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FOODBORNE ILLNESS-CAMPYLOBACTER

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Campylobacter jejuni is a gram-negative, curved, motile, microaerophilic rod-shaped bacteria. Estimates indicate that Campylobacter jejuni is the third leading cause of bacterial foodborne illness in the United States.

Specific Substances

    1) Campylobacter (synonym)
    2) Campylobacter jejuni (synonym)
    3) Campylobacterosis (synonym)
    4) Campylobacter enteritis (synonym)
    5) Campylobacter gastroenteritis (synonym)
    6) Food poisoning Campylobacter (synonym)
    7) Campylobacter food poisoning (synonym)
    8) Campylobacter fetus (synonym)

Available Forms Sources

    A) FORMS
    1) Greater than 80% (Center for Food Safety and Applied Nutrition (CFSAN), 2012) of Campylobacter enteritis cases are caused by C jejuni, but C coli may also cause disease (Engberg, 2006). A strain recognized as Campylobacter fetus causes fetal and neonatal infections (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    2) Specific Campylobacter jejuni toxins that may be responsible for causing the symptoms of infection have not been identified. Motile C. jejuni invade gastrointestinal mucosa but the mechanism for pathogenesis is not known (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    B) SOURCES
    1) INCIDENCE
    a) Estimates indicate that Campylobacter jejuni is the third leading cause of bacterial foodborne illness in the United States. In 2008, 12.68 cases were reported for every 100,000 individuals. Annually, an estimated 845,024 cases occur and approximately 99 deaths are attributed to C. jejuni in the United States. Additionally, it is thought that for each reported case of campylobacteriosis, 30 cases remain unreported (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    2) ANIMAL SOURCES
    a) Campylobacter occurs as natural gut microflora of most food-producing animals including chickens, turkeys, swine, cattle, and sheep (Center for Food Safety and Applied Nutrition (CFSAN), 2012). Surveys have found that anywhere from 20% to 100% of chickens available in the retail market are contaminated with C. jejuni. (Center for Food Safety and Applied Nutrition (CFSAN), 2009). A contaminated poultry carcass may contain 100 to 100,000 Campylobacter cells (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    3) FOOD CONTAMINATION
    a) Common food sources include improperly handled or undercooked poultry, unpasteurized milk and cheese, and nonchlorinated water (ponds and streams). Campylobacter jejuni has also been detected in seafood and vegetables (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    4) TARGET POPULATION
    a) Campylobacter infection most commonly affects children under the age of 5 years. In developing countries, it is most common in children up to age 2 years, and causes relatively mild symptoms, primarily watery diarrhea. In developed countries there is a second peak in young adults aged 15 to 24 years, which tends to be associated with more severe clinical manifestations (abdominal cramps, bloody diarrhea, and fever) (Havelaar et al, 2009). This peak does not occur in developing countries, and this difference is believed to be related to host immunity (Zilbauer et al, 2008). The highest incidence of Campylobacter infection is among infants 6 to 12 months of age (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    b) While most infections are self-limited, immunocompromised patients are at risk for more severe infections. Among similar age groups, the incidence of Campylobacter infection is about 40 times greater for individuals who have HIV/AIDS (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    c) Campylobacter infection in pregnant women may lead to fetal or neonatal infection, miscarriage, or stillbirths (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    5) TRANSMISSION
    a) Campylobacter jejuni is primarily transmitted through contaminated food. In humans, infection has been linked to eating and handling undercooked or raw meat and poultry (fresh or frozen) (Center for Food Safety and Applied Nutrition (CFSAN), 2012). There is also evidence of transmission from animal contact, environmental sources, and rarely human-to-human transmission (Havelaar et al, 2009). Campylobacter fetus infections are frequently the result of animal contact but may also develop after consumption of contaminated food (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    6) DISEASE
    a) Pathogenesis varies based on the virulence of the infecting organism. Campylobacteriosis results in a form of gastritis called Campylobacter enteritis, which is most often self-limiting and requires no treatment. In rare cases, bacteremia, meningitis, hepatitis, cholecystitis, or pancreatitis may develop. Bacteremia occurs in about 1.5 cases for every 1000 cases of gastroenteritis (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    1) LONG-TERM COMPLICATIONS: Some autoimmune disorders such as Guillan-Barre syndrome (GBS) and reactive arthritis are associated with campylobacteriosis. Studies show that 40% of GBS patients had a prior Campylobacter infection; approximately one case of GBS occurs for every 2000 Campylobacter jejuni infections. The onset of GBS after C. jejuni infection is about 2 to 3 weeks. Reactive arthritis develops in approximately 2% of C. jejuni gastroenteritis cases. One explanation for the association between autoimmune disorders and Campylobacter infection is that C. jejuni possesses antigens similar to those found in human nervous tissues, which triggers an autoimmune reaction (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    2) Recurrent colitis and hemolytic uremic syndrome have been reported after C. jejuni infection (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    b) Most cases of Campylobacter enteritis are sporadic. A small number of outbreaks have been reported. Sources have included raw milk and contaminated water (Engberg, 2006).
    7) TIME TO ONSET
    a) Symptoms usually develop about 2 to 5 days after ingestion of contaminated food or water (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    8) DURATION
    a) Campylobacter infections are typically self-limited. Symptoms resolve within 2 to 14 days (mean 10 days), but relapses develop in about 25% of patients (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Engberg, 2006).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) CAUSATIVE ORGANISM
    1) Campylobacter jejuni is a gram-negative, curved, motile, microaerophilic rod-shaped bacteria.
    B) TOXIN
    1) Specific Campylobacter jejuni toxins that may be responsible for causing the symptoms of infection have not been identified.
    C) EPIDEMIOLOGY
    1) Campylobacter jejuni is estimated to be the third leading cause of bacterial foodborne illness in the United States. Illness is usually self-limited. Approximately 99 deaths annually are attributed to Campylobacter jejuni infection in the United States.
    D) TARGET POPULATION
    1) Children under the age or 5, and young adolescents and young adults aged 15 to 29 years are most often affected. Fatalities are most common among individuals who are in otherwise poor health.
    E) MECHANISM
    1) Unknown.
    F) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) Diarrhea can be watery or sticky, and may contain blood or white blood cells. Fever, abdominal pain, nausea, vomiting, headache and muscle pain may also develop. Patients who develop Campylobacter septicemia can have secondary infections of virtually any organ. Myocarditis is a rare complication.
    2) CHRONIC SYMPTOMS
    a) Most patients recover without complications, but reactive arthritis, hemolytic uremic syndrome, and Guillain-Barre syndrome have been reported in a small minority of patients.
    3) ROUTE OF EXPOSURE
    a) Most common sources of exposure are undercooked chicken, raw milk and, less often, non-chlorinated water.
    4) TIME TO ONSET
    a) Usually 2 to 5 days after ingestion of contaminated food or water.
    5) DURATION
    a) Symptoms generally last 2 to 14 days; relapse is common, developing in about 25% of patients.
    0.2.20) REPRODUCTIVE
    A) Campylobacter jejuni and more specifically C. fetus may lead to fetal or neonatal infection. C. fetus infections are associated with a mortality rate of up to 70% among neonates and fetuses of pregnant women. There are 20 cases of septic abortion induced by C jejuni reported in the medical literature.

