dehydration occurs in approximately 10% of these children.
    • Inflammatory diarrhea symptoms are indistinguishable from those caused by Shigella organisms, Escherichia coli, and Salmonella species. They are characterized by malaise, fever, abdominal cramps, tenesmus, bloody stools, and fecal leukocytes on light microscopy. Rarely, in young adults and adolescents, inflammatory diarrhea can be severe and can be confused with Crohn disease and ulcerative colitis. Toxic megacolon with massive bleeding may occasionally occur. In asymptomatic neonates, C jejuni has been isolated from blood-streaked formed stools or hematochezia.
  • Extraintestinal infections
    • Bacteremia with C jejuni is uncommon and is most frequently found in patients with immunodeficiency, patients with chronic illness, and patients at extremes of ages. Bloodstream infections and systemic infections by C fetus are rare. The 3 patterns of bacteremia are as follows:
      • Transient bacteremia in a normal host with acute Campylobacter enteritis: These patients usually completely recover without treatment.
      • Secondary bacteremia or deep focus of infection such as meningitis, pneumonia, endocarditis, and thrombophlebitis in a normal host: Bacteremia usually originates from the intestinal tract and responds to antimicrobial therapy. 
      • Chronic bacteremia with relapses that can persist for several months occurring in an immunocompromised host: In these patients, bacteremia can also arise from an infected indwelling catheter. Many such patients do not have acute enteritis.
    • Localized extraintestinal infections are uncommon manifestations and include cholecystitis, arthritis, urinary tract infection, pancreatitis, osteomyelitis, and meningitis. These manifestations may be the initial presentation of C jejuni infection or may occur simultaneously with bacteremia. They frequently are seen in patients who are immunocompromised or who are at extremes of age. Appropriate treatment is necessary.
  • Because of the affinity of C fetus for the genital tract (and by the tropism for fetal tissue), C fetus and, rarely, C jejuni are associated with perinatal infection. Abortion or stillbirth and premature labor have been described. Infants are often premature and develop signs and symptoms suggestive of sepsis, including fever, cough, respiratory distress, vomiting, diarrhea, cyanosis, convulsions, and jaundice. Infection typically progresses to meningitis, which may be rapidly fatal or may result in serious neurologic sequelae. The source of the organism in these cases has been the mother.

Physical

  • The abdomen is frequently tender upon palpation, especially the right lower quadrant.
  • Rarely, splenomegaly may be present.

Causes

  • Individuals at increased risk for Campylobacter enteritis include the following:
    • Those with occupational exposure to cattle, sheep, and other farm animals
    • Laboratory workers
    • Those in contact with the excreta of infected persons
    • Homosexual men
  • The following underlying conditions increase risk for Campylobacter bacteremia, suggesting the importance of both humoral and cell-mediated immunity:
    • Hypogammaglobulinemia
    • Human immunodeficiency virus (HIV) infection
    • Kwashiorkor
    • Pregnancy
    • Malignancy
    • Extremes of age
    • Alcoholism
    • Diabetes mellitus
    • Postsplenectomy status
    • Human leukocyte antigen B27 (HLA-B27) - Increases risk for immunoreactive complications, such as reactive arthritis or Reiter syndrome

More on Campylobacter Infections

Overview: Campylobacter Infections
Differential Diagnoses & Workup: Campylobacter Infections
Treatment & Medication: Campylobacter Infections
Follow-up: Campylobacter Infections
References

References

  1. CDC. Preliminary FoodNet data on the incidence of infection with pathogens transmitted commonly through food--10 states, 2006. MMWR Morb Mortal Wkly Rep. Apr 13 2007;56(14):336-9. [Medline].

  2. Long SS, ed. Principles and Practice of Pediatric Infectious Diseases. 2nd ed. Churchill Livingstone; 2003:890-4.

  3. Allos BM. Campylobacter jejuni infection as a cause of the Guillain-Barre syndrome. Infect Dis Clin North Am. Mar 1998;12(1):173-84. [Medline].

  4. Allos BM. Campylobacter jejuni Infections: update on emerging issues and trends. Clin Infect Dis. Apr 15 2001;32(8):1201-6. [Medline].

  5. Blaser M. Development of Guillain-Barre syndrome following Campylobacter infection. J Infect Dis. 1997;176 Supp 2:S91-200. [Medline].

