Current Diagnosis

• Campylobacter jejuni and Campylobacter coli are the leading causes of childhood and traveler’s diarrhea worldwide.

• Raw or undercooked poultry (or cross-contamination with poultry juices) is the best-known source of infection.

• Infection is characterized by abrupt onset of crampy abdominal pain, nausea, and profuse diarrhea or dysentery.

• A prodrome of high fever and myalgias precedes diarrheal illness in one third of cases.

• Campylobacter gastroenteritis can mimic acute appendicitis and inflammatory bowel disease.

• Late complications of Campylobacter infection include reactive arthritis and Guillain-Barré syndrome 1 to 2 weeks after diarrhea.

Current Therapy

• Antibiotics are not essential for most healthy patients because the illness is self-limited.

• Azithromycin (Zithromax)1  500 mg daily × 3 days (pediatric dosage, 10 mg/kg/day) is effective if given early in the course (less than 5% resistance).

• Quinolone antibiotics have been effective, but resistance is developing, particularly in South and Southeast Asia owing to the use of quinolones in poultry feed.

• Prevention entails reducing Campylobacter colonization of poultry and using proper food-handling techniques. Vaccination may be possible in the future.

1 Not FDA approved for this indication.


Campylobacter enteritis is one of the most common forms of bacterial diarrhea in the world and the most common food-related illness in North America. Most cases (95%) are caused by Campylobacter jejuni, a commensal gram-negative bacteria found in the gut of animals, particularly poultry. The related Campylobacter coli causes a clinically identical but much less common (5%) infection. Children in developing countries are usually infected before age 2 years.

Foodborne outbreaks affect adults in developed counties as well as travelers to developing nations. Campylobacter is a common cause of traveler’s diarrhea, and 13% of U.S. Campylobacter infections are acquired abroad. Most infections are due to cross-contamination of food with raw poultry (unwashed cutting boards) or from drinking unpasteurized milk or contaminated water. Infections increase in spring and peak during the summer months. The typical incubation period is 3 to 4 days (range, 1–8 days), with the illness lasting up to a week. After recovery, the bacteria are excreted in the feces for several weeks and may be transmitted by improper hand washing, although person-to-person transmission is unusual.

Risk Factors

Anyone exposed to improperly prepared food, unpasteurized milk, or unchlorinated water is at risk. Improperly cooked poultry or food contaminated by raw poultry is the most common source. Contact with infected pets is a common cause of childhood exposure. Elderly, immunocompromised, or very young patients are at additional risk for prolonged symptoms, invasive disease, and hospitalization.

Proton-pump inhibitors, by reducing protective stomach acid, appear to increase the risk of campylobacteriosis and other bacterial enteritides.


Campylobacter infection starts in the small intestine (jejunum, ileum) and spreads to the colon. Symptoms can begin with enteritis (profuse watery stools) or with frank colitis (bloody stools). Colitis thus can mimic inflammatory bowel disease or appendicitis. Inflammatory bowel disease may be excluded by colon biopsies, which demonstrate acute but not chronic inflammatory change.


Proper food-handling techniques are the best means of prevention. Poultry products should be cooked until an internal temperature of 165 °F is reached and all juices run clear. Hands must be washed with soap after contact with raw poultry or animal feces and after using the rest room. Cross-contamination should be avoided by careful disinfection of countertops and utensils after preparing meats or, better yet, using entirely separate surfaces. Only one drop of poultry juice (< 500 organisms) is sufficient to cause disease. Although not currently feasible, Campylobacter vaccination has been proposed for prevention.

Clinical Manifestations

Campylobacter enteritis typically manifests as sudden onset of cramping, nausea, vomiting, and diarrhea, often indistinguishable from other bacterial diarrheas. Most cases are self-limited, with recovery in 3 to 4 days. About a third of patients experience a febrile prodrome with myalgias occurring for about a day before onset of diarrheal illness. Dysenteric (bloody) stools are common (15%) and imply more-invasive disease. Like Yersinia, Campylobacter infection can mimic acute appendicitis (ileocecitis), especially if this occurs in the absence of significant diarrhea. Computed tomography or ultrasound in bacterial pseudoappendicitis usually documents mesenteric adenitis, and surgery can be avoided. In young children, seizures can occur before the onset of diarrhea and fever, and dysenteric illness (50%) is more common.


Most cases are diagnosed by stool culture in the setting of acute diarrhea and crampy abdominal pain. On microscopic examination, C. jejuni is a gram-negative, spiral-shaped rod with a single polar flagellum at one or both ends. It can be isolated in culture media containing cephalothin, to which it is usually resistant. Darkfield microscopic stool examination is occasionally attempted for early diagnosis, but this is not very sensitive. Polymerase chain reaction analysis of stool samples is a very promising diagnostic approach, although it is not yet available in many laboratories. Later diagnosis, subsequent to resolution of diarrhea, requires serologic testing.

Differential Diagnosis

Campylobacter infections are clinically indistinguishable from other bacterial enteritides such as salmonellosis and shigellosis. All of these produce fever, cramps, diarrhea, and dysentery. However, Campylobacter colitis is more likely to mimic inflammatory bowel disease and appendicitis and to later cause Guillain-Barré syndrome.


Most cases of Campylobacter infection are mild and self-limited, and antibiotics are not required. If antibiotics are to be used, they are most effective if given early to high-risk patients, because delayed treatment (e.g., after positive stool culture results) is less likely to affect outcome. First-line choices include macrolides, such as azithromycin (< 5% resistance), or fluoroquinolones, such as ciprofloxacin (Cipro). Azithromycin (Zithromax)1 is preferred for traveler’s diarrhea acquired in South and Southeast Asia, where quinolone-resistant Campylobacter is common. Azithromycin has supplanted erythromycin (Ery-Tab)1 because it is better tolerated and has fewer GI side effects. Rarely, intravenous aminoglycosides or carbapenems are necessary in very ill patients unable to take oral medication.