Laboratory Monitoring

    A) Monitor serum electrolytes in patients with severe diarrhea or vomiting. Monitor for clinical evidence of dehydration.
    B) Stool cultures are rarely necessary as most infections are self-limited. If necessary Campylobacter jejuni can be isolated from stool, but the organism requires special handling.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is primarily symptomatic and supportive. Illness is often mild. Significant nausea and vomiting may be controlled with an antiemetic agent. Patients with moderate to severe dehydration may require IV rehydration.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Antibiotics should be considered in patients with severe disease, extra-intestinal manifestations, and those who are immunocompromised.
    C) DECONTAMINATION
    1) PREHOSPITAL or HOSPITAL: GI decontamination is not indicated
    D) ANTIBIOTIC THERAPY
    1) Most infections are self-limited and do not require antibiotic treatment. Antibiotics should be considered in patients with severe disease, extra-intestinal manifestations, and those who are immunocompromised. Macrolides are the drugs of choice. ERYTHROMYCIN: ADULT: 500 mg twice a day for 5 days. AZITHROMYCIN: ADULT: 500 mg daily for 3 days. PEDIATRIC: 10 mg/kg orally once daily for 3 days.
    E) MONITORING OF PATIENT
    1) In most cases, routine laboratory studies are not indicated. Monitor serum electrolytes in patients with severe diarrhea or vomiting. Evaluate for evidence of dehydration. Stool cultures are rarely necessary as most infections are self-limited. If necessary, Campylobacter jejuni can be isolated from stool, but the organism requires special handling.
    F) PATIENT DISPOSITION
    1) HOME CRITERIA: Most patients will develop mild, self-limited symptoms that can be managed at home with oral rehydration.
    2) ADMISSION CRITERIA: All patients with significant toxicity, severe dehydration, clinical instability, abnormal electrolyte concentrations, or significant underlying health problems should be admitted for intravenous rehydration therapy.
    3) OBSERVATION CRITERIA: Patients with severe symptoms should be sent to a healthcare facility for evaluation and treatment.
    G) PITFALLS
    1) While most infections are self-limited, immunocompromised patients are at risk for more severe infections.
    H) DIFFERENTIAL DIAGNOSIS
    1) The differential diagnosis includes infection with other bacteria (eg, Clostridium perfringens or Staphylococcus aureus) or exposure to nonbacterial (eg, viruses, plants or mushroom ingestion) causes of acute gastroenteritis or exposure to chemicals (eg, insecticides, pesticides).

