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

The family Campylobacteraceae includes 2 genera: Campylobacter and Arcobacter. The genus Campylobacter includes 18 species and subspecies; 11 of these are considered pathogenic to humans and cause enteric and extraintestinal illnesses. The major pathogens are Campylobacter jejuni and Campylobacter fetus. The following Campylobacter species and subspecies are pathogenic to humans:

• Enteric
• • C jejuni subspecies jejuni
  • C jejuni subspecies doylei
  • Campylobacter coli
  • Campylobacter upsaliensis
  • Campylobacter lari
  • C fetus subspecies fetus
  • Campylobacter hyointestinalis
  • Campylobacter concisus
• Extraintestinal
• • C jejuni subspecies jejuni
  • C upsaliensis
  • C lari
  • C fetus subspecies fetus
  • C concisus
  • Campylobacter sputorum
  • Campylobacter curvus
  • Campylobacter rectus

Campylobacter pylori has been reclassified as Helicobacter pylori and is not addressed in this article (see Helicobacter Pylori Infection).

Campylobacter pathogens are small, curved, motile, microaerophilic, gram-negative rods. They vary in width from 0.2-0.9 mm and vary in length from 0.5-5.0 mm. They exhibit rapid, darting motility in corkscrew fashion using a single flagellum or 2 flagella (monotrichous, amphitrichous). They also possess a lipopolysaccharide endotoxin.

Campylobacteriosis infects humans and animals. The animal reservoir is the gastrointestinal tract of dogs, cats, and other pets that can carry the organism. Transmission of C jejuni to humans occurs by ingestion of contaminated food or water, including unpasteurized milk and undercooked poultry, or by direct contact with fecal material from infected animals or persons. The 2 types of illnesses associated with Campylobacter infections in humans are intestinal infection and extraintestinal infection. The prototype for intestinal infection is C jejuni, and the prototype for extraintestinal infection is C fetus.

Pathophysiology

Factors responsible for the diseases caused by C jejuni are not well known. Based on clinical illness, researchers have postulated 3 mechanisms, as follows:

• Adherence and production of heat-labile enterotoxins, inducing secretory diarrhea
• Invasion and proliferation within the intestinal epithelium, leading to cell damage and inflammatory response
• Translocation of the organism into the intestinal mucosa and proliferation in the lamina propria and mesenteric lymph nodes, leading to extraintestinal infections such as meningitis, cholecystitis, urinary tract infection, and mesenteric adenitis

Information on the pathogenesis of Campylobacter infections other than C jejuni is scarce. Bacteremia is more common with C fetus infection. A surface protein in C fetus inhibits the C3b binding responsible for both the serum and phagocytic resistance of the organism, making the organism resistant to the bactericidal effects of human serum. After oral ingestion, C fetus may colonize the intestinal tract, resulting in portal bacteremia. In immunocompetent hosts, the organism is phagocytosed by the reticuloendothelial cells in the liver, preventing further spread. However, in patients that have predisposing factors that might serve as a local site of infection such as a gravid uterus, bacteremia can lead to severe complications. Infants may be affected hematogenously or by ascending infection during amnionitis and premature rupture of membranes.

Frequency

United States

In the United States, 2 million symptomatic enteric Campylobacter infections are estimated per year (1% of the US population per year). Incidence in the rural population is 5-6 times higher because of increased consumption of raw milk. In 2005, the overall incidence rate of laboratory-confirmed Campylobacter infections in the United States was 12.7 cases per 100,000 population.¹ However, the incidence rate of symptomatic Campylobacter infections has been estimated to be 760-1100 cases per 100,000 population.²

International

In developing countries, C jejuni is often isolated from stools of healthy individuals and is especially common during the first 5 years of life. Isolation rates in children who are asymptomatic or in children with diarrhea range from 8-45%, with an annual incidence rate as high as 2.1 episodes of Campylobacter-associated diarrhea per child.

In developed countries, the average incidence rate of Campylobacter bacteremia is estimated to be 1.5 per 1000 patients with enteritis.

