Campylobacteriosis

Last updated October 16, 2006

Agent
Pathogenesis
Epidemiology
Clinical Features
Differential Diagnosis
Laboratory Diagnosis
Treatment
Vaccines
Travel Implications
Disease Prevention and Control
Infection Control Measures in Healthcare Settings
References

Agent

Classification

Campylobacter, Sulfurospirillum, and Arcobacter are three genera that make up the family Campylobacteraceae (see References: Nachamkin 2003). A related family, Helicobacteraceae, contains a number of closely related species in the genus, Helicobacter.
Campylobacteriosis is the group of infections caused by gram-negative bacteria within the genus Campylobacter.
The genus Campylobacter has 14 species; recent reclassification has placed some former Campylobacter species into the genus Helicobacter (see References: Blaser 2005).
Campylobacter species are mainly zoonotic, with several animal species serving as reservoirs for human infection. Campylobacter can cause both diarrheal and systemic illnesses; in some countries, it lives as a commensal organism in humans (see References: Moore 2006).
The species that are most often associated with human gastrointestinal disease include (see References: Blaser 2005):

C jejuni
C coli
C lari
C fetus subsp fetus
C upsaliensis

Species most commonly associated with extraintestinal infections include (see