Range Of Toxicity

    A) Infectious dose varies based on the health of the individual and the type of contaminated food ingested. Ingestion of as few as 500 bacteria cells may cause illness in some individuals, but it is thought that ingestion of a minimum of 10,000 cells is needed to cause infection. About 5% to 10% of patients may require hospitalization. The case fatality ratio is estimated to be between 0.05 (5 deaths in 10,000 cases) and 0.1 (one death per thousand infections). Fatalities are very rare in healthy individuals. Immunocompromised patients are at increased risk.

Clinical Effects

Summary Of Exposure

    A) CAUSATIVE ORGANISM
    1) Campylobacter jejuni is a gram-negative, curved, motile, microaerophilic rod-shaped bacteria.
    B) TOXIN
    1) Specific Campylobacter jejuni toxins that may be responsible for causing the symptoms of infection have not been identified.
    C) EPIDEMIOLOGY
    1) Campylobacter jejuni is estimated to be the third leading cause of bacterial foodborne illness in the United States. Illness is usually self-limited. Approximately 99 deaths annually are attributed to Campylobacter jejuni infection in the United States.
    D) TARGET POPULATION
    1) Children under the age or 5, and young adolescents and young adults aged 15 to 29 years are most often affected. Fatalities are most common among individuals who are in otherwise poor health.
    E) MECHANISM
    1) Unknown.
    F) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) Diarrhea can be watery or sticky, and may contain blood or white blood cells. Fever, abdominal pain, nausea, vomiting, headache and muscle pain may also develop. Patients who develop Campylobacter septicemia can have secondary infections of virtually any organ. Myocarditis is a rare complication.
    2) CHRONIC SYMPTOMS
    a) Most patients recover without complications, but reactive arthritis, hemolytic uremic syndrome, and Guillain-Barre syndrome have been reported in a small minority of patients.
    3) ROUTE OF EXPOSURE
    a) Most common sources of exposure are undercooked chicken, raw milk and, less often, non-chlorinated water.
    4) TIME TO ONSET
    a) Usually 2 to 5 days after ingestion of contaminated food or water.
    5) DURATION
    a) Symptoms generally last 2 to 14 days; relapse is common, developing in about 25% of patients.