Mortality/Morbidity

• The vast majority of patients fully recover from C jejuni infection within 5 days (range, 2-10 d), either spontaneously or after appropriate antimicrobial therapy. The symptomatic Campylobacter infection–associated mortality rate in the United States is estimated to be 24 deaths per 10,000 culture-confirmed cases (200 deaths per year).
• Infection with C fetus is a concern in immunocompromised patients, pregnant women, and neonates.
• Previously healthy patients usually recover without complications.

Race

• Campylobacter infection has no race predilection.

Sex

• In individuals aged 45 years or younger, the C jejuni isolation rate is higher in males than in females. In individuals older than 45 years, no sexual predilection is reported.
• In the adult population, the male-to-female C fetus infection ratio is 3:1.
• No sex predilection is noted in children.

Age

• Individuals of any age can be infected with C jejuni enteritis. The rate of infection differs between developed and developing countries. In developed countries, the peak attack rates are in infants younger than 1 year; a second, broader peak attack rate occurs in persons aged 15-30 years. In developing countries, symptomatic infection chiefly affects children younger than 5 years and declines with age. This is likely due to the development of protective immunity secondary to a high level of exposure to the organism early in life.
• In contrast to the age-specific distribution of Campylobacter enteritis, the highest rate of bacteremia occurs in patients aged 65 years and older. In this age group, the incidence rate of Campylobacter bacteremia is 1 case per 170 intestinal infections; in children younger than 14 years, the incidence rate is 1 case per 3000 intestinal infections. Roughly 60-90% of isolates are C jejuni or C coli; 8-15% are C fetus. In children from developing countries, bacteremia appears common, occurring in 45 per 1000 cases of intestinal infection. C jejuni subspecies jejuni accounts for 41% of these infections, C jejuni subspecies doylei accounts for 24%, and C upsaliensis accounts for 5.6%.

CLINICAL

Section 3 of 10  

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

History

Clinical manifestations of all Campylobacter species infections that cause enteric illness overlap and appear identical. These manifestations include the following:

• Diarrhea
• • Mild episodes of diarrhea subside within 7 days in 60-70% of cases, last for 2 weeks in 20-30%, and persist longer than 2 weeks in 5-10% of cases. In one third to one half of patients, initial symptoms include periumbilical cramping, intense abdominal pain that mimics appendicitis, malaise, myalgias, headache, and vomiting.
  • Watery secretory diarrhea consists of more than 10 stools per day and is frequently seen in younger children. Dehydration occurs in approximately 10% of these children.
  • Inflammatory diarrhea symptoms are indistinguishable from those caused by Shigella organisms, Escherichia coli, and Salmonella species. They are characterized by malaise, fever, abdominal cramps, tenesmus, bloody stools, and fecal leukocytes on light microscopy. Rarely, in young adults and adolescents, inflammatory diarrhea can be severe and can be confused with Crohn disease and ulcerative colitis. Toxic megacolon with massive bleeding may occasionally occur. In asymptomatic neonates, C jejuni has been isolated from blood-streaked formed stools or hematochezia.
• Extraintestinal infections
• • Bacteremia with C jejuni is uncommon and is most frequently found in patients with immunodeficiency, patients with chronic illness, and patients at extremes of ages. Bloodstream infections and systemic infections by C fetus are rare. The 3 patterns of bacteremia are as follows:
  • • Transient bacteremia in a normal host with acute Campylobacter enteritis: These patients usually completely recover without treatment.
    • Secondary bacteremia or deep focus of infection such as meningitis, pneumonia, endocarditis, and thrombophlebitis in a normal host: Bacteremia usually originates from the intestinal tract and responds to antimicrobial therapy. 
    • Chronic bacteremia with relapses that can persist for several months occurring in an immunocompromised host: In these patients, bacteremia can also arise from an infected indwelling catheter. Many such patients do not have acute enteritis.
• • Localized extraintestinal infections are uncommon manifestations and include cholecystitis, arthritis, urinary tract infection, pancreatitis, osteomyelitis, and meningitis. These manifestations may be the initial presentation of C jejuni infection or may occur simultaneously with bacteremia. They frequently are seen in patients who are immunocompromised or who are at extremes of age. Appropriate treatment is necessary.
• Because of the affinity of C fetus for the genital tract (and by the tropism for fetal tissue), C fetus and, rarely, C jejuni are associated with perinatal infection. Abortion or stillbirth and premature labor have been described. Infants are often premature and develop signs and symptoms suggestive of sepsis, including fever, cough, respiratory distress, vomiting, diarrhea, cyanosis, convulsions, and jaundice. Infection typically progresses to meningitis, which may be rapidly fatal or may result in serious neurologic sequelae. The source of the organism in these cases has been the mother.