  6. Blaser MJ. Campylobacter fetus--emerging infection and model system for bacterial pathogenesis at mucosal surfaces. Clin Infect Dis. Aug 1998;27(2):256-8. [Medline].

  7. Blaser MJ. Epidemiologic and clinical features of Campylobacter jejuni infections. J Infect Dis. Dec 1997;176 Suppl 2:S103-5. [Medline].

  8. Feigin RD, Cherry J, Demmler G, Kaplan S, eds. Textbook of Pediatric Infectious Diseases. Vol 1. 5th ed. WB Saunders; 2003:1612-1628.

  9. Gurtler M, Alter T, Kasimir S, Fehlhaber K. The importance of Campylobacter coli in human campylobacteriosis: prevalenceand genetic characterization. Epidemiol Infect. Dec 2005;133(6):1081-7. [Medline].

  10. Hahn AF. Guillain-Barre syndrome. Lancet. Aug 22 1998;352(9128):635-41. [Medline].

  11. Hein I, Schneck C, Knogler M, et al. Campylobacter jejuni isolated from poultry and humans in Styria, Austria: epidemiology and ciprofloxacin resistance. Epidemiol Infect. Jun 2003;130(3):377-86. [Medline].

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

  13. Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Diseases. 6th ed. Churchill Livingstone; 2005:2455-8.

  14. Pickering LK, et al. Report of the Committee on Infectious Diseases. In: Red Book. 27th ed. American Academy of Pediatrics; 2006:240-2.

  15. Remington JS, Klein JO, eds. Infectious Diseases of the Fetus and Newborn Infant. 5th ed. WB Saunders; 2001:1275-81.

  16. Ruiz J, Marco F, Oliveira I, Vila J, Gascon J. Trends in antimicrobial resistance in Campylobacter spp. causing traveler's diarrhea. APMIS. Mar 2007;115(3):218-24. [Medline].

  17. Serichantalergs O, Dalsgaard A, Bodhidatta L, et al. Emerging fluoroquinolone and macrolide resistance of Campylobacter jejuni and Campylobacter coli isolates and their serotypes in Thai children from 1991 to 2000. Epidemiol Infect. Feb 19 2007;1-8. [Medline].

Further Reading

Keywords

Campylobacter infections, campylobacteriosis, Campylobacteraceae, Campylobacter, Campylobacter jejuni, C jejuni, Campylobacter fetus, C fetus, Arcobacter, C jejuni subspecies doylei, Campylobacter coli, Campylobacter upsaliensis, Campylobacter Lari, C fetus subspecies fetus, Campylobacter hyointestinalis, Campylobacter concisus, Campylobacter sputorum, Campylobacter curvus, Campylobacter rectus, Campylobacter pylori, Helicobacter pylori, meningitis, cholecystitis , urinary tract infection, mesenteric adenitis, bacteremia, gravid uterus, enteritis, arthritis, pancreatitis, osteomyelitis

Contributor Information and Disclosures

Author

Jocelyn Y Ang, MD, Assistant Professor, Department of Pediatrics, Division of Infectious Diseases, Children's Hospital of Michigan and Wayne State University
Jocelyn Y Ang, 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.

Coauthor(s)

Sharon Nachman, MD, Chief of Pediatric Infectious Diseases, Associate Professor, Department of Pediatrics, Division of Infectious Diseases, State University of New York at Stony Brook
Sharon Nachman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

Medical Editor

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 Federation for Medical Research, American Medical Association, 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, and Southern Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Nothing to disclose.

Managing Editor

Mark R Schleiss, MD, American Legion Chair of Pediatrics, Professor of Pediatrics, Division Director, Division of Infectious Diseases and Immunology, Department of Pediatrics, University of Minnesota School of Medicine
Mark R Schleiss, MD is a member of the following medical societies: American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Robert W Tolan Jr, MD, Chief 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 Consulting; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching; sanofi pasteur Grant/research funds Unrestricted research grant; sanofi pasteur  Consulting; sanofi pasteur Honoraria Speaking and teaching; Tap Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD, Professor and Vice Chairman, Department of Pediatrics, Head, Division of Infectious Diseases, Louisiana State University Health Sciences Center
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: None None None

 
 
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