AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Campylobacter infections are among the most common bacterial infections in humans. They produce both diarrheal and systemic illnesses. In industrialized regions, enteric infection produces 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.

Campylobacter-like organisms can produce an enterocolitis/proctocolitis syndrome in homosexual males, who are at increased risk for infections caused by Helicobacter cinaedi and Helicobacter fennelliae. C jejuni may also produce serious bacteremic conditions in individuals with AIDS. Most reported bacteremias have been due to Campylobacter fetus fetus. 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 developing 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 transmission are 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 outbreaks.

Transmission occurs most commonly from 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 infections. In most colonized animals, a lifelong carrier state develops.

The infectious dose is 1000-10,000 bacteria. Infection has occurred after ingestion of 500 organisms by a volunteer; however, illness is infrequent with a dose of less than 10,000 organisms. Campylobacter species are sensitive to hydrochloric acid in the stomach, and antacid treatment can reduce the amount of inoculum needed to cause disease.

Symptoms 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 organisms 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. The organism produces diffuse, bloody, edematous, and exudative enteritis. The inflammatory infiltrate consists of neutrophils, mononuclear cells, and eosinophils. Crypt abscesses in the epithelial glands and ulceration of the mucosal epithelium are present.

Cytotoxin production has been reported in strains from patients with bloody diarrhea. In a small number of cases, the infection may be 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, infections may be more frequent, 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 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 infection in patients with AIDS and hypogammaglobulinemia indicates that both cell-mediated and humoral immunity are important in preventing and terminating infection.

Frequency

United States

Exact figures are not available, but an estimated 2 million cases of Campylobacter enteritis occur annually, accounting for 5-7% of cases of gastroenteritis. A large animal reservoir is present, with up to 100% of poultry, including chickens, turkeys, and waterfowl having asymptomatic infections in their intestinal tracts. The major reservoirs of C fetus are cattle and sheep.

International

C jejuni infections are extremely common worldwide. Exact figures are not available. The highest national rate of campylobacteriosis was reported by New Zealand, which peaked in May 2006 at 400 per 100,000 population.¹

Mortality/Morbidity

The disease is usually self-limited without any mortality. Exact figures are unavailable, but occasional deaths occur in young, previously healthy individuals because of volume depletion and in persons who are elderly or immunocompromised.

Race

No clear racial predominance is evident.

Sex

The organism is 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

Infection 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 highest age-specific attack rate occurs in young children, but the greatest number of positive fecal cultures occurs in adults and older children.
• Asymptomatic infection is infrequent in adults.
• In developing countries, 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 may be infected asymptomatically.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

The spectrum of disease can range from asymptomatic to severe, life-threatening colitis with toxic megacolon.

• Clinical manifestations of infections from all of the Campylobacter species that cause enteric illnesses appear identical.
• • 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 as long as 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 is present in greater than 90% of patients, may be low or high grade and can persist for a week.
  • Patients with C jejuni who report vomiting, bloody diarrhea, or both tend to have a longer illness and require hospital admission.²
  • Abdominal pain and tenderness may be localized. If pain is in the right lower quadrant, it may mimic acute appendicitis (pseudoappendicitis).
  • Tenesmus occurs in approximately 25% of patients.
  • Sometimes, acute abdominal pain may be the only symptom, with pain typically in the right lower quadrant. Among the symptoms, abdominal pain is more likely to occur with Campylobacter infection than with Salmonella and Shigella infections.
• In contrast to C jejuni, C fetus causes diarrheal illness less frequently. However, when it does occur, the clinical manifestations are similar. C fetus is an opportunistic agent in debilitated hosts, but healthy hosts may also be affected.
• • Bacteremia is common, and C fetus fetus is frequently isolated from the bloodstream. This may be because it resists the bactericidal activity of serum, while the more common C jejuni does not.
  • Systemic illness with a predilection for vascular sites is characteristic. Meningitis, vascular infections, and abscesses may be present.
  • C fetus may cause intermittent diarrhea or nonspecific abdominal pain.