Physical

• The abdomen is frequently tender upon palpation, especially the right lower quadrant.
• Rarely, splenomegaly may be present.

Causes

• Individuals at increased risk for Campylobacter enteritis include the following:
• • Those with occupational exposure to cattle, sheep, and other farm animals
  • Laboratory workers
  • Those in contact with the excreta of infected persons
  • Homosexual men
• The following underlying conditions increase risk for Campylobacter bacteremia, suggesting the importance of both humoral and cell-mediated immunity:
• • Hypogammaglobulinemia
  • Human immunodeficiency virus (HIV) infection
  • Kwashiorkor
  • Pregnancy
  • Malignancy
  • Extremes of age
  • Alcoholism
  • Diabetes mellitus
  • Postsplenectomy status
  • Human leukocyte antigen B27 (HLA-B27) - Increases risk for immunoreactive complications, such as reactive arthritis or Reiter syndrome

DIFFERENTIALS

Section 4 of 10  

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

Other Problems to be Considered

• Other bacterial causes of inflammatory diarrhea
• • Shigella organism
  • Enteroinvasive E coli
  • E coli O157:H7
  • Salmonella species
  • Yersinia enterocolitica
  • Aeromonas species 
  • Vibrio parahaemolyticus
• Inflammatory bowel disease
• Pseudomembranous enterocolitis secondary to Clostridium difficile infection
• Intussusception in infants
• Acute abdomen 
• Acute appendicitis

WORKUP

Section 5 of 10  

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

Lab Studies

• Microbiologic studies
• • Presumptive diagnosis can be made by examination of fecal specimens by darkfield or phase-contrast microscopy, which demonstrates the characteristic darting motility, and a Gram stain of the stool, which shows Vibrio forms (slim, short, curved rods). RBCs and neutrophils are present in stool in approximately 75% of patients with Campylobacter enteritis.
  • Definitive diagnosis of infection is based on isolation of organisms from stool culture or from another site.
  • Culture of C jejuni from stool requires special isolation techniques and special media such as Campy-BAP or Skirrow. These media contain antibiotics that reduce the emergence of other enteric microorganisms. Inoculated media should be incubated in 5% oxygen and 10% carbon dioxide at 42°C. If C fetus or other atypical enteric species are suspected, isolation from stool requires inoculation on media lacking antibiotics and at 37°C. Filtration technique may be needed. Routine media are adequate for isolation of Campylobacter from normally sterile sites such as blood, body fluids, and tissues.
• Hematology and blood chemistries
• • Peripheral WBC count is usually within the reference range; however, a left shift may occur.
  • The alanine aminotransferase level and the erythrocyte sedimentation rate (ESR) may be slightly elevated.
  • Other laboratory evaluations are within the reference ranges.
• Serology
• • Diagnostic rise usually occurs after symptoms have resolved. Because the median duration of fecal excretion in the convalescent phase is less than 3 weeks, serology testing may be more sensitive than culture for the diagnosis of recent C jejuni infection.
  • Although serologic testing is also useful for epidemiologic investigations it is not recommended for routine diagnosis.

Other Tests

• DNA probes and polymerase chain reaction are mainly research tools at this time and are not routinely performed.

