eMedicine Specialties > Infectious Diseases > Bacterial Infections

Campylobacter Infections

Mahmud H Javid, MD, Chief, Section of Infectious Diseases, Shifa Hospital, Islamabad, Pakistan
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

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.

Differential Diagnoses

Other Problems to Be Considered

Entamoeba histolytica infection
Intussusception
Toxigenic Escherichia coli infection
Enteropathogenic E coli infection

Workup

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% O₂.⁵
• 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.⁶
• Real-time polymerase chain reaction (PCR) can be used to quickly and accurately detect C jejuni directly in diarrheal stool.⁷

Procedures

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.

Treatment

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 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:
  • High fever
  • Bloody diarrhea
  • Excessive bowel movements (ie, >8 stools per day)
  • Worsening symptoms
  • Failure of symptoms to improve
  • 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 bacteremia may require fresh frozen plasma with antibiotics.
• Patients with severe dysentery or a relapsing course may require hospitalization.
• Patients with endovascular C fetus infections 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

• Suspected toxic megacolon or aneurysms should be evaluated surgically.

Consultations

• Toxic megacolon or infected aneurysms:⁸ Consult a surgeon.
• Endovascular C fetus infections: Consult an infectious disease specialist.

Activity

Patients with Campylobacter infection may engage in activities as tolerated.

Medication

Azithromycin therapy would be a primary antibiotic choice for Campylobacter infections, when indicated (see Medical Care),⁹ with a typical regimen of 500 mg/d for 3 days. However, erythromycin is the classic antibiotic of choice. Its resistance remains low,¹⁰ and it can be used in pregnant women and children.

Ciprofloxacin and tetracycline are alternatives but should be avoided in young children. In addition, the use of fluoroquinolones in food animals has resulted in fluoroquinolone-resistant Campylobacter strains worldwide.^11,12 A recent study from the United Kingdom found fluoroquinolone-resistant Campylobacter species in 22% of poultry and 75% of pig farms.¹³

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.

Antibiotics

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

Azithromycin (Zithromax)

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.

Dosing

Adult

500mg PO qd for 3 d

Pediatric

<6 months: Not established
>6 months:
Day 1: 10 mg/kg PO once; not to exceed 500 mg/d
Days 2-5: 5 mg/kg PO qd; not to exceed 250 mg/d

Interactions

May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine

Contraindications

Documented hypersensitivity; hepatic impairment; do not administer with pimozide

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Site reactions can occur with IV route; bacterial or fungal overgrowth may result from prolonged antibiotic use; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function or prolonged QT intervals

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

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.

Dosing

Adult

500 mg erythromycin stearate, base, or estolate salts (or 400 mg ethylsuccinate) PO q6h; alternatively, 333 mg (as base) PO q8h

Pediatric

30-50 mg/kg/d, base or ethylsuccinate, PO divided q6-8h for 5-7 d; not to exceed 1 g/d

Interactions

Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis; inhibits CYP1A2, CYP 3A4 isoenzymes

Contraindications

Documented hypersensitivity; hepatic impairment

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients with liver disease; estolate formulation may cause cholestatic jaundice; adverse GI effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occurs

Ciprofloxacin (Cipro)

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.

Dosing

Adult

500 mg PO bid for 5-7 d

Pediatric

<18 years: Not recommended
>18 years: Administer as in adults

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)

Contraindications

Documented hypersensitivity

Precautions

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

Clindamycin (Cleocin)

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.

Dosing

Adult

150-300 mg/dose PO q8h

Pediatric

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

Interactions

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption of clindamycin

Contraindications

Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis

Precautions

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

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

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.

Dosing

Adult

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

<8 years: Not recommended
>8 years: 2-5 mg/kg/d PO in 1-2 divided doses; PO not to exceed 200 mg/d

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

Contraindications

Documented hypersensitivity; severe hepatic dysfunction

Precautions

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.

Levofloxacin (Levaquin)

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

Dosing

Adult

500 mg PO qd

Pediatric

<18 years: Not recommended
>18 years: Administer as in adults

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)

Contraindications

Documented hypersensitivity

Precautions

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

Ceftriaxone (Rocephin)

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.

Dosing

Adult

1 g IV qd

Pediatric

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

Interactions

Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

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

Gentamicin (Garamycin, Gentacidin)

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.

Dosing

Adult

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

<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

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)

Contraindications

Documented hypersensitivity; non–dialysis-dependent renal insufficiency

Precautions

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

Imipenem and cilastatin (Primaxin)

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.

Dosing

Adult

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

<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

Interactions

Coadministration with cyclosporine, may increase adverse CNS effects of both agents; coadministration with ganciclovir may result in generalized seizures

Contraindications

Documented hypersensitivity

Precautions

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

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.
• 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 Campylobacter organisms.
• Unpasteurized milk and untreated surface water should not be consumed. Consumption of unpasteurized milk is the most commonly reported cause of Campylobacter infection outbreaks.
• 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.
• 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.^14,15
• 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.¹⁶
• Fresh chicken can be the dominant source of Campylobacter infection, and replacing this with frozen chicken can reduce Campylobacter levels.²

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 jejuni infection.¹⁷ )
• Reactive arthritis^18,19
• 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.^20,21 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 controls.²² )
• Infected aortoiliac aneurysms⁸

Prognosis

• 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.

Miscellaneous

Medicolegal Pitfalls

• Steroids worsen Campylobacter infections; therefore, treatable infections such as Campylobacter infections should be excluded before inflammatory bowel disease is diagnosed.
• 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

1. 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. Jun 2008;5(3):329-37. [Medline].

2. 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].

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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
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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
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