Vital Signs

    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) Fever is a fairly common finding (Galanis, 2007).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) MYOCARDITIS
    1) WITH POISONING/EXPOSURE
    a) Myocarditis is a rare complication that can occur within a week of Campylobacter enteritis.
    b) CASE REPORT: A 24-year-old man with Noonan syndrome developed multiple episodes of chest pain over 2 days. He also reported 6 days of diarrhea, fevers and diaphoresis which started after eating from a buffet at a wedding. An initial ECG showed widespread ST elevation, troponin T was elevated, and an echocardiogram showed a small pericardial effusion and an akinetic left ventricular apical segment. He was treated with aspirin, thrombolytics and opioids. Angiogram showed normal coronary arteries and Campylobacter jejuni was isolated from a stool. A cardiac MR 4 weeks later was consistent with recent myocarditis (Turley et al, 2008).
    c) CASE REPORT: A 19-year-old man presented with severe left sided chest pain 4 days after developing acute gastroenteritis. ECG showed ST elevation in posterior and lateral leads, and right heart strain, and troponin T was elevated. Coronary angiography was normal, but there was hypokinesis of the left ventricular apex. Stool culture revealed Campylobacter jejuni (Kratzer et al, 2010).
    d) CASE REPORT: A 43-year-old man presented with chest pain radiating to his jaw one week after an episode of enteritis. An ECG showed anterolateral ST elevation and troponin T was elevated. He was treated with thrombolytics. An echocardiogram showed possible apical akineses. Stool cultures grew Campylobacter jejuni and later angiography showed normal coronary arteries. He recovered (Mera et al, 2007).
    e) CASE REPORT: A 16-year-old boy presented with chest pain and dyspnea which developed after 5 days of bloody diarrhea, fever, headache and abdominal pain. An ECG showed ST elevation in leads I, II and V4-6, an echocardiogram showed reduce left ventricular ejection fraction, and troponin T was elevated. Campylobacter jejuni was isolated from stool. The patient recovered (Heinzl et al, 2010).
    f) CASE REPORT: A 17-year-old man presented with one day of chest pain radiating to his left arm, and 2 days of fever and diarrhea. An ECG showed ST elevation in leads I, AVL, and V4 and V5, and an echocardiogram was normal. Troponin T was elevated. Campylobacter jejuni was isolated from stool. Magnetic resonance tomography was consistent with myocarditis. He recovered (Heinzl et al, 2010).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache is fairly common (Engberg, 2006).
    B) GUILLAIN-BARRé SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Campylobacter enteritis is the most common infection preceding the development of Guillain-Barre syndrome (Kuwabara, 2011). Guillain-Barre develops in about 0.1% of patients with Campylobacter enteritis (Galanis, 2007).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting may develop, but are not common findings (Galanis, 2007).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea is characteristic and may be watery, bloody (Galanis, 2007), or sticky, and may contain leukocytes (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    C) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Abdominal pain is fairly common and can be severe and localized enough to mimic appendicitis (Galanis, 2007).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) HEMOLYTIC UREMIC SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Hemolytic uremic syndrome is a rare complication of Campylobacter enteritis (Center for Food Safety and Applied Nutrition (CFSAN), 2012).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) HEMOLYTIC UREMIC SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Hemolytic uremic syndrome is a rare complication of Campylobacter enteritis (Center for Food Safety and Applied Nutrition (CFSAN), 2012).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) ARTHRITIS
    1) WITH POISONING/EXPOSURE
    a) Reactive arthritis develops in about 1% to 5% of patients with Campylobacter enteritis (Galanis, 2007; Pope et al, 2007).

Reproductive

    3.20.1) SUMMARY
    A) Campylobacter jejuni and more specifically C. fetus may lead to fetal or neonatal infection. C. fetus infections are associated with a mortality rate of up to 70% among neonates and fetuses of pregnant women. There are 20 cases of septic abortion induced by C jejuni reported in the medical literature.
    3.20.3) EFFECTS IN PREGNANCY
    A) SEPTIC ABORTION
    1) Campylobacter fetus is a strain of Campylobacter that may cause fetal or neonatal infections. C. fetus may be transmitted by consumption of contaminated food or water but is often the result of animal contact. C. fetus infections are associated with a mortality rate of up to 70% among neonates and fetuses of pregnant women. C. jejuni may also cause fetal infections leading to miscarriage or stillbirth (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    2) There are 20 cases of septic abortion induced by C jejuni reported in the medical literature (Center for Food Safety and Applied Nutrition (CFSAN), 2009).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor serum electrolytes in patients with severe diarrhea or vomiting. Monitor for clinical evidence of dehydration.
    B) Stool cultures are rarely necessary as most infections are self-limited. If necessary Campylobacter jejuni can be isolated from stool, but the organism requires special handling.
    4.1.2) SERUM/BLOOD
    A) Monitor serum electrolytes in patients with severe diarrhea or vomiting. Monitor for clinical evidence of dehydration.
    B) Stool cultures are rarely necessary as most infections are self-limited.

Methods

    A) Campylobacter species can be identified rapidly in stool or food by latex agglutination tests (Miller et al, 2008).
    B) Campylobacter jejuni can be isolated from stool, but the organism requires special handling (antibiotic-containing culture media and 5% oxygen atmosphere) (Center for Food Safety and Applied Nutrition (CFSAN), 2012).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) All patients with significant toxicity, severe dehydration, clinical instability, abnormal electrolyte concentrations, or significant underlying health problems should be admitted for intravenous rehydration therapy.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Most patients will develop mild, self-limited symptoms that can be managed at home with oral rehydration.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with severe symptoms should be sent to a healthcare facility for evaluation and treatment.