Procedures

• Normal mucosa is found in 50% of patients who undergo proctoscopy secondary to a prolonged course of Campylobacter enteritis. Mucosal edema, congestion, friability, and granularity are seen in the remaining half.

Histologic Findings

The spectrum of histologic findings in the intestinal tract ranges from minimal edema with acute and chronic inflammatory cells without vascular congestion, to moderate inflammation and cryptitis, to crypt abscess formation. For perinatal infections secondary to C jejuni and C fetus, the placenta may have areas of necrosis, infarction, microabscesses, and inflammation.

TREATMENT

Section 6 of 10  

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

Medical Care

• Evaluation can usually be performed on an outpatient basis.
• Intravenous hydration and inpatient care may be necessary for patients who are severely dehydrated and cannot tolerate oral hydration.

Surgical Care

• Occasionally, acute abdominal pain may be the only presenting symptom, often mimicking acute appendicitis and resulting in immediate laparotomy.

Consultations

• Consultation with an infectious disease specialist and a gastroenterologist may be necessary for complicated cases.

Diet

• Because rehydration and electrolyte replacement are the mainstays for treating diarrheal disease, oral rehydration with an electrolyte and glucose solution is necessary.

Activity

• Permit activity as tolerated.

MEDICATION

Section 7 of 10  

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

Most C jejuni infections are generally mild and self-limited. The need to administer antimicrobials in uncomplicated cases is still controversial. Correction of electrolyte abnormalities and rehydration are the mainstay of treatment for enteritis due to Campylobacter species. Antimicrobial therapy should be considered in immunocompromised hosts or in individuals with fever, increasing bloody diarrhea, or symptoms that last longer than 1 week.

C jejuni is usually sensitive to erythromycin, azithromycin, gentamicin, tetracycline, and chloramphenicol. Reports of ciprofloxacin-resistant strains are increasing in most countries, especially in Thailand. In adults, placebo-controlled studies of erythromycin demonstrate no improvement in the clinical symptoms if administered late in the course of illness but have resulted in decreased fecal shedding. If an appropriate antibiotic therapy was initiated within the first 4 days of illness, a reduction in the excretion of the organism was noted; however, results regarding the resolution of symptoms were controversial. In contrast, early erythromycin treatment for children with bloody diarrhea shortened both the duration of diarrhea and excretion of microbes in the stool.

The recommended duration for antibiotic treatment for gastroenteritis is 5-7 days. Antimicrobial therapy for all immunocompromised patients with C jejuni bacteremia should be selected based on a laboratory susceptibility test. Begin therapy with gentamicin, imipenem, third-generation cephalosporins, or chloramphenicol until susceptibility test results are available. Because infections with C fetus usually are systemic, intravenous antibiotics are usually required. Aminoglycosides, such as gentamicin, are usually the drugs of choice (DOC).

Alternatives for C fetus bacteremia include ampicillin, imipenem, chloramphenicol, and third-generation cephalosporins. Reported synergistic combinations include ampicillin with gentamicin and imipenem with gentamicin. Duration of therapy is empiric.

Patients with CNS infection require treatment for 2-3 weeks with a third-generation cephalosporin, ampicillin, or chloramphenicol. Those with endovascular infection should be treated for at least 4 weeks with gentamicin as the DOC. Treatment with ampicillin or third-generation cephalosporins are other alternatives. Erythromycin is the DOC in patients with diarrheal illness secondary to C fetus infection.

Drug Category: Macrolide antibiotics

Ease of administration, lack of serious adverse effects, and fewer propensities to select for plasmid-mediated antibiotic resistance make erythromycin the DOC.

Drug Name	Azithromycin (Zithromax)
Description	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. Single dose is recommended. May become DOC because of safety profile, ease of use, and improved GI tract tolerability relative to erythromycin. Administer caps and oral susp on an empty stomach, at least 1 h before or 2 h after meals. Tab and oral powder (sachet) may be administered with food.
Adult Dose	Day 1: 500 mg PO Days 2-5: 250 mg/d PO
Pediatric Dose	<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/d PO; not to exceed 250 mg/d
Contraindications	Documented hypersensitivity; hepatic impairment; do not administer with pimozide
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
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, prolonged QT intervals, or pneumonia; caution in hospitalized, geriatric, or debilitated patients

Drug Category: Tetracyclines

These agents may be used in children but are not approved for children younger than 9 years because of the risk of dental staining.

