Campylobacter Infections



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 (see image below) is usually the most common cause of community-acquired inflammatory enteritis. In developing regions, the diarrhea may be watery.

View Image

Scanning electron microscope image of Campylobacter jejuni, illustrating its corkscrew appearance and bipolar flagella. Source: Virginia-Maryland Regi....

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.[1] Bacteremia can also occur with H fennelliae.[2] 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.


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 can extend to involve the colon and rectum. 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.

Campylobacter species also produce the bacterial toxin cytolethal distending toxin (CDT), which produces a cell block at the G2 stage preceding mitosis. CDT inhibits cellular and humoral immunity via destruction of immune response cells and necrosis of epithelial-type cells and fibroblasts involved in the repair of lesions. This leads to slow healing and results in disease symptoms.[3]

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.

The oral cavity contains numerous Campylobacter species, such as Campylobacter concisus, that have been associated with a subtype of inflammatory bowel disease.[4, 5]



United States

An estimated 0.8 million cases of campylobacteriosis occur annually in the United States.[6]


C jejuni infections are extremely common worldwide, although exact figures are not available, particularly in low- and middle-income countries. In high-income countries, the incidence has been estimated to be 4.4-9.3 per 1000 population.[7] New Zealand reported the highest national campylobacteriosis rate, which peaked in May 2006 at 400 per 100,000 population.[8] After implementation of a national strategy to reduce foodborne Campylobacter infections, the rates subsequently fell in 2006-2008.[9]


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.


Campylobacter infections have no clear racial predilection.


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 H fennelliae.


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. In the United States, the highest incidence of Campylobacter infection in 2010 was in children younger than 5 years and was 24.4 cases per 100,000 population,[10] However, 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 Campylobacter Infections.


Campylobacter infections can range from asymptomatic to, rarely, severe life-threatening colitis with toxic megacolon.[11]

All Campylobacter species associated with enteric illnesses cause identical clinical manifestations.


The symptoms and severity of the gastroenteritis produced can vary.

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.[12]

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.

Differences based on Campylobacter species

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.[13]

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.[14]

Systemic illness with a predilection for vascular sites is characteristic. Meningitis,[15] vascular infections, thrombophlebitis, peritonitis and cellulitis can occur.[16]

C fetus infection may cause intermittent diarrhea or nonspecific abdominal pain. It should also be considered in individuals with nonspecific fever who are either immunocompromised or have had exposure to cattle and sheep.[17]


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.


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.

Laboratory Studies

Clinical diagnosis of enteric Campylobacter infection is established by demonstrating the organism via direct examination of feces or by isolation of the organisms.

Campylobacter organisms multiply more slowly than other enteric bacteria; thus, unusual techniques are used for isolation from fecal specimens.

These include growth at 42°C, use of antibiotic-containing media, and micropore filtration to keep larger bacilli from contaminating the culture.

Specific types of selective media are blood-based, antibiotic-containing media such as Skirrow, Butzler, and Campy-BAP.

Micropore filtration is based on filters with pores small enough to prevent the passage of microbes but large enough to allow passage of organism-free fluid. Filters with a pore diameter of 25 nm to 0.45 µm are usually used in this procedure, which can also be used to remove microorganisms from water and air for microbiological testing.

Multiple media types can be used to cultivate C jejuni, although Mueller-Hinton broth and agar best support C jejuni growth. The optimum atmosphere for C jejuni growth is 85% N2, 10% CO2, and 5% O2.[18]

Campylobacter organisms are oxidase positive with C jejuni hydrolysing hippurate.[19]

Results of stool cultures usually do not remain positive beyond 2 weeks.

Darkfield or phase-contrast microscopy of fecal specimens can also be used to assess for characteristic darting motility within 2 hours of passage.

A Gram stain of stool samples for characteristic curved rods is specific, with a sensitivity of 50-75%.

Fecal leukocytes and erythrocytes are present in 75% of patients with Campylobacter enteritis and can be detected with direct light microscopic examination using methylene blue or Gram stain.

Peripheral blood leukocytosis may be present.

Dehydration may be clinically evident in patients who are moderately to severely ill.

If infection with C fetus or another atypical species is suspected, incubation at 37°C and use of media without cephalosporins are required.

Serodiagnosis of C jejuni infections can be improved by using highly specific recombinant antigens in an enzyme-linked immunoassay (ELISA) technique.[20]

Real-time polymerase chain reaction (PCR) can be used to quickly and accurately detect C jejuni directly in diarrheal stool.[21]

The newer methods such as molecular biology techniques (PCR) and immunoenzymatic methods[22] are more sensitive than traditional culture methods.[23, 24]

Culture-independent tests, such as rapid tests for detection of antigens in stool specimens, are available.[25, 26, 27] However, their use as standalone tests has been questioned.[28]


Up to 80% of patients with Campylobacter infection demonstrate evidence of proctocolitis on sigmoidoscopy. However, findings may be identical to those observed in pseudomembranous colitis or inflammatory bowel disease. Sigmoidoscopic abnormalities range from focal mucosal edema and hyperemia with patchy petechiae to diffuse or aphthoid ulceration.