Monitoring

    A) Monitor serum electrolytes in patients with severe diarrhea or vomiting. Monitor for clinical evidence of dehydration.
    B) Stool cultures are rarely necessary as most infections are self-limited. If necessary Campylobacter jejuni can be isolated from stool, but the organism requires special handling.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) GI decontamination is not indicated.
    6.5.2) PREVENTION OF ABSORPTION
    A) GI decontamination is not indicated
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) In most cases, routine laboratory studies are not indicated.
    2) Monitor serum electrolytes in patients with severe diarrhea or vomiting. Evaluate for evidence of dehydration.
    3) Stool cultures are rarely necessary as most infections are self-limited. If necessary, Campylobacter jejuni can be isolated from stool, but the organism requires special handling.
    B) FLUID/ELECTROLYTE BALANCE REGULATION
    1) GENERAL: Initial assessment must determine the degree of dehydration. Correct deficits as indicated, and monitor intake and output in symptomatic patients.
    2) ORAL FLUIDS: Patients with mild fluid deficits can often be managed with oral fluid therapy consisting of clear liquids or specially formulated glucose and electrolyte solutions.
    3) IV FLUIDS: Patients with moderate to severe dehydration are generally treated with IV fluids.
    C) ANTIEMETIC
    1) INDICATIONS: Significant nausea and vomiting may be controlled with an antiemetic agent.
    D) ANTIBIOTIC THERAPY
    1) Most patients have self-limited disease and do not require antibiotics. Antibiotic therapy should be considered in patients who are immunocompromised, those who have severe disease, and those who have extra-intestinal manifestations.
    2) Resistance to erythromycin in developed countries is about 5% (Pickering, 2008). The incidence of Campylobacter jejuni resistant to fluoroquinolones has been rapidly increasing, and has been as high as 19% (Dingle et al, 2005).
    3) ERYTHROMYCIN: ADULT: 500 mg twice a day for 5 days (longer therapy may be required for immunocompromised patients) (Guerrant et al, 2001).
    4) AZITHROMYCIN: ADULT: 500 mg daily for 3 days (Tribble et al, 2007). PEDIATRIC: 10 mg/kg orally once daily for 3 days (Mackell, 2005).

Range Of Toxicity

Summary

    A) Infectious dose varies based on the health of the individual and the type of contaminated food ingested. Ingestion of as few as 500 bacteria cells may cause illness in some individuals, but it is thought that ingestion of a minimum of 10,000 cells is needed to cause infection. About 5% to 10% of patients may require hospitalization. The case fatality ratio is estimated to be between 0.05 (5 deaths in 10,000 cases) and 0.1 (one death per thousand infections). Fatalities are very rare in healthy individuals. Immunocompromised patients are at increased risk.

Minimum Lethal Exposure

    A) The case fatality ratio is estimated to be between 0.05 (5 deaths in 10,000 cases) (Galanis, 2007) and 0.1 (one death per thousand infections) (Center for Food Safety and Applied Nutrition (CFSAN), 2009). In the United States, there are about 99 deaths each year related to campylobacteriosis. Fatalities are very rare in healthy individuals. Immunocompromised patients are at an increased risk (Center for Food Safety and Applied Nutrition (CFSAN), 2012).

Maximum Tolerated Exposure

    A) Infectious dose varies based on the health of the individual and the type of contaminated food ingested. Ingestion of as few as 500 Campylobacter cells caused illness in volunteers. However, in general, it is thought that ingestion of a minimum of 10,000 cells is needed to cause infection (Center for Food Safety and Applied Nutrition (CFSAN), 2012). About 5% to 10% of patients may require hospitalization (Galanis, 2007).