Drug Category: Lincosamide antibiotics

These drugs represent an alternative to tetracycline.

Drug Category: Aminoglycoside antibiotics

Reserve these drugs for treatment of infections caused by organisms not sensitive to less toxic agents.

Drug Category: Fluoroquinolone antibiotics

Ciprofloxacin and other fluoroquinolones are alternative agents to erythromycin but are not approved for those younger than 18 years.

Drug Category: Antibiotics, other

Alternatives for C fetus bacteremia include ampicillin, imipenem, chloramphenicol, and third-generation cephalosporins. Reported synergistic combinations include ampicillin with gentamicin and imipenem with gentamicin. Duration of therapy is empiric.

Drug Name	Chloramphenicol (Chloromycetin)
Description	Binds to 50 S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effective against gram-negative and gram-positive bacteria.
Adult Dose	50-100 mg/kg/d IV divided q6h; not to exceed 4 g/d
Pediatric Dose	Neonates: Loading dose: 20 mg/kg IV Maintenance dose: Administer first maintenance dose 12h after loading dose <7 days: 25 mg/kg/d IV qd >7 days: <2 kg: 25 mg/kg/d IV qd >2 kg: 50 mg/kg/d IV divided q12h Infants/children: 50-100 mg/kg/d IV divided q6h; not to exceed 4 g/d
Contraindications	Trivial infections or prophylaxis; previous toxic reactions to chloramphenicol; G-6-PD deficiency
Interactions	Avoid other agents that cause bone marrow depression; may increase effects of hydantoins or sulfonylureas; may increase serum iron levels, decrease response to iron, vitamin B-12 When administered concurrently with barbiturates, chloramphenicol serum levels may decrease and barbiturate levels may increase, causing toxicity; rifampin may reduce serum chloramphenicol levels, presumably through hepatic enzyme induction; may increase effects of anticoagulants
Pregnancy	D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions	Caution in pregnancy at term or during labor because of potential toxic effects on fetus (gray baby syndrome) Perform blood tests at baseline and q2d during therapy; discontinue if blood dyscrasias, optic neuritis, or peripheral neuritis develops; avoid repeat therapy; monitor serum levels; breastfeeding women

Drug Name	Ceftriaxone (Rocephin)
Description	Third-generation cephalosporin. Arrests bacterial growth by binding to one or more penicillin-binding proteins.
Adult Dose	1-4 g/d IV divided q12-24h; not to exceed 4 g/d
Pediatric Dose	Infants and children: 50-75 mg/kg/d IM/IV divided q12-24h Meningitis: 100 mg/kg/d IV/IM divided q12-24h; not to exceed 4 g/d
Contraindications	Documented hypersensitivity
Interactions	May cause false-positive Clinitest results; potentiated by probenecid
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Penicillin or other allergy; concomitant renal and hepatic impairment, (not to exceed 2 g/d); chronic hepatic disease or malnutrition, monitor prothrombin time; GI disease

Drug Name	Ampicillin (Marcillin, Omnipen)
Description	Broad-spectrum penicillin. Bactericidal activity against susceptible organisms.
Adult Dose	500-3000 mg IV q4-6h; not to exceed 12 g/d IV
Pediatric Dose	Neonates <7 days: <2 kg: 50-100 mg/kg/d IV divided q12h >2 kg: 75-150 mg/kg/d IV divided q8h Neonates >7 days: <1.2 kg: 50-100 mg/kg/d IV divided q12h 1.2-2 kg: 75-150 mg/kg/d IV divided q8h >2 kg: 100-200 mg/kg/d IV divided q6h Children: Mild-to-moderate infections: 100-200 mg/kg/d IV divided q6h Severe infections: 200-400 mg/kg/d IV divided q4-6h
Contraindications	Documented hypersensitivity; contraindicated in infections caused by penicillinase-producing organism
Interactions	May cause false-positive Clinitest result; potentiated by probenecid
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	May have cross-sensitivity with cephalosporins or imipenem; high incidence of rash with mononucleosis; monitor blood, renal, and liver function with long-term use