Medical Care

Replacement of fluids and electrolytes is the mainstay of therapy in patients with Campylobacter infections. Promote rehydration with oral glucose-electrolyte solutions. Failure to achieve hydration with oral intake may require intravenous fluids.

The use of antibiotics to treat uncomplicated Campylobacter infections is controversial, with studies showing that erythromycin rapidly eliminated Campylobacter organisms from the stool without affecting the duration of illness. Studies in children with C jejuni dysentery have shown benefit from early treatment with erythromycin. Antibiotics may be indicated if any of the following occur:

Surgical Care

Suspected toxic megacolon or aneurysms should be evaluated surgically.


Toxic megacolon or infected aneurysms:[29] Consult a surgeon.

Endovascular C fetus infections: Consult an infectious disease specialist.


Patients with Campylobacter infection may engage in activities as tolerated.

Medication Summary

Azithromycin therapy would be a primary antibiotic choice for Campylobacter infections, when indicated (see Medical Care),[30] with a typical regimen of 500 mg/d for 3 days. If the patient is bacteremic, treatment can be extended to two weeks.[31] However, erythromycin is the classic antibiotic of choice. Its resistance remains low,[32] and it can be used in pregnant women and children.

The use of fluoroquinolones in food animals has resulted in fluoroquinolone-resistant Campylobacter strains worldwide.[33, 34] Quinolone resistance of C jejuni and Campylobacter coli is conferred by the mutation gyrA C-257-T, which can be identified with methods such as multiplex PCR.[35] A 2008 study from the United Kingdom found fluoroquinolone-resistant Campylobacter species in 22% of poultry and 75% of pig farms.[36] High levels of ciprofloxacin resistance have also been reported in developing countries, with resistance ranging from 30% to greater than 70%.[37, 38] Some evidence has shown that multidrug resistance in pediatric patients in developing countries may be related to the food chain.[39] Consequently, their use as empiric therapy should be avoided.

Infections involving macrolide resistance could be treated with amoxicillin-clavulanate.[40]

Specific antibiotic doses to treat Campylobacter infections have not been fully defined for tetracycline, therefore, the doses below are empirical. Tetracyclines should be avoided in pregnancy and children.

Antibiotic treatment does not prolong carriage of C jejuni.[41]

CNS infections can be treated with meropenem.[42, 43] Life-threatening infections can be treated with carbapenems and aminoglycosides.

Azithromycin (Zithromax)

Clinical Context:  Acts by binding to 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Nucleic acid synthesis is not affected.

Concentrates in phagocytes and fibroblasts as demonstrated by in vitro incubation techniques. In vivo studies suggest that concentration in phagocytes may contribute to drug distribution to inflamed tissues.

Treats mild-to-moderate microbial infections.

Plasma concentrations are very low, but tissue concentrations are much higher, giving it value in treating intracellular organisms. Has a long tissue half-life.

Effective against a wide range of organisms, including the most common gram-positive and gram-negative organisms. Has additional coverage of so-called atypical infections such as Chlamydia, Mycoplasma, and Legionella species.

Indicated for treatment of patients with mild-to-moderate infections, including acute bronchitic infections that may be observed with bronchiectasis.

Erythromycin (E-Mycin, Ery-Tab, E.E.S.)

Clinical Context:  DOC for Campylobacter infections. Macrolide antibiotic that inhibits bacterial growth by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For C jejuni (not C fetus) infections.

Doxycycline (Bio-Tab, Doryx, Vibramycin, Doxy, Vibra-Tabs)

Clinical Context:  Inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. For C jejuni (not C fetus) infections.

Imipenem and cilastatin (Primaxin)

Clinical Context:  For treatment of multiple organism infections in which other agents do not have wide-spectrum coverage or are contraindicated because of potential for toxicity. For C fetus (not C jejuni) infection.

Gentamicin (Garamycin, Gentacidin)

Clinical Context:  Aminoglycoside antibiotic. May be needed in severe infections. Dosing regimens are numerous; adjust dose based on CrCl and changes in volume of distribution. Can be used for C fetus infections. May be administered IV/IM.

Meropenem (Merrem IV)

Clinical Context:  Inhibits cell-wall synthesis by binding to penicillin-binding proteins; resistant to most beta-lactamases. Can be used for C fetus meningitis.

Ampicillin (Ampi, Omnipen, Penglobe)

Clinical Context:  Broad-spectrum penicillin; interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms; alternative to amoxicillin when unable to take medication orally.

Amoxicillin/clavulanate (Augmentin, Augmentin ES-600, Augmentin XR)

Clinical Context:  Amoxicillin binds to penicillin-binding proteins, thus inhibiting final transpeptidation step of peptidoglycan synthesis in bacterial cell walls; addition of clavulanate inhibits beta-lactamase-producing bacteria, allowing amoxicillin extended spectrum of action.