Physical

• The patient may appear to be ill.
• The abdomen is diffusely tender, frequently in the right or left lower quadrant.
• Among symptoms, only abdominal pain is more likely with Campylobacter infections than with 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.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Entamoeba histolytica
Intussusception
Toxigenic Escherichia coli
Enteropathogenic E coli

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• The clinical diagnosis of enteric infection is established by demonstrating the organism by direct examination of feces or by isolation of the organisms.
• Since Campylobacter organisms multiply more slowly than other enteric bacteria, unusual techniques are used to isolate them 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. The technique of micropore filtration is based on filters with pores small enough to prevent the passage of microbes but large enough to allow the organism-free fluid to pass through. Filters with a pore diameter from 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.
• Results of stool cultures usually do not remain positive beyond 2 weeks.
• Darkfield or phase-contrast microscopy of fecal specimens for characteristic darting motility within 2 hours of passage can also be used.
• 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. Fecal leukocytes and erythrocytes can be detected with direct light microscopic examination using methylene blue or Gram stain.
• Peripheral blood leukocytosis may be present.
• Laboratory evidence of dehydration may be noted in patients who are moderately to severely ill.
• If 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.³

Procedures

• Up to 80% of patients demonstrate evidence of proctocolitis when examined by 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.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

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

• The use of antibiotics is controversial, with studies showing that erythromycin rapidly eliminated Campylobacter from the stool without affecting the duration of illness. Studies in children with dysentery due to C jejuni have shown benefit from early treatment with erythromycin. Antibiotics may be indicated if any of the following possibilities occur:
• • High fever
  • Bloody diarrhea
  • Excessive bowel movements (ie, >8 stools per d)
  • Worsening symptoms
  • Failure of symptoms to lessen
  • Persistence of symptoms for longer than 1 week
  • Pregnancy
  • HIV infection and other immunocompromised states
• Avoid antimotility agents because they prolong the duration of symptoms and have been associated with fatalities.
• Individuals with hypogammaglobulinemia who have recurrent C jejuni bacteremias may require fresh frozen plasma with antibiotics.
• Patients with severe dysentery or a relapsing course may require hospitalization.
• Patients with endovascular infections due to C fetus require at least 4 weeks of treatment; gentamicin is believed to be the agent of choice. Treatment with ampicillin or third-generation cephalosporins is an alternative.
• Treat C fetus CNS infections for 2-3 weeks with third-generation cephalosporins, ampicillin, or chloramphenicol.

Surgical Care

• Surgical evaluation may be needed if toxic megacolon develops.

Consultations

• Toxic megacolon: Consult a surgeon.
• Endovascular infections with C fetus: Consult an infectious disease specialist.

Activity

Patients may engage in activities as tolerated.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Erythromycin is the antibiotic of choice. Ciprofloxacin and tetracycline are alternative choices; however, they should be avoided in young children. Also, the use of fluoroquinolones in food animals has resulted in fluoroquinolone-resistant strains worldwide. Erythromycin resistance remains low, and it can be used in children or patients who are pregnant. Erythromycin resistance remains low and it can be used in pregnancy and children. Clindamycin is another therapeutic alternative. Specific antibiotic doses to treat Campylobacter infections have not been fully defined for tetracycline and clindamycin; therefore, the doses below are empirical. Therapy with the newer macrolides, such as clarithromycin or azithromycin, should also be effective, and their use may increase.

Drug Category: Antibiotics

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

Drug Name	Ciprofloxacin (Cipro)
Description	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.
Adult Dose	500 mg PO bid for 5-7 d
Pediatric Dose	<18 years: Not recommended >18 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	Antacids, iron, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine and probenecid may increase levels of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; fluoroquinolones may increase serum levels of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in patients with renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy; do not use in pediatrics as first-line agent because of cartilage damage in young animals; may cause CNS toxicity

Drug Name	Clindamycin (Cleocin)
Description	Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Adult Dose	150-300 mg/dose PO q8h
Pediatric Dose	8-20 mg/kg/d PO as hydrochloride (caps) or 8-25 mg/kg/d PO as palmitate (oral susp) divided tid/qid; not to exceed 1.8 g/d 20-40 mg/kg/d IV divided tid/qid; not to exceed 4.8 g/d
Contraindications	Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
Interactions	Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption of clindamycin
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Adjust dose in severe hepatic dysfunction; no adjustment necessary in patients with renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile

Drug Name	Doxycycline (Bio-Tab, Doryx, Vibramycin, Doxy, Vibra-Tabs)
Description	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.
Adult Dose	200 mg PO/IV immediately and 100 mg hs, followed by 100 mg bid for 3 d; alternatively, 100-200 mg PO for 14 d
Pediatric Dose	<8 years: Not recommended >8 years: 2-5 mg/kg/d PO in 1-2 divided doses; PO not to exceed 200 mg/d
Contraindications	Documented hypersensitivity; severe hepatic dysfunction
Interactions	Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy
Pregnancy	D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions	Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines.