Unfortunately, quinolone resistance is not limited to Asia.

Resistance has also increased in the United States. The widespread practice of using antibiotics, especially fluoroquinolones (enrofloxacin [Baytril]),2 as additives to chicken feed has resulted in increasing quinolone resistance in Campylobacter strains found in poultry, the major source of infection. The Foodborne Diseases Active Surveillance Network (FoodNet) of the Centers for Disease Control and Prevention (CDC) found that 40% of U.S. poultry products were contaminated with Campylobacter, and 10% of these strains were ciprofloxacin resistant. Although fluoroquinolones were removed from U.S. animal feed in 2005, they continue to be used overseas. A newer strategy involves supplementing poultry feed with bacteriocins, nontoxic antimicrobial peptides, to reduce Campylobacter colonization.

Irradiation of poultry meat might also be effective.

Empiric self-treatment of traveler’s diarrhea is intended to shorten the duration of symptoms and involves immediate ciprofloxacin (Cipro) or azithromycin (Zithromax)1 at the onset of diarrheal illness. One or two doses of antibiotics are usually sufficient to abort symptoms, and prolonged treatment is usually unnecessary.

Loperamide (Imodium) might help control diarrhea in adults, but it should be avoided in dysenteric illness and in young children.


Campylobacter complications can occur either acutely or following the illness. Acute complications include cholecystitis, pseudoappendicitis, peritonitis, sepsis, and chest pain (pericarditis) (Box 1). Rashes, such as vasculitis or erythema nodosum, can occur. Rarely, focal extraintestinal infections such as septic arthritis or osteitis develop. Childhood complications include meningitis and encephalopathy, and dysenteric illness in infants occasionally mimics intussusception.

Campylobacter can provoke postinfectious irritable bowel syndrome and is suspected of contributing to inflammatory bowel disease by damaging the intestinal epithelium, leading to chronic inflammation.

Box 1
Acute and Chronic Campylobacter


Acute Complications

Acute colitis, dysentery


Pseudoappendicitis (mesenteric adenitis)


Pericarditis (chest pain)

Postinfectious irritable bowel syndrome

Chronic Complications

Inflammatory bowel disease (possible contributor)

Guillain-Barré syndrome (1:1000 cases)

Reactive arthritis

Late-term complications include Guillain-Barré syndrome and reactive arthritis. About one in a thousand Campylobacter infections is complicated by Guillain-Barré syndrome, which occurs several weeks after infection and carries a worse prognosis when associated with Campylobacter. As much as 30% to 40% of all Guillain-Barré syndrome has been attributed to Campylobacter infection, and even subclinical cases have been associated by later serologic testing.

Reactive arthritis following Campylobacter infection is common and also appears unrelated to the severity of the preceding diarrhea.

Swelling and arthralgia in the hands, wrists, knees, or ankles develops 1 to 2 weeks following diarrhea and can persist for weeks to months.

Nonsteroidal antiinflammatory drugs are usually helpful, and complete recovery is the rule.


1.     Centers for Disease Control and Prevention. Campylobacter: General information. Available at 2014 [accessed July 9, 2015].

2.    Gupta A., Nelson J.M., Barrett T.J., et al. Antimicrobial resistance among Campylobacter strains, United States, 1997–2001. Emerg Infect Dis. 2004;10:1102–1109.

3.     Kalischuk L., Buret A. A role for Campylobacter jejuni–induced enteritis in inflammatory bowel disease? Am J Physiol Gastrointest Liver Physiol. 2010;298:G1–9.

4.    Nachamkin I., Allos B.M., Ho T. Campylobacter species and Guillain-Barré syndrome. Clin Microbiol Rev. 1998;11:555–567.

5.     Neal K.R., Scott H.M., Slack R.C., Logan R.F. Omeprazole as a risk factor for Campylobacter gastroenteritis: Case control study. BMJ. 1996;312:414–415.

6.      Neal K.R., Wright J.M. Reactive arthritis–like symptoms following gastroenteritis—an increased risk with severe Campylobacter infection. Int J Med Microbiol. 2001;291:110.

7.    Nelson J.M., Chiller T.M., Powers J.H., Angulo F.J. Fluoroquinolone-resistant Campylobacter species and the withdrawal of fluoroquinolones from use in poultry: A public health success story. Clin Infect Dis. 2007;44:977–980.

8.    Nelson J.M., Smith K.E., Vugia D.J., et al. Prolonged diarrhea due to ciprofloxacin-resistant Campylobacter infection. J Infect Dis. 2004;190:1150–1157.

9.       Skirrow M.B., Blaser M.J. Campylobacter jejuni. In: Blaser M.J., Smith P.D., Radin J.I., et al., eds. Infections of the Gastrointestinal Tract. ed 2nd Philadelphia: Lippincott Willians & Wilkins; 2002 p. 719–739.

10.       Svetich E., Stern N. Bacteriocins to control Campylobacter spp. in poultry—a review. Poult Sci. 2010;89:1763–1768.

11.    Ternhag A., Asikainen T., Giesecke J., Ekdahl K. A meta-analysis on the effects of antibiotic treatment on duration of symptoms caused by infection with Campylobacter species. Clin Infect Dis. 2007;44:696–700.

12.       Tribble D.R., Sanders J.W., Pang L.W., et al. Traveler’s diarrhea in Thailand: Randomized, double-blind trial comparing single-dose and 3-day azithromycin-based regimens with a 3- day levofloxacin regimen. Clin Infect Dis. 2007;44:338–346.

2  Not available in the United  States.

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