It is a semisynthetic antibiotic with a broad spectrum of bactericidal activity, covering both gram-negative and gram-positive microorganisms.

Ciprofloxacin (Cipro)

Clinical Context:  Synthetic, broad-spectrum antibacterial compounds. Novel mechanism of action, targeting bacterial topoisomerases II and IV, leads to a sudden cessation of DNA replication. Oral bioavailability is nearly 100%. For C jejuni (not C fetus) infections.

Levofloxacin (Levaquin)

Clinical Context:  For pseudomonal infections and infections due to multidrug resistant gram-negative organisms. For C jejuni (not for C fetus) infections.

Class Summary

Therapy must be comprehensive and cover all likely pathogens in the context of the clinical setting.

Further Inpatient Care

In some cases, systemic Campylobacter infections are diagnosed retrospectively following empirical antibiotic therapy with clinical resolution. In such cases, follow-up blood cultures should be obtained, and treatment can be stopped if they are negative.

Oral erythromycin may not be adequate for systemic C jejuni or C fetus endovascular infections.


Pasteurization of milk and chlorination of drinking water destroy Campylobacter organisms.

Unpasteurized milk and untreated surface water should not be consumed.

Raw milk may not be safe, even if it conforms to routine testing by somatic cell and coliform counts.[44]

Treatment with antibiotics can reduce fecal excretion.

Health care workers with Campylobacter infections should not provide direct patient care or prepare food while they have diarrhea or are shedding Campylobacter organisms in the stool. However, person-to-person transmission is unusual.

After diarrhea resolves, infective organisms may be present in the stool for up to 3 weeks.

Separate cutting boards should be used for foods of animal origin and other foods. After preparing raw food of animal origin, all cutting boards and countertops should be carefully cleaned with soap and hot water.[45, 46]

Chicken should be adequately cooked.

When outbreaks occur, community education can be directed at proper food-handling techniques, including thorough cooking of poultry.

As noted above, handling and consumption of poultry meat is a significant source of illness. One control strategy that has been suggested is to keep colonized and noncolonized flocks separate.[47]

Fresh chicken can be the dominant source of Campylobacter infection, and replacing this with frozen chicken can reduce Campylobacter levels.[8]

Eating raw animal products such as beef and cattle liver should be avoided.[48]

Cross-contamination of food items not normally associated with Campylobacter infections should be considered and prevented.[49]


Potential complications of Campylobacter infections include the following:


Generally, Campylobacter infections carry an excellent prognosis. The disease is almost always self-limited, with or without specific therapy.

The illness usually lasts less than a week, but some patients develop a longer-relapsing diarrheal illness that lasts several weeks.

The occasional deaths attributable to C jejuni infection usually occur in elderly or immunocompromised hosts.

Attributable deaths may also occur in young, healthy individuals secondary to volume depletion.

The rarer C fetus infection may also be fatal in debilitated hosts.

Patient Education

Many Campylobacter infections are potentially preventable through education.

Meat and poultry should be cooked well.

Hands should be washed carefully after preparing food.

Parents should be informed that sick pets (eg, puppies, kittens) may harbor human pathogens and must be kept away from young children.

Untreated surface water and unpasteurized milk should be avoided.

What are Campylobacter infections?What are the signs and symptoms of Campylobacter infections?How are Campylobacter infections transmitted?What is the infectious dose of Campylobacter?What is the pathogenesis of Campylobacter infections?What is the pathophysiology of diarrhea in Campylobacter infections?What are the characteristics of Campylobacter infections in patients with HIV infection?What is the pathophysiology of C fetus Campylobacter infections?What is the pathophysiology of C jejuni Campylobacter infections?What is the incidence of Campylobacter infections in the US?What is the global incidence of Campylobacter infections?What are the risk factors for Campylobacter infection caused mortality?What are the racial predilections for Campylobacter infections?How does the incidence of Campylobacter infections vary by sex?Which age groups are at greatest risk for Campylobacter infections?What is the typical history in patients with Campylobacter infections?What are the signs and symptoms of Campylobacter infections?How do the clinical histories vary among different Campylobacter species?What are the physical findings characteristic of Campylobacter infections?How are Campylobacter organisms characterized?What are the differential diagnoses for Campylobacter Infections?How are Campylobacter infections diagnosed?What is the role of sigmoidoscopy in the diagnosis of Campylobacter infections?What is the initial therapy for Campylobacter infections?What is the role of antibiotics in the treatment of Campylobacter infections?What is the role of surgery in the treatment of Campylobacter infections?When should specialists be consulted in the treatment of Campylobacter infections?What activity restrictions are needed during the treatment of Campylobacter infections?Which antibiotics are used in the treatment of Campylobacter infections?Which medications in the drug class Antibiotics are used in the treatment of Campylobacter Infections?What are the limitations of oral erythromycin in the treatment of Campylobacter infections?How are Campylobacter infections prevented?What are potential complications of Campylobacter infections?What is the prognosis of Campylobacter infections?What is included in patient education for Campylobacter infections?