FOLLOW-UP

Section 8 of 10  

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

Further Inpatient Care

• Evaluate protracted cases further to rule out other causes of fever, diarrhea, and sepsis.
• Provide close monitoring and support in the intensive care unit for immunoreactive complications such as Guillain-Barré syndrome (GBS).

Further Outpatient Care

• Assess the resolution of illness and patient compliance with medication.

In/Out Patient Meds

• Rehydrate intravenously or orally.
• Administer antibiotics as indicated.

Transfer

• Patients with immunoreactive complications such as GBS may require transfer to a chronic care facility for rehabilitation after their condition stabilizes.

Complications

• Guillain-Barré syndrome
• • GBS is a disorder of peripheral nerves and is characterized by ascending paralysis.
  • GBS occurs more often in males (male-to-female ratio of 3:1), during summertime, and in adults.
  • A disproportionate amount of GBS-associated C jejuni belongs to a rare serotype called Penner (lipopolysaccharide) type 0:19. Other variants of GBS include the following:
  • • Acute motor axonal neuropathy (AMAN) or Chinese paralytic syndrome: This syndrome is characterized by a rapid onset of paralysis with progression to tetraplegia and respiratory failure and occurs in children in northern China during summer and fall.
    • Fisher syndrome is characterized by ophthalmoplegia, areflexia, and cerebellar ataxia.
  • Strong evidence suggests an association between preceding C jejuni infection and GBS. The antigenic similarity between specific regions (terminal tetrasaccharide) of lipopolysaccharide of C jejuni and human gangliosides (GM1) led to the concept of molecular mimicry. This concept implies the sharing of homologous epitopes between the bacterial lipopolysaccharide and ganglioside surface components of the peripheral nerve. Immune response from simple C jejuni infection could induce antibodies that cross-react to the gangliosides and trigger GBS.
• Reactive arthritis
• • Sixty percent of patients are positive for HLA-B27; this is more common in young men.
  • Arthritis starts a few days to several weeks after the episode of diarrhea. Joint involvement is usually monoarticular and affects the knees. The course is self-limited, ranging from 1 week to several months.
  • Synovial fluid is sterile, fever and leukocytosis are absent, and ESR is elevated
• Other infrequently reported complications are as follows:
• • Reiter syndrome
  • Erythema nodosum
  • Hepatitis
  • Intestinal nephritis
  • Hemolytic-uremic syndrome
  • Immunoglobulin A (IgA) nephropathy

Prognosis

• Most patients fully recover after C jejuni infection, with or without antibiotics.
• Campylobacter septicemia in patients with immune deficiencies (including congenital hypogammaglobulinemia, acquired hypogammaglobulinemia, malnutrition, HIV) and in neonates is associated with a high mortality rate.
• Even with plasmapheresis and intravenous immunoglobulin, as many as 20% of patients with GBS may require mechanical ventilation. Between 15% and 20% of all patients may develop severe neurologic deficit. GBS disease may result in mortality in 5-10% of all patients. Because GBS secondary to C jejuni may be more severe, the number of patients who require mechanical ventilation, experience severe neurologic sequelae, and die may also be higher.
• Previously healthy persons infected with C fetus usually recover without sequelae. This infection may be lethal to patients with altered immune status and neonates. Prognosis for these patients depends on the early administration of fluids and appropriate antimicrobial therapy.