Drug Name	Levofloxacin (Levaquin)
Description	For pseudomonal infections and infections due to multidrug resistant gram-negative organisms. For C jejuni (not for C fetus) infections.
Adult Dose	500 mg PO qd
Pediatric Dose	<18 years: Not recommended >18 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; levofloxacin reduces therapeutic effects of phenytoin; probenecid may increase levofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy

Drug Name	Ceftriaxone (Rocephin)
Description	Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins. For C fetus (not C jejuni) infections.
Adult Dose	1 g IV qd
Pediatric Dose	Neonates > 7 d: 25-50 mg/kg/d IV/IM; not to exceed 125 mg/d Infants and children: 50-75 mg/kg/d IV/IM divided q12h; not to exceed 2 g/d
Contraindications	Documented hypersensitivity
Interactions	Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections, and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy; caution in breastfeeding women

Drug Name	Gentamicin (Garamycin, Gentacidin)
Description	Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes. Not the DOC. Consider if penicillins or other less toxic drugs are contraindicated, when clinically indicated, and in mixed infections caused by susceptible staphylococci and gram-negative organisms. Dosing regimens are numerous; adjust dose based on CrCl and changes in volume of distribution. May be administered IV/IM. For C fetus (not C jejuni) infections.
Adult Dose	Serious infections and normal renal function: 3 mg/kg/dose IV q8h Loading dose and maintenance dose: 1-2.5 mg/kg IV and 1-1.5 mg/kg IV, respectively, q8h or may be administered as a single daily dose
Pediatric Dose	<5 years: 2.5 mg/kg/dose IV/IM q8h >5 years: 1.5-2.5 mg/kg/dose IV/IM q8h or 6-7.5 mg/kg/d divided q8h; not to exceed 300 mg/d; monitor as in adults
Contraindications	Documented hypersensitivity; non–dialysis-dependent renal insufficiency
Interactions	Coadministration with other aminoglycosides, cephalosporins, penicillins, and amphotericin B may increase nephrotoxicity; because aminoglycosides enhance effects of neuromuscular blocking agents prolonged respiratory depression may occur; coadministration with loop diuretics may increase auditory toxicity of aminoglycosides; possible irreversible hearing loss of varying degrees may occur (monitor regularly)
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Narrow therapeutic index (not intended for long-term therapy); caution in renal failure (not on dialysis), myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; adjust dose in renal impairment

Drug Name	Imipenem and cilastatin (Primaxin)
Description	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.
Adult Dose	Base initial dose on severity of infection, and administer in equally divided doses; dose may range from 250-500 mg q6h IV for a maximum of 3-4 g/d; alternatively, 500-750 mg q12h IM or intra-abdominally
Pediatric Dose	<3 months: Not established Infants > 3 months and children <12 years: 15-25 mg/kg/dose IV q6h Fully susceptible organisms: Not to exceed 2 g/d Infections with moderately susceptible organisms: Not to exceed 4 g/d >12 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	Coadministration with cyclosporine, may increase adverse CNS effects of both agents; coadministration with ganciclovir may result in generalized seizures
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Adjust dose in renal insufficiency; avoid use in children <12 y

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Systemic infections are sometimes diagnosed retrospectively following previous empirical antibiotic therapy with clinical resolution. In such cases, follow-up blood cultures should be obtained.
• Oral erythromycin may not be adequate for systemic C jejuni or C fetus endovascular infections.

Deterrence/Prevention

• Pasteurization of milk and chlorination of drinking water destroy the organism.
• Unpasteurized milk and untreated surface water should not be consumed. Consumption of unpasteurized milk is the most frequently reported cause of outbreaks.
• Treatment with antibiotics can reduce fecal excretion.
• Infected health care workers 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.
• 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.
• 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.⁴
• Fresh chicken can be the dominant source of infection, and replacing this with frozen chicken can reduce Campylobacter levels.¹