Mahmud H Javid, MBBS, Consultant in Infectious Diseases, Shifa International Hospital, Pakistan

Disclosure: Nothing to disclose.


Shadab Hussain Ahmed, MD, AAHIVS, FACP, FIDSA, Professor of Clinical Medicine, The School of Medicine at Stony Brook University Medical Center; Adjunct Clinical Associate Professor, Department of Medicine, New York College of Osteopathic Medicine of New York Institute of Technology; Attending Physician, Department of Medicine, Division of Infectious Diseases, Director of HIV Prevention Services, Administrative HIV Designee, Nassau University Medical Center

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Michael Stuart Bronze, MD, David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD, David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Disclosure: Nothing to disclose.


  1. Totten PA, Fennell CL, Tenover FC, Wezenberg JM, Perine PL, Stamm WE, et al. Campylobacter cinaedi (sp. nov.) and Campylobacter fennelliae (sp. nov.): two new Campylobacter species associated with enteric disease in homosexual men. J Infect Dis. 1985 Jan. 151 (1):131-9. [View Abstract]
  2. Saito S, Tsukahara M, Ohkusu K, Kurai H. Helicobacter fennelliae Bacteremia: Three Case Reports and Literature Review. Medicine (Baltimore). 2016 May. 95 (18):e3556. [View Abstract]
  3. Smith JL, Bayles DO. The contribution of cytolethal distending toxin to bacterial pathogenesis. Crit Rev Microbiol. 2006 Oct-Dec. 32 (4):227-48. [View Abstract]
  4. Zhang L. Oral Campylobacter species: Initiators of a subgroup of inflammatory bowel disease?. World J Gastroenterol. 2015 Aug 21. 21 (31):9239-44. [View Abstract]
  5. Kaakoush NO, Mitchell HM, Man SM. Role of emerging Campylobacter species in inflammatory bowel diseases. Inflamm Bowel Dis. 2014 Nov. 20 (11):2189-97. [View Abstract]
  6. Bolinger H, Kathariou S. The Current State of Macrolide Resistance in Campylobacter spp.: Trends and Impacts of Resistance Mechanisms. Appl Environ Microbiol. 2017 Jun 15. 83 (12):[View Abstract]
  7. World Health Organization. "The global view of campylobacteriosis: report of an expert consultation, Utrecht, Netherlands, 9-11 July 2012." (2013).
  8. Baker M, Wilson N, Ikram R, Chambers S, Shoemack P, Cook G. Regulation of chicken contamination is urgently needed to control New Zealand's serious campylobacteriosis epidemic. N Z Med J. 2006. 119(1243):U2264. [View Abstract]
  9. Jeffs E, Williman J, Martin N, Brunton C, Walls T. Epidemiology of Campylobacter Gastroenteritis in New Zealand Children and the Effect of The Campylobacter Strategy: A 20-year Observational Study. Pediatr Infect Dis J. 2019 Jun. 38 (6):569-576. [View Abstract]
  10. Vital signs: incidence and trends of infection with pathogens transmitted commonly through food--foodborne diseases active surveillance network, 10 U.S. sites, 1996-2010. MMWR Morb Mortal Wkly Rep. 2011 Jun 10. 60(22):749-55. [View Abstract]
  11. Kwok M, Maurice A, Lisec C, Brown J. Campylobacter colitis: Rare cause of toxic megacolon. Int J Surg Case Rep. 2016. 27:141-143. [View Abstract]
  12. Gillespie IA, O'brien SJ, Frost JA, Tam C, Tompkins D, Neal KR. Investigating vomiting and/or bloody diarrhoea in Campylobacter jejuni infection. J Med Microbiol. 2006 Jun. 55(Pt 6):741-6. [View Abstract]
  13. Ishihara A, Hashimoto E, Ishioka H, Kobayashi H, Gomi H. Campylobacter fetus meningitis associated with eating habits of raw meat and raw liver in a healthy patient: A case report and literature review. IDCases. 2018. 11:97-100. [View Abstract]
  14. Pacanowski J, Lalande V, Lacombe K, Boudraa C, Lesprit P, Legrand P, et al. Campylobacter bacteremia: clinical features and factors associated with fatal outcome. Clin Infect Dis. 2008 Sep 15. 47(6):790-6. [View Abstract]
  15. van Samkar A, Brouwer MC, van der Ende A, van de Beek D. Campylobacter Fetus Meningitis in Adults: Report of 2 Cases and Review of the Literature. Medicine (Baltimore). 2016 Feb. 95 (8):e2858. [View Abstract]
