Basics
Description
- Campylobacter species are motile, curved, gram-negative bacilli that are commensal flora of birds, pigs, and cattle and commonly cause bacterial gastroenteritis in humans.
Epidemiology
- Campylobacter infections are among the most common causes of enteritis worldwide, with the highest attack rates in children <4 years.
- Asymptomatic infection occurs in 30-100% of chickens, turkeys, and water fowl. Other reservoirs of infection include swine, cattle, sheep, horses, rodents, and household pets (especially young pets).
- Contaminated water and unpasteurized milk are other sources of infection.
- Infections typically occur sporadically, without outbreaks.
Incidence
- Estimated rates of Campylobacter infection vary widely worldwide. In the United States, the estimated annual incidence in 2012 was 14.3/100,000 overall, 14% higher than in 2006-2008 (95% CI, 7-21%).
- The highest U.S. incidence is for those <5 years at 24.08/100,000 population.
- Among speciated U.S. infections, 90% were C. jejuni and 8% were C. coli. Of all U.S. infections, 15% resulted in hospitalization and 0.1% in death.
- The incidence is seasonal and generally peaks in summer worldwide.
Prevalence
- Although surveillance data are limited, the highest prevalence of Campylobacter infections occur in resource-poor settings.
- Campylobacter is the most common cause of travelers' diarrhea in Southeast Asia, accounting for a third of all infections.
Risk Factors
- Approximately 40% of Campylobacter enteritis is estimated to be attributable to undercooked chicken consumption, which had an odds ratio (OR) of 3.4 (95% CI, 2.2-4.5) for infection.
- Other risk factors for Campylobacter enteritis include international travel (OR 4.9, 95% CI, 2.9-8.2), direct contact with farm animals (OR 2.6, 95% CI, 2.0-3.4), chronic disease, poor food preparation hygiene, consumption of chicken prepared outside the home, and use of acid-suppressive medications.
- Children are at higher risk relative to adults.
- Frequent exposure to Campylobacter (e.g., among food handlers and abattoir workers) may protect against disease.
- Person-to-person transmission of C. jejuni has been reported when index cases were young children incontinent of feces or as vertical transmission from mother to neonate.
- Asymptomatic hospital personnel or food handlers have not been implicated as sources.
General Prevention
- Hand washing after contact with animals or animal products, cleaning cooking utensils and cutting boards after contact with raw poultry, proper cooling and storage of foods, pasteurization of milk, and chlorination of water supplies decrease the risk for infection.
- Diapered infants with symptomatic infection should be excluded from child care until resolution of diarrhea.
- No licensed vaccines currently exist, but C. jejuni strains with decreased risk of secondary Guillain-Barr © syndrome (GBS) are being developed as candidates for capsular polysaccharide conjugate vaccines.
Pathophysiology
- Transmission of disease is by the fecal-oral route from contaminated food and water or by direct contact with fecal material from animals or persons infected with the organism.
- As few as 500 organisms may be required to produce infection.
- Campylobacter spp. possess 1 or 2 flagella that provide the organism's motility and facilitate intestinal colonization.
- C. jejuni adheres to epithelial cells and mucus, secretes cytotoxins (which play a role in the development of watery diarrhea), can invade intestinal epithelial cells using a microtubule entry system, and induces an inflammatory ileocolitis.
- Campylobacter can cause a range of clinical manifestations, including enteritis and rare localized extraintestinal infections.
- Bacteremia, although uncommon, can occur, especially in the neonate and immunocompromised host; C. fetus is the species most likely to be isolated. C. fetus can also cause neonatal meningitis.
- C. upsaliensis, C. lari, and C. hyointestinalis have been identified in immunocompromised individuals and are usually associated with a self-limiting enteritis but can occasionally cause systemic illness.
Etiology
- Campylobacter is a motile, curved, microaerophilic, non-lactose-fermenting, oxidase-positive, gram-negative rod that requires oxygen and carbon dioxide for optimal growth.