Complications

• Toxic megacolon
• Pseudomembranous colitis
• Colonic hemorrhage
• Hemolytic uremic syndrome
• Thrombotic thrombocytopenic purpura
• Immunoproliferative small intestinal disease (This is a type of lymphoma that involves mucosa-associated lymphoid tissue [MALT]. It has been found to be associated with C jejuni⁵).
• Reactive arthritis
• Reiter syndrome
• Bacteremia
• Endocarditis
• Cholecystitis
• Urinary tract infection
• Pancreatitis
• Stillbirths, septic abortions (C fetus)
• Guillain-Barré syndrome (GBS) (GBS may develop secondary to cross-immunoreactivity between human gangliosides GM1 and GD1a and C jejuni lipopolysaccharides. In one study, up to 25% of patients with GBS had stool cultures positive for C jejuni. However, because of shortcomings of standard serological methods, the role of C jejuni may have been underestimated. In a study using a highly specific ELISA based on recombinant antigens, 80% of 36 patients with acute GBS were found to have serological evidence of preceding C jejuni infection, compared with 3.5% of controls⁶).

Prognosis

• Generally, affected patients have an excellent prognosis. The disease is self-limited, with or without specific therapy.
• The illness usually lasts less than a week, but the patient can sometimes develop a longer-relapsing diarrheal illness that lasts several weeks.
• The occasional deaths in patients with C jejuni usually occurred in hosts who were elderly or immunocompromised.
• Deaths may also occur in young, healthy individuals because of volume depletion.
• The rarer C fetus infection may also be fatal in hosts who are debilitated.

Patient Education

• Many infections are potentially preventable through education.
• Meat and poultry should be cooked well.
• Careful handwashing must be performed 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.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Steroids worsen Campylobacter infections; therefore, before making a diagnosis of inflammatory bowel disease, treatable infectious causes such as Campylobacter infections should be excluded.
• A single negative stool culture result does not exclude infection.
• Physicians who diagnose campylobacteriosis and laboratories that identify the organism should report their findings to the local health department.

Special Concerns

• C fetus is missed on most routine stool cultures for C jejuni.
• C jejuni is capable of surviving in milk, other foods, or water maintained at 4°C for several weeks. However, it cannot withstand drying or freezing temperatures and is destroyed by pasteurization and chlorine at concentrations used for water disinfection.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

1. 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. [Medline].
2. 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. Jun 2006;55(Pt 6):741-6. [Medline].
3. Schmidt-Ott R, Brass F, Scholz C, Werner C, Gross U. Improved serodiagnosis of Campylobacter jejuni infections using recombinant antigens. J Med Microbiol. Aug 2005;54(Pt 8):761-7. [Medline].
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5. Lecuit M, Abachin E, Martin A. Immunoproliferative small intestinal disease associated with Campylobacter jejuni. N Engl J Med. Jan 15 2004;350(3):239-48. [Medline].
6. 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. Jul 2006;13(7):779-83. [Medline].
7. Allos BM. Campylobacter jejuni Infections: update on emerging issues and trends. Clin Infect Dis. Apr 15 2001;32(8):1201-6. [Medline].
8. Blaser MJ. Campylobacter fetus--emerging infection and model system for bacterial pathogenesis at mucosal surfaces. Clin Infect Dis. Aug 1998;27(2):256-8. [Medline].
9. Blaser MJ, Wells JG, Feldman RA, et al. Campylobacter enteritis in the United States. A multicenter study. Ann Intern Med. Mar 1983;98(3):360-5. [Medline].
10. Butzler JP. Campylobacter, from obscurity to celebrity. Clin Microbiol Infect. Oct 2004;10(10):868-76. [Medline].
11. 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). Jul 1985;64(4):244-50. [Medline].
12. Crushell E, Harty S, Sharif F, Bourke B. Enteric campylobacter: purging its secrets?. Pediatr Res. Jan 2004;55(1):3-12. [Medline].
13. 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. Jul 1981;56(7):414-23. [Medline].
14. Fennell CL, Totten PA, Quinn TC, et al. Characterization of Campylobacter-like organisms isolated from homosexual men. J Infect Dis. Jan 1984;149(1):58-66. [Medline].
15. Francioli P, Herzstein J, Grob JP, et al. Campylobacter fetus subspecies fetus bacteremia. Arch Intern Med. Feb 1985;145(2):289-92. [Medline].
16. Friis LM, Pin C, Pearson BM, Wells JM. In vitro cell culture methods for investigating Campylobacter invasion mechanisms. J Microbiol Methods. May 2005;61(2):145-60. [Medline].
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Article Last Updated: Feb 20, 2007