  16. Ausselet N, Huang D, Vandercam B, Yombi JC. Campylobacter fetus cellulitis in an immunocompromised patient: case report and review of the literature. Acta Clin Belg. 2009 Jul-Aug. 64 (4):346-8. [View Abstract]
  17. Wagenaar JA, van Bergen MA, Blaser MJ, Tauxe RV, Newell DG, van Putten JP. Campylobacter fetus infections in humans: exposure and disease. Clin Infect Dis. 2014 Jun. 58 (11):1579-86. [View Abstract]
  18. Davis L, DiRita V. Growth and laboratory maintenance of Campylobacter jejuni. Curr Protoc Microbiol. 2008 Aug. Chapter 8:Unit 8A.1.1-8A.1.7. [View Abstract]
  19. Nakari UM, Puhakka A, Siitonen A. Correct identification and discrimination between Campylobacter jejuni and C. coli by a standardized hippurate test and species-specific polymerase chain reaction. Eur J Clin Microbiol Infect Dis. 2008 Jul. 27(7):513-8. [View Abstract]
  20. Schmidt-Ott R, Brass F, Scholz C, Werner C, Gross U. Improved serodiagnosis of Campylobacter jejuni infections using recombinant antigens. J Med Microbiol. 2005 Aug. 54(Pt 8):761-7. [View Abstract]
  21. Lin S, Wang X, Zheng H, Mao Z, Sun Y, Jiang B. Direct detection of Campylobacter jejuni in human stool samples by real-time PCR. Can J Microbiol. 2008 Sep. 54(9):742-7. [View Abstract]
  22. Tolcin R, LaSalvia MM, Kirkley BA, Vetter EA, Cockerill FR 3rd, Procop GW. Evaluation of the Alexon-trend ProSpecT Campylobacter microplate assay. J Clin Microbiol. 2000 Oct. 38(10):3853-5. [View Abstract]
  23. Bessède E, Delcamp A, Sifré E, Buissonnière A, Mégraud F. New methods for detection of campylobacters in stool samples in comparison to culture. J Clin Microbiol. 2011 Mar. 49(3):941-4. [View Abstract]
  24. Buss JE, Cresse M, Doyle S, Buchan BW, Craft DW, Young S. Campylobacter culture fails to correctly detect Campylobacter in 30% of positive patient stool specimens compared to non-cultural methods. Eur J Clin Microbiol Infect Dis. 2019 Jun. 38 (6):1087-1093. [View Abstract]
  25. Tissari P, Rautelin H. Evaluation of an enzyme immunoassay-based stool antigen test to detect Campylobacter jejuni and Campylobacter coli. Diagn Microbiol Infect Dis. 2007 Jun. 58 (2):171-5. [View Abstract]
  26. Couturier BA, Couturier MR, Kalp KJ, Fisher MA. Detection of non-jejuni and -coli Campylobacter species from stool specimens with an immunochromatographic antigen detection assay. J Clin Microbiol. 2013 Jun. 51 (6):1935-7. [View Abstract]
  27. Gómez-Camarasa C, Gutiérrez-Fernández J, Rodríguez-Granger JM, Sampedro-Martínez A, Sorlózano-Puerto A, Navarro-Marí JM. Evaluation of the rapid RIDAQUICK Campylobacter® test in a general hospital. Diagn Microbiol Infect Dis. 2014 Feb. 78 (2):101-4. [View Abstract]
  28. Fitzgerald C, Patrick M, Gonzalez A, Akin J, Polage CR, Gillim-Ross L, et al. Multicenter Evaluation of Clinical Diagnostic Methods for Detection and Isolation of Campylobacter spp. from Stool. J Clin Microbiol. 2016 May. 54 (5):1209-15. [View Abstract]
  29. Cochennec F, Gazaigne L, Lesprit P, Desgranges P, Allaire E, Becquemin JP. Aortoiliac aneurysms infected by Campylobacter fetus. J Vasc Surg. 2008 Oct. 48(4):815-20. [View Abstract]
  30. Gilbert DN, Moellering RC Jr, eds. The Sanford Guide To Antimicrobial Therapy 2007. 37th ed. Antimicrobial Therapy, Inc.; 2007. 15.
  31. The Sanford Guide to Antimicrobial Therapy. Antimicrobial Therapy, Inc; 28 July, 2019.
  32. Bardon J, Kolar M, Cekanova L, Hejnar P, Koukalova D. Prevalence of Campylobacter jejuni and its Resistance to Antibiotics in Poultry in the Czech Republic. Zoonoses Public Health. 2008 Sep 2. [View Abstract]
  33. Hannula M, Hänninen ML. Effects of low-level ciprofloxacin challenge in the in vitro development of ciprofloxacin resistance in Campylobacter jejuni. Microb Drug Resist. 2008 Sep. 14(3):197-201. [View Abstract]
  34. Price LB, Johnson E, Vailes R, Silbergeld E. Fluoroquinolone-resistant campylobacter isolates from conventional and antibiotic-free chicken products. Environ Health Perspect. 2005 May. 113(5):557-60. [View Abstract]
