Infection is caused by gram-negative, spiral-shaped microaerophilic bacteria of the family Campylobacteriaceae. Most infections are caused by Campylobacter jejuni; other species, including C. coli, also cause infection. C. jejuni and C. coli are carried normally in the intestinal tracts of many domestic and wild animals.
The major modes of transmission include eating contaminated foods (especially undercooked chicken and foods contaminated by raw chicken), drinking contaminated water or milk (unpasteurized milk, most commonly), and having contact with animals, particularly farm animals such as cows and chickens, as well as domestic cats and dogs. Campylobacter can also be transmitted from person to person by the fecal-oral route.
Campylobacter is a leading cause of bacterial diarrheal disease worldwide; in the United States, it is estimated to cause 1.3 million human illnesses every year. Campylobacter is the most common laboratory-confirmed enteric pathogen reported in travelers returning to the United States from every region of the world. The risk of infection is highest in travelers to Africa and South America, especially in areas with poor restaurant hygiene and inadequate sanitation. The infectious dose is thought to be small; <500 organisms can cause disease.
Incubation period is typically 2–4 days. Campylobacteriosis is characterized by diarrhea (frequently bloody), abdominal pain, fever, and occasionally nausea and vomiting. More severe illness can occur, including dehydration, bloodstream infection, and symptoms mimicking acute appendicitis or ulcerative colitis. Campylobacter is the most frequently observed antecedent infection in cases of Guillain-Barré syndrome (GBS). Symptoms of GBS usually begin 1–3 weeks after the onset of Campylobacter enteritis.
Diagnosis is traditionally based on isolation of the organism from stools by using selective media incubated under reduced oxygen tension at 42°C (107.6°F) for 72 hours. Visualization of motile and curved, spiral, or S-shaped rods by stool phase-contrast or dark-field microscopy can provide rapid presumptive evidence for Campylobacter enteritis. Rapid culture-independent tests, including both antigen tests and nucleic acid–based tests, are becoming more widely available and commonly used. The sensitivity and specificity of stool antigen tests are variable, and in settings of low prevalence, the positive predictive value is likely to be low. Therefore, laboratories should confirm positive results of stool antigen tests by culture. Nucleic acid–based tests have recently been approved and appear to have higher sensitivity and specificity than the antigen tests.
The disease is generally self-limited, lasting a week or less. Antibiotic therapy decreases the duration of symptoms if administered early in the course of disease. Because campylobacteriosis generally cannot be distinguished from other causes of travelers’ diarrhea without a diagnostic test, the use of empiric antibiotics in travelers should follow the guidelines for travelers’ diarrhea.
Rates of antibiotic resistance, especially fluoroquinolone resistance, have risen sharply in the past 20 years, and high rates of resistance are now seen in many regions of the world. Travel abroad is a risk factor for infection with resistant Campylobacter. Clinicians should suspect resistant infection in returning travelers with campylobacteriosis in whom empiric fluoroquinolone treatment has failed. When fluoroquinolone resistance is proven or suspected, azithromycin is usually the next choice of treatment, although resistance to macrolides has also been reported.
No vaccine is available; food and water precautions are recommended (see Chapter 2, Food & Water Precautions). Antibiotic prophylaxis is not recommended.
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