Patient Education

• Tips for preventing campylobacteriosis
• • Thoroughly cook all poultry products. If served undercooked poultry in a restaurant, return it for further cooking.
  • Wash hands with soap before and after handling raw foods of animal origin.
  • Prevent cross-contamination in the kitchen
  • • Use separate cutting boards for foods of animal origin and other foods.
    • Carefully clean all cutting boards, countertops, and utensils with soap and hot water after preparing raw food of animal origin.
  • Avoid consuming unpasteurized milk and untreated surface water.
  • Make sure that persons with diarrhea, especially children, carefully and frequently wash their hands with soap to reduce the risk of spreading infection.
  • Wash hands with soap after contact with pet feces.

MISCELLANEOUS

Section 9 of 10  

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

Medical/Legal Pitfalls

• Failure by physicians and clinical laboratories to report diagnosis of campylobacteriosis to local health departments to further prevent possible outbreaks.

Special Concerns

• Because of the widespread use of antibiotics, especially quinolones, in humans and animal food, increasing resistance to these agents is reported.

REFERENCES

Section 10 of 10

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

1. CDC. Preliminary FoodNet data on the incidence of infection with pathogens transmitted commonly through food--10 states, 2006. MMWR Morb Mortal Wkly Rep. Apr 13 2007;56(14):336-9. [Medline].
2. Long SS, ed. Principles and Practice of Pediatric Infectious Diseases. 2^nd ed. Churchill Livingstone; 2003:890-4.
3. Allos BM. Campylobacter jejuni infection as a cause of the Guillain-Barre syndrome. Infect Dis Clin North Am. Mar 1998;12(1):173-84. [Medline].
4. Allos BM. Campylobacter jejuni Infections: update on emerging issues and trends. Clin Infect Dis. Apr 15 2001;32(8):1201-6. [Medline].
5. Blaser M. Development of Guillain-Barre syndrome following Campylobacter infection. J Infect Dis. 1997;176 Supp 2:S91-200. [Medline].
6. 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].
7. Blaser MJ. Epidemiologic and clinical features of Campylobacter jejuni infections. J Infect Dis. Dec 1997;176 Suppl 2:S103-5. [Medline].
8. Feigin RD, Cherry J, Demmler G, Kaplan S, eds. Textbook of Pediatric Infectious Diseases. Vol 1. 5^th ed. WB Saunders; 2003:1612-1628.
9. Gurtler M, Alter T, Kasimir S, Fehlhaber K. The importance of Campylobacter coli in human campylobacteriosis: prevalenceand genetic characterization. Epidemiol Infect. Dec 2005;133(6):1081-7. [Medline].
10. Hahn AF. Guillain-Barre syndrome. Lancet. Aug 22 1998;352(9128):635-41. [Medline].
11. Hein I, Schneck C, Knogler M, et al. Campylobacter jejuni isolated from poultry and humans in Styria, Austria: epidemiology and ciprofloxacin resistance. Epidemiol Infect. Jun 2003;130(3):377-86. [Medline].
12. Helms M, Simonsen J, Molbak K. Foodborne bacterial infection and hospitalization: a registry-based study. Clin Infect Dis. Feb 15 2006;42(4):498-506. [Medline].
13. Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Diseases. 6^th ed. Churchill Livingstone; 2005:2455-8.
14. Pickering LK, et al. Report of the Committee on Infectious Diseases. In: Red Book. 27^th ed. American Academy of Pediatrics; 2006:240-2.
15. Remington JS, Klein JO, eds. Infectious Diseases of the Fetus and Newborn Infant. 5^th ed. WB Saunders; 2001:1275-81.
16. Ruiz J, Marco F, Oliveira I, Vila J, Gascon J. Trends in antimicrobial resistance in Campylobacter spp. causing traveler's diarrhea. APMIS. Mar 2007;115(3):218-24. [Medline].
17. Serichantalergs O, Dalsgaard A, Bodhidatta L, et al. Emerging fluoroquinolone and macrolide resistance of Campylobacter jejuni and Campylobacter coli isolates and their serotypes in Thai children from 1991 to 2000. Epidemiol Infect. Feb 19 2007;1-8. [Medline].

Article Last Updated: Sep 7, 2007