  35. Hormeño L, Palomo G, Ugarte-Ruiz M, Porrero MC, Borge C, Vadillo S, et al. Identification of the main quinolone resistance determinant in Campylobacter jejuni and Campylobacter coli by MAMA-DEG PCR. Diagn Microbiol Infect Dis. 2016 Mar. 84 (3):236-9. [View Abstract]
  36. Taylor NM, Davies RH, Ridley A, Clouting C, Wales AD, Clifton-Hadley FA. A survey of fluoroquinolone resistance in Escherichia coli and thermophilic Campylobacter spp. on poultry and pig farms in Great Britain. J Appl Microbiol. 2008 Nov. 105(5):1421-31. [View Abstract]
  37. Meng CY, Smith BL, Bodhidatta L, Richard SA, Vansith K, Thy B, et al. Etiology of diarrhea in young children and patterns of antibiotic resistance in Cambodia. Pediatr Infect Dis J. 2011 Apr. 30(4):331-5. [View Abstract]
  38. Pandey P, Bodhidatta L, Lewis M, Murphy H, Shlim DR, Cave W, et al. Travelers' diarrhea in Nepal: an update on the pathogens and antibiotic resistance. J Travel Med. 2011 Mar-Apr. 18(2):102-8. [View Abstract]
  39. Noreen Z, Siddiqui F, Javed S, Wren BW, Bokhari H. Transmission of Multidrug Resistant Campylobacter jejuni to Children from Different Sources in Pakistan. J Glob Antimicrob Resist. 2019 Jul 23. [View Abstract]
  40. Schiaffino F, Colston JM, Paredes-Olortegui M, François R, Pisanic N, Burga R, et al. Antibiotic Resistance of Campylobacter Species in a Pediatric Cohort Study. Antimicrob Agents Chemother. 2019 Feb. 63 (2):[View Abstract]
  41. Mandal BK, Ellis ME, Dunbar EM, Whale K. Double-blind placebo-controlled trial of erythromycin in the treatment of clinical campylobacter infection. J Antimicrob Chemother. 1984 Jun. 13(6):619-23. [View Abstract]
  42. Burch KL, Saeed K, Sails AD, Wright PA. Successful treatment by meropenem of Campylobacter jejuni meningitis in a chronic alcoholic following neurosurgery. J Infect. 1999 Nov. 39(3):241-3. [View Abstract]
  43. Shioyama M, Mitui Y, Ueda H, Takada K, Kureshiro J, Kitaguchi M, et al. [Bacterial meningitis with Campylobacter fetus manifesting chronic clinical course]. Rinsho Shinkeigaku. 2006 Oct. 46(10):699-701. [View Abstract]
  44. Davis KR, Dunn AC, Burnett C, McCullough L, Dimond M, Wagner J, et al. Campylobacter jejuni Infections Associated with Raw Milk Consumption - Utah, 2014. MMWR Morb Mortal Wkly Rep. 2016 Apr 1. 65 (12):301-5. [View Abstract]
  45. van Asselt ED, de Jong AE, de Jonge R, Nauta MJ. Cross-contamination in the kitchen: estimation of transfer rates for cutting boards, hands and knives. J Appl Microbiol. 2008 Nov. 105(5):1392-401. [View Abstract]
  46. de Jong AE, Verhoeff-Bakkenes L, Nauta MJ, de Jonge R. Cross-contamination in the kitchen: effect of hygiene measures. J Appl Microbiol. 2008 Aug. 105(2):615-24. [View Abstract]
  47. Wagenaar JA, Mevius DJ, Havelaar AH. Campylobacter in primary animal production and control strategies to reduce the burden of human campylobacteriosis. Rev Sci Tech. 2006 Aug. 25(2):581-94. [View Abstract]
  48. Ishihara A, Hashimoto E, Ishioka H, Kobayashi H, Gomi H. Campylobacter fetus meningitis associated with eating habits of raw meat and raw liver in a healthy patient: A case report and literature review. IDCases. 2018. 11:97-100. [View Abstract]
  49. Kang CR, Bang JH, Cho SI. Campylobacter jejuni Foodborne Infection Associated with Cross-contamination: Outbreak in Seoul in 2017. Infect Chemother. 2019 Mar. 51 (1):21-27. [View Abstract]
  50. Lecuit M, Abachin E, Martin A. Immunoproliferative small intestinal disease associated with Campylobacter jejuni. N Engl J Med. 2004 Jan 15. 350(3):239-48. [View Abstract]
  51. Kosunen TU, Kauranen O, Martio J, et al. Reactive arthritis after campylobacter jejuni enteritis in patients with HLA-B27. Lancet. 1980 Jun 14. 1(8181):1312-3. [View Abstract]
  52. Pönkä A, Martio J, Kosunen TU. Reiter's syndrome in association with enteritis due to Campylobacter fetus ssp. jejuni. Ann Rheum Dis. 1981 Aug. 40(4):414-5. [View Abstract]