- Three main Campylobacter species involved in human infections include C. jejuni, C. coli (which cause enteritis), and C. fetus (implicated in systemic illness in neonates and compromised hosts). Rarer human pathogens include C. concisus, C. curvus, C. hyointestinalis, C. lari, C. rectus, C. sputorum, and C. upsaliensis.
Commonly Associated Conditions
- Campylobacteriosis occurs in both healthy and immunocompromised individuals.
Diagnosis
History
- Enteritis is characterized by fever, abdominal pain, and bloody diarrhea.
- Symptoms can last for 24 hours and be indistinguishable from viral gastroenteritis or appendicitis, or can be relapsing, thus mimicking inflammatory bowel disease.
- In some patients, illness can be severe, resembling dysentery.
- Incubation period is usually 2-5 days and is usually self-limited by 5-7 days.
Physical Exam
- Abdominal pain, diarrhea, malaise, and fever are common signs and symptoms of infection.
- Stools can contain occult or visible blood.
- Inflammatory ileocolitis is the most common manifestation in children.
- If the infection establishes a chronic phase (20% of infected patients), symptoms may mimic inflammatory bowel disease and other immunoreactive complications may occur.
Alert
- Not all bacterial colitis presents with blood or mucus in the stool. Therefore, increased suspicion for bacterial colitis should exist if the diarrhea is prolonged or the patient has appropriate exposures.
Diagnostic Tests & Interpretation
Lab
- Stool culture requires selective media (Skirrow, Butzler, or campy-BAP), microaerophilic conditions, and an incubation temperature of 42 °C to isolate important Campylobacter species.
- C. fetus, C. hyointestinalis, and C. upsaliensis may not be detected on Campylobacter-selective media due to their sensitivity to antimicrobial agents in the media.
Imaging
- Imaging is not often required for diagnosis.
Diagnostic Procedures/Other
- Rapid DNA-based testing to detect and differentiate Campylobacter spp. from other enteropathogens is being developed and has moderate sensitivity compared to the current gold standard of stool culture.
Pathologic Findings
- Examination of fecal specimen for darting motility of C. jejuni by darkfield or phase-contrast microscopy within 2 hours of passage can permit presumptive diagnosis.
Differential Diagnosis
- Campylobacter infection should be considered in all patients with a diarrheal illness, especially those with blood or mucus in their stool, recurrent gastritis, or in immunocompromised hosts.
- Symptoms can overlap with those of appendicitis or inflammatory bowel disease.
- Additional intestinal bacterial pathogens include Aeromonas, Campylobacter, Clostridium difficile, Escherichia coli, Listeria, Plesiomonas, Salmonella, Shigella, Vibrio species, and Yersinia.
- Other viral and parasitic pathogens include amebiasis, adenovirus types 40 and 41, Cryptosporidium, Cyclospora, Cystoisospora, Giardia, norovirus, and rotavirus.
Treatment
Medication
- Most patients have self-limited infection.
- Select patient populations (HIV and other immunocompromised individuals, pregnant women) may benefit from early therapy.
- If treated in the first 3 days of enteritis, erythromycin (for 5 days) or azithromycin (for 3 days) appear effective in eradicating the organism from the stool within 2-3 days and shortening the course of diarrhea.
- Ciprofloxacin, tetracycline, aminoglycosides, and imipenem are alternatives if resistant or bacteremic strains are present, although fluoroquinolone resistance is increasingly common and thought to be related to human and agricultural antibiotic use.
- Macrolide resistance is approximately 5%.
- Treatment duration for enteritis is 3-5 days.
- Appropriate bacteremia treatment should be based on antimicrobial susceptibility testing.
Additional Treatment
General Measures
Immunocompetent children with diarrhea usually improve with rehydration alone.
Issues for Referral
Specific follow-up is unnecessary.
Additional Therapies
Antimotility agents can prolong symptoms and should be avoided.
Inpatient Considerations
Initial Stabilization
Correct initial dehydration.
Admission Criteria
Admit those requiring IV fluids.