References

General Bibliography

    1) Center for Food Safety and Applied Nutrition (CFSAN): Bacillus cereus and other Bacillus species. In: Bad Bug Book Foodborne Pathogenic Microorganisms and Natural Toxins Handbook Second Edition. U.S. Food and Drug Administration (FDA). College Park, MD. 2012a. Available from URL: http://www.fda.gov/downloads/Food/FoodSafety/FoodborneIllness/FoodborneIllnessFoodbornePathogensNaturalToxins/BadBugBook/UCM297627.pdf. As accessed 2013-03-06.
    2) Center for Food Safety and Applied Nutrition (CFSAN): Campylobacter jejuni. In: Bad Bug Book Foodborne Pathogenic Microorganisms and Natural Toxins Handbook Second Edition. U.S. Food and Drug Administration (FDA. College Park, MD. 2012. Available from URL: http://www.fda.gov/downloads/Food/FoodSafety/FoodborneIllness/FoodborneIllnessFoodbornePathogensNaturalToxins/BadBugBook/UCM297627.pdf. As accessed 2013-03-06.
    3) Center for Food Safety and Applied Nutrition (CFSAN): Campylobacter jejuni. In: Bad Bug Book: Foodborne Pathogenic Microorganisms and Natural Toxins Handbook. U.S. Food and Drug Administration (FDA). Silver Spring, MD. 2009. Available from URL: http://www.fda.gov/Food/FoodSafety/FoodborneIllness/FoodborneIllnessFoodbornePathogensNaturalToxins/BadBugBook/ucm070024.htm. As accessed 2011-08-01.
    4) Dingle KE, Clarke L, & Bowler IC: Ciprofloxacin resistance among human Campylobacter isolates 1991-2004: an update. J Antimicrob Chemother 2005; 56(2):435-437.
    5) Engberg J: Contributions to the epidemiology of Campylobacter infections. A review of clinical and microbiological studies. Dan Med Bull 2006; 53(4):361-389.
    6) Fernandez-Cruz A, Munoz P, Mohedano R, et al: Campylobacter bacteremia: clinical characteristics, incidence, and outcome over 23 years. Medicine (Baltimore) 2010; 89(5):319-330.
    7) Galanis E: Campylobacter and bacterial gastroenteritis. CMAJ 2007; 177(6):570-571.
    8) Guerrant RL, Van Gilder T, Steiner TS, et al: Practice guidelines for the management of infectious diarrhea. Clin Infect Dis 2001; 32(3):331-351.
    9) Havelaar AH, van Pelt W, Ang CW, et al: Immunity to Campylobacter: its role in risk assessment and epidemiology. Crit Rev Microbiol 2009; 35(1):1-22.
    10) Heinzl B, Kostenberger M, Nagel B, et al: Campylobacter jejuni infection associated with myopericarditis in adolescents: report of two cases. Eur J Pediatr 2010; 169(1):63-65.
    11) Kratzer C, Wolf F, Graninger W, et al: Acute cardiac disease in a young patient with Campylobacter jejuni infection: a case report. Wien Klin Wochenschr 2010; 122(9-10):315-319.
    12) Kuwabara S: Does Campylobacter jejuni infection elicit axonal or demyelinating Guillain-Barre syndrome, or both?. J Neurol Neurosurg Psychiatry 2011; 82(3):238-.
    13) Mackell S: Traveler's diarrhea in the pediatric population: etiology and impact. Clin Infect Dis 2005; 41(Suppl 8):S547-S552.
    14) Mera V, Lopez T, & Serralta J: Take traveller's diarrhoea to heart. Travel Med Infect Dis 2007; 5(3):202-203.
    15) Miller RS, Speegle L, Oyarzabal OA, et al: Evaluation of three commercial latex agglutination tests for identification of Campylobacter spp. J Clin Microbiol 2008; 46(10):3546-3547.
    16) Pickering LK: Antimicrobial resistance among enteric pathogens. Adv Exp Med Biol 2008; 609:154-163.
    17) Pope JE, Krizova A, Garg AX, et al: Campylobacter reactive arthritis: a systematic review. Semin Arthritis Rheum 2007; 37(1):48-55.
    18) Tribble DR, Sanders JW, Pang LW, et al: Traveler's diarrhea in Thailand: randomized, double-blind trial comparing single-dose and 3-day azithromycin-based regimens with a 3-day levofloxacin regimen. Clin Infect Dis 2007; 44(3):338-346.
    19) Turley AJ, Crilley JG, & Hall JA: Acute myocarditis secondary to Campylobacter jejuni enterocolitis. Resuscitation 2008; 79(1):165-167.
    20) Wysok B & Uradzinski J: Campylobacter spp.--a significant microbiological hazard in food. I. Characteristics of Campylobacter species, infection source, epidemiology. Pol J Vet Sci 2009; 12(1):141-148.
    21) Zilbauer M, Dorrell N, Wren BW, et al: Campylobacter jejuni-mediated disease pathogenesis: an update. Trans R Soc Trop Med Hyg 2008; 102(2):123-129.