  53. Kuperman-Shani A, Vaknin Z, Mendlovic S, Zaidenstein R, Melcer Y, Maymon R. Campylobacter coli infection causing second trimester intrauterine growth restriction (IUGR): a case report and review of the literature. Prenat Diagn. 2015 Dec. 35 (12):1258-61. [View Abstract]
  54. Mishu B, Blaser MJ. Role of infection due to Campylobacter jejuni in the initiation of Guillain-Barre syndrome. Clin Infect Dis. 1993 Jul. 17(1):104-8. [View Abstract]
  55. Mishu B, Ilyas AA, Koski CL, et al. Serologic evidence of previous Campylobacter jejuni infection in patients with the Guillain-Barre syndrome. Ann Intern Med. 1993 Jun 15. 118(12):947-53. [View Abstract]
  56. Schmidt-Ott R, Schmidt H, Feldmann S, Brass F, Krone B, Gross U. Improved serological diagnosis stresses the major role of Campylobacter jejuni in triggering Guillain-Barré syndrome. Clin Vaccine Immunol. 2006 Jul. 13(7):779-83. [View Abstract]
  57. Baker MG, Kvalsvig A, Zhang J, Lake R, Sears A, Wilson N. Declining Guillain-Barré syndrome after campylobacteriosis control, New Zealand, 1988–2010. Emerg Infect Dis. Feb 2012.
  58. Harvala H, Rosendal T, Lahti E, Engvall EO, Brytting M, Wallensten A, et al. Epidemiology of Campylobacter jejuni infections in Sweden, November 2011-October 2012: is the severity of infection associated with C. jejuni sequence type?. Infect Ecol Epidemiol. 2016. 6:31079. [View Abstract]
  59. Kogawa S, Furukawa K. [Campylobacter jejuni meningitis in an immunocompetent adult male]. Rinsho Shinkeigaku. 2010 Apr. 50(4):262-4. [View Abstract]
  60. Kitamura S, Matsumura N, Ohtake N, Kita M, Konishi I. Tubo-ovarian abscess with endometrial cyst probably infected by Campylobacter fetus: Two cases. J Obstet Gynaecol Res. 2016 Apr 14. [View Abstract]
  61. Kato H, Wakasugi H, Mukuta T, Furukawa M, Yokota M, Yamada Y, et al. Campylobacter fetus subspecies fetus meningitis with chronic alcoholism and diabetes mellitus. Jpn J Med. 1990 Sep-Oct. 29(5):542-4. [View Abstract]
  62. Rao KV, Ralston RA. Meningitis due to Campylobacter fetus intestinalis in a kidney transplant recipient. A case report. Am J Nephrol. 1987. 7(5):402-3. [View Abstract]
  63. Ailes E, Demma L, Hurd S, Hatch J, Jones TF, Vugia D, et al. Continued decline in the incidence of Campylobacter infections, FoodNet 1996-2006. Foodborne Pathog Dis. 2008 Jun. 5(3):329-37. [View Abstract]
  64. Allos BM. Campylobacter jejuni Infections: update on emerging issues and trends. Clin Infect Dis. 2001 Apr 15. 32(8):1201-6. [View Abstract]
  65. Blaser MJ. Campylobacter fetus--emerging infection and model system for bacterial pathogenesis at mucosal surfaces. Clin Infect Dis. 1998 Aug. 27(2):256-8. [View Abstract]
  66. Blaser MJ, Wells JG, Feldman RA, et al. Campylobacter enteritis in the United States. A multicenter study. Ann Intern Med. 1983 Mar. 98(3):360-5. [View Abstract]
  67. Butzler JP. Campylobacter, from obscurity to celebrity. Clin Microbiol Infect. 2004 Oct. 10(10):868-76. [View Abstract]
  68. Caldwell DB, Wang Y, Lin J. Development, stability, and molecular mechanisms of macrolide resistance in Campylobacter jejuni. Antimicrob Agents Chemother. 2008 Nov. 52(11):3947-54. [View Abstract]
  69. Carbone KM, Heinrich MC, Quinn TC. Thrombophlebitis and cellulitis due to Campylobacter fetus ssp. fetus. Report of four cases and a review of the literature. Medicine (Baltimore). 1985 Jul. 64(4):244-50. [View Abstract]
  70. Crushell E, Harty S, Sharif F, Bourke B. Enteric campylobacter: purging its secrets?. Pediatr Res. 2004 Jan. 55(1):3-12. [View Abstract]
  71. Drake AA, Gilchrist MJ, Washington JA 2nd, et al. Diarrhea due to Campylobacter fetus subspecies jejuni. A clinical review of 63 cases. Mayo Clin Proc. 1981 Jul. 56(7):414-23. [View Abstract]
  72. Fennell CL, Totten PA, Quinn TC, et al. Characterization of Campylobacter-like organisms isolated from homosexual men. J Infect Dis. 1984 Jan. 149(1):58-66. [View Abstract]
  73. Francioli P, Herzstein J, Grob JP, et al. Campylobacter fetus subspecies fetus bacteremia. Arch Intern Med. 1985 Feb. 145(2):289-92. [View Abstract]
  74. Friis LM, Pin C, Pearson BM, Wells JM. In vitro cell culture methods for investigating Campylobacter invasion mechanisms. J Microbiol Methods. 2005 May. 61(2):145-60. [View Abstract]
  75. Giesendorf BA, Quint WG. Detection and identification of Campylobacter spp. using the polymerase chain reaction. Cell Mol Biol (Noisy-le-grand). 1995 Jul. 41(5):625-38. [View Abstract]
  76. Kosunen TU, Ponka A, Kauranen O, et al. Arthritis associated with Campylobacter jejuni enteritis. Scand J Rheumatol. 1981. 10(2):77-80. [View Abstract]
  77. Mee AS, Shield M, Burke M. Campylobacter colitis: differentiation from acute inflammatory bowel disease. J R Soc Med. 1985 Mar. 78(3):217-23. [View Abstract]
  78. Pasternak J, Bolivar R, Hopfer RL, et al. Bacteremia caused by Campylobacter-like organisms in two male homosexuals. Ann Intern Med. 1984 Sep. 101(3):339-41. [View Abstract]
  79. Perlman DM, Ampel NM, Schifman RB, et al. Persistent Campylobacter jejuni infections in patients infected with the human immunodeficiency virus (HIV). Ann Intern Med. 1988 Apr. 108(4):540-6. [View Abstract]
  80. Robinson DA. Infective dose of Campylobacter jejuni in milk. Br Med J (Clin Res Ed). 1981 May 16. 282(6276):1584. [View Abstract]
  81. Taylor DN, Blaser MJ. The epidemiology of Helicobacter pylori infection. Epidemiol Rev. 1991. 13:42-59. [View Abstract]
  82. Taylor DN, Blaser MJ, Echeverria P, et al. Erythromycin-resistant Campylobacter infections in Thailand. Antimicrob Agents Chemother. 1987 Mar. 31(3):438-42. [View Abstract]
  83. Taylor DN, McDermott KT, Little JR, et al. Campylobacter enteritis from untreated water in the Rocky Mountains. Ann Intern Med. 1983 Jul. 99(1):38-40. [View Abstract]
  84. Taylor DN, Perlman DM, Echeverria PD, et al. Campylobacter immunity and quantitative excretion rates in Thai children. J Infect Dis. 1993 Sep. 168(3):754-8. [View Abstract]
  85. Tee W, Mijch A. Campylobacter jejuni bacteremia in human immunodeficiency virus (HIV)-infected and non-HIV-infected patients: comparison of clinical features and review. Clin Infect Dis. 1998 Jan. 26(1):91-6. [View Abstract]
  86. Tee W, Mijch A, Wright E, Yung A. Emergence of multidrug resistance in Campylobacter jejuni isolates from three patients infected with human immunodeficiency virus. Clin Infect Dis. 1995 Sep. 21(3):634-8. [View Abstract]
  87. Walker RI, Caldwell MB, Lee EC, et al. Pathophysiology of Campylobacter enteritis. Microbiol Rev. 1986 Mar. 50(1):81-94. [View Abstract]
  88. Wassenaar TM, Blaser MJ. Pathophysiology of Campylobacter jejuni infections of humans. Microbes Infect. 1999 Oct. 1(12):1023-33. [View Abstract]
  89. Yamashita K, Aoki Y, Hiroshima K. Pyogenic vertebral osteomyelitis caused by Campylobacter fetus subspecies fetus. A case report. Spine. 1999 Mar 15. 24(6):582-4. [View Abstract]
  90. Castaño-Rodríguez N, Kaakoush NO, Lee WS, Mitchell HM. Dual role of Helicobacter and Campylobacter species in IBD: a systematic review and meta-analysis. Gut. 2015 Oct 27. [View Abstract]
  91. Laprade N, Cloutier M, Lapen DR, Topp E, Wilkes G, Villemur R, et al. Detection of virulence, antibiotic resistance and toxin (VAT) genes in Campylobacter species using newly developed multiplex PCR assays. J Microbiol Methods. 2016 May. 124:41-7. [View Abstract]

Scanning electron microscope image of Campylobacter jejuni, illustrating its corkscrew appearance and bipolar flagella. Source: Virginia-Maryland Regional College of Veterinary Medicine, Blacksburg, Virginia.

Scanning electron microscope image of Campylobacter jejuni, illustrating its corkscrew appearance and bipolar flagella. Source: Virginia-Maryland Regional College of Veterinary Medicine, Blacksburg, Virginia.