IV Fluids
Use normal saline to correct dehydration. IV fluids should contain dextrose if being used for maintenance fluid requirements.
Nursing
Contact precautions are recommended for admitted infected infants and children incontinent of stool and should be maintained until they receive 48 hours of antibiotics.
Discharge Criteria
Discharge rehydrated patients able to maintain hydration orally.
Ongoing Care
Follow-up Recommendations
Patient Monitoring
In untreated patients, the median organism excretion is 2-3 weeks but can be up to 3 months. Asymptomatic carriage is uncommon.
Diet
Avoid undercooked poultry and unpasteurized milk. Resume a normal diet when tolerated.
Patient Education
Symptoms resolve in 1 week for most people.
Prognosis
For patients with enteritis, the prognosis is very good, regardless of whether antibiotic treatment is given.
Complications
- Postinfectious immunologic complications include reactive arthritis, GBS, Miller-Fisher syndrome (a GBS variant predominantly affecting eye movement), reactive arthritis, and erythema nodosum.
- GBS is estimated to affect 1 in 1,000 patients with Campylobacter infection.
- C. jejuni (serotypes O:19 and O:41) is the most frequently identified GBS cause and is responsible for up to 40% of U.S. GBS cases.
- HLA-B27 antigen is associated with reactive arthropathy. The estimated incidence of reactive arthritis after Campylobacter infection ranges from 0 to 7%.
- Children with high fever may develop seizures.
- Some studies have demonstrated associations between Campylobacter infection and both irritable bowel syndrome and inflammatory bowel disease.
- Spontaneous abortion and hemolytic uremic syndrome are described with C. upsaliensis.
Additional Reading
- Centers for Disease Control and Prevention. Incidence and trends of infection with pathogens transmitted commonly through food-foodborne diseases active surveillance network, 10 U.S. sites, 1996-2012. MMWR Morb Mortal Wkly Rep. 2013;62(15):283-287. [View Abstract]
- Domingues AR, Pires SM, Halasa T, et al. Source attribution of human campylobacteriosis using a meta-analysis of case-control studies of sporadic infections. Epidemiol Infect. 2012;140(6):970-981. [View Abstract]
- Kirkpatrick BD, Tribble DR. Update on human Campylobacter jejuni infections. Curr Opin Gastroenterol. 2011;27(1):1-7. [View Abstract]
- Lal A, Hales S, French N, et al. Seasonality in human zoonotic enteric diseases: a systematic review. PLoS One. 2012;7(4):e31883. [View Abstract]
- Liu J, Gratz J, Amour C, et al. A laboratory-developed Taqman Array Card for simultaneous detection of 19 enteropathogens. J Clin Microbiol. 2013;51(2):472-480. [View Abstract]
- Ross AGP, Olds GR, Cripps AW, et al. Enteropathogens and chronic illness in returning travelers. N Engl J Med. 2013;368(19):1817-1825. [View Abstract]
Codes
ICD09
- 008.43 Intestinal infection due to campylobacter
ICD10
- A04.5 Campylobacter enteritis
SNOMED
- 18081009 enteric campylobacteriosis (disorder)
- 447354007 Intestinal infection due to Campylobacter jejuni (disorder)
- 446122002 Intestinal infection due to Campylobacter coli (disorder)
FAQ
- Q: Is treatment necessary for asymptomatic children when Campylobacter is isolated as the pathogen causing the enteritis?
- A: No treatment is needed in this situation.
- Q: Can one develop immunity to Campylobacter infections?
- A: Immunity to C. jejuni is acquired after 1 or more infections. For children living in endemic areas, effective natural immunity is a result of significant repeated early exposure.
- Q: How are C. jejuni infection and GBS related?
- A: Many strains of C. jejuni have surface glycolipids that are similar to gangliosides, which are abundant in the central and peripheral nervous systems. Anti-Campylobacter antibodies bind to the gangliosides through molecular mimicry, causing the demyelinating process characteristic of GBS.