eMedicine Specialties > Infectious Diseases > Bacterial Infections

Campylobacter Infections

Author: Mahmud H Javid, MD, Chief, Section of Infectious Diseases, Shifa Hospital, Islamabad, Pakistan
Coauthor(s): Shadab Hussain Ahmed, MD, FACP, FIDSA, MACGS, AAHIVS, Associate Professor of Clinical Medicine, State University of New York at Stony Brook; Attending Physician, Division of Infectious Diseases, Director of HIV Prevention Services, Nassau University Medical Center
Contributor Information and Disclosures

Updated: Feb 17, 2009

Introduction

Background

Campylobacter infections are among the most common bacterial infections in humans. They produce both diarrheal and systemic illnesses. In industrialized regions, enteric Campylobacter infections produce an inflammatory, sometimes bloody, diarrhea or dysentery syndrome.

Campylobacter jejuni is usually the most common cause of community-acquired inflammatory enteritis. In developing regions, the diarrhea may be watery.

Infections with Campylobacter -like organisms can produce an enterocolitis/proctocolitis syndrome in homosexual males, who are at increased risk for Helicobacter cinaedi and Helicobacter fennelliae infections. C jejuni infections may also produce serious bacteremic conditions in individuals with AIDS. Most reported bacteremias have been due to Campylobacter fetus fetus infection. Campylobacter lari, which is found in healthy seagulls, has also been reported to produce mild recurrent diarrhea in children. Campylobacter upsaliensis may cause diarrhea or bacteremia, while Campylobacter hyointestinalis, which has biochemical characteristics similar to those of C fetus, causes occasional bacteremia in immunocompromised individuals.

Campylobacter organisms may also be an important cause of traveler's diarrhea, especially in Thailand and surrounding areas of Southeast Asia. In a study of American military personnel deployed in Thailand, more than half of those with diarrhea were found to be infected with Campylobacter species.

These organisms are related to Helicobacter pylori, which was previously known as Campylobacter pylori. No reservoir other than the human gastric mucosa has been identified for H pylori.

Pathophysiology

The known routes of Campylobacter transmission include fecal-oral, person-to-person sexual contact, unpasteurized raw milk and poultry ingestion, and waterborne (ie, through contaminated water supplies). Exposure to sick pets, especially puppies, has also been associated with Campylobacter outbreaks.

Transmission of Campylobacter organisms to humans usually occurs via infected animals and their food products. Most human infections result from the consumption of improperly cooked or contaminated foodstuffs. Chickens may account for 50-70% of human Campylobacter infections. Most colonized animals develop a lifelong carrier state.

The infectious dose is 1000-10,000 bacteria. Campylobacter infection has occurred after ingestion of 500 organisms by a volunteer; however, a dose of less than 10,000 organisms is not a common cause of illness. Campylobacter species are sensitive to hydrochloric acid in the stomach, and antacid treatment can reduce the amount of inoculum needed to cause disease.

Symptoms of Campylobacter infection begin after an incubation period of up to a week. The sites of tissue injury include the jejunum, the ileum, and the colon. C jejuni appears to invade and destroy epithelial cells. C jejuni are attracted to mucus and fucose in bile, and the flagella may be important in both chemotaxis and adherence to epithelial cells or mucus. Adherence may also involve lipopolysaccharides or other outer membrane components. Such adherence would promote gut colonization. PEB 1 is a superficial antigen that appears to be a major adhesin and is conserved among C jejuni strains.

Some strains of C jejuni produce a heat-labile, choleralike enterotoxin, which is important in the watery diarrhea observed in infections. Infection with the organism produces diffuse, bloody, edematous, and exudative enteritis. The inflammatory infiltrate consists of neutrophils, mononuclear cells, and eosinophils. Crypt abscesses develop in the epithelial glands, and ulceration of the mucosal epithelium occurs.

Cytotoxin production has been reported in Campylobacter strains from patients with bloody diarrhea. In a small number of cases, the infection is associated with hemolytic-uremic syndrome and thrombotic thrombocytopenic purpura through a poorly understood mechanism. Endothelial cell injury, mediated by endotoxins or immune complexes, is followed by intravascular coagulation and thrombotic microangiopathy in the glomerulus and the gastrointestinal mucosa.

In patients with HIV infection, Campylobacter infections may be more common, may cause prolonged or recurrent diarrhea, and may be more commonly associated with bacteremia and antibiotic resistance.

C fetus is covered with a surface S-layer protein that functions like a capsule and disrupts c3b binding to the organisms, resulting in both serum and phagocytosis resistance.

C jejuni infections also show recurrence in children and adults with immunoglobulin deficiencies. Acute C jejuni infection confers short-term immunity. Patients develop specific immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies in serum; IgA antibodies also develop in intestinal secretions. The severity and persistence of C jejuni infections in individuals with AIDS and hypogammaglobulinemia indicates that both cell-mediated and humoral immunity are important in preventing and terminating infection.

Frequency

United States

An estimated 2 million cases of Campylobacter enteritis occur annually, accounting for 5-7% of cases of gastroenteritis. Campylobacter organisms have a large animal reservoir, with up to 100% of poultry, including chickens, turkeys, and waterfowl having asymptomatic intestinal infections. The major reservoirs of C fetus are cattle and sheep. Nonetheless, the incidence of Campylobacter infections has been declining. Changes in the incidence of culture-confirmed Campylobacter infections have been monitored by the Foodborne Diseases Active Surveillance Network (FoodNet) since 1996. In 2006, the incidence of culture-confirmed Campylobacter infection in the FoodNet sites was 12.7 per 100,000 persons. This represents a 30% decline compared with the 1996-1998 illness baseline; with most of the decline occurring between 1996 and 1999.1

International

C jejuni infections are extremely common worldwide, although exact figures are not available. New Zealand reported the highest national campylobacteriosis rate, which peaked in May 2006 at 400 per 100,000 population.2

Mortality/Morbidity

Campylobacter infections are usually self-limited and rarely cause mortality. Exact figures are unavailable, but occasional deaths have been attributed to Campylobacter infections, typically in elderly or immunocompromised persons and secondary to volume depletion in young, previously healthy individuals.

Race

Campylobacter infections have no clear racial predilection.

Sex

Campylobacter organisms are isolated more frequently from males than females. Homosexual men appear to be at increased risk for infection with atypical Campylobacter species such as Helicobacter cinaedi and Helicobacter fennelliae.

Age

Campylobacter infections can occur in all age groups.

  • Studies show a peak incidence in children younger than 1 year and in persons aged 15-29 years. The age-specific attack rate is highest in young children, but the rate of fecal cultures positive for Campylobacter species is greatest in adults and older children.
  • Asymptomatic Campylobacter infection is uncommon in adults.
  • In developing countries, Campylobacter infection is very common in the first 5 years of life. Asymptomatic infection is also more common. In Bangladesh, up to 39% of all children younger than 2 years have asymptomatic infection.
  • For additional information on pediatric Campylobacter infections, see the article Campylobacter Infections in eMedicine’s Pediatrics: General Medicine volume.

Clinical

History

Campylobacter infections can range from asymptomatic to severe life-threatening colitis with toxic megacolon.

  • All Campylobacter species associated with enteric illnesses cause identical clinical manifestations.
    • Patients may have a history of ingestion of inadequately cooked poultry, unpasteurized milk, or untreated water. The incubation period is 1-7 days and is probably related to the dose of organisms ingested.
    • A brief prodrome of fever, headache, and myalgias lasting up to 24 hours is followed by crampy abdominal pain, fever as high as 40°C, and as many as 10 watery, frequently bloody, bowel movements per day. Fever, which develops in more than 90% of patients, may be low or high grade and can persist for a week.
    • Patients with C jejuni infection who report vomiting, bloody diarrhea, or both tend to have a longer illness and require hospital admission.3
    • Abdominal pain and tenderness may be localized. Pain in the right lower quadrant may mimic acute appendicitis (pseudoappendicitis).
    • Tenesmus occurs in approximately 25% of patients.
    • In some cases, acute abdominal pain is the only symptom, with pain typically in the right lower quadrant. Among the symptoms, abdominal pain is more likely to result from Campylobacter infection than from Salmonella or Shigella infections.
  • In contrast to C jejuni infection, C fetus infection causes diarrheal illness less frequently and is the most commonly identified species in bacteremia. However, C fetus infection that produces diarrheal illness results in clinical manifestations that are similar to those of C jejuni infection. C fetus is an opportunistic agent in debilitated hosts, but healthy hosts may also be affected.
    • Campylobacter bacteremia is common, and C fetus fetus is frequently isolated from the bloodstream, possibly because it resists the bactericidal activity of serum, while the more common C jejuni does not. Persons who develop Campylobacter bacteremia are usually older and are more likely to have cellulitis, endovascular infection, or a device-related infection.4
    • Systemic illness with a predilection for vascular sites is characteristic. Meningitis, vascular infections, and abscesses may be present.
    • C fetus infection may cause intermittent diarrhea or nonspecific abdominal pain.

Physical

  • Patients with Campylobacter infection may appear to be ill.
  • The patient’s abdomen is diffusely tender, frequently in the right or left lower quadrant.
  • Among symptoms, only abdominal pain is more likely to result from Campylobacter infections than from Salmonella and Shigella infections.

Causes

Campylobacter organisms are curved or spiral, motile, non–spore-forming, gram-negative rods. Organisms from young cultures have a vibriolike appearance, but, after 48 hours of incubation, organisms appear coccoid. Campylobacter organisms are motile by means of unipolar or bipolar flagellae. They are both oxidase- and catalase-positive and microaerophilic, requiring reduced oxygen (5-10%) and increased carbon dioxide (3-10%). The organisms grow slowly, with 3-4 days required for primary isolation from stool samples, and even longer from blood.

More on Campylobacter Infections

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

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Further Reading

Keywords

Campylobacter infection, diarrhea, dysentery, enteric infection, enteritis, gastroenteritis, campylobacteriosis, Campylobacter jejuni, C jejuni, Campylobacter fetus, C fetus, Campylobacter lari, C lari, Campylobacter upsaliensis, C upsaliensis, Campylobacter hyointestinalis, C hyointestinalis, Campylobacter pylori, C pylori, Helicobacter pylori, H pylori, Helicobacter cinaedi, H cinaedi, Helicobacter fennelliae, H fennelliae, enterocolitis, proctocolitis, bacteremia, acquired immunodeficiency syndrome, AIDS, human immunodeficiency virus, HIV, traveler's diarrhea, toxic megacolon, pseudoappendicitis, inflammatory bowel disease, IBD, Guillain-Barré syndrome, Campylobacter enteritis

Contributor Information and Disclosures

Author

Mahmud H Javid, MD, Chief, Section of Infectious Diseases, Shifa Hospital, Islamabad, Pakistan
Mahmud H Javid, MD is a member of the following medical societies: Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

Shadab Hussain Ahmed, MD, FACP, FIDSA, MACGS, AAHIVS, Associate Professor of Clinical Medicine, State University of New York at Stony Brook; Attending Physician, Division of Infectious Diseases, Director of HIV Prevention Services, Nassau University Medical Center
Shadab Hussain Ahmed, MD, FACP, FIDSA, MACGS, AAHIVS is a member of the following medical societies: American College of Physicians, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and International AIDS Society
Disclosure: Nothing to disclose.

Medical Editor

Douglas A Drevets, MD, Assistant Professor, Department of Medicine, Section of Infectious Disease, Oklahoma University Health Sciences Center
Douglas A Drevets, MD is a member of the following medical societies: American Association of Immunologists, American Society for Microbiology, Central Society for Clinical Research, and Christian Medical & Dental Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Michael Stuart Bronze, MD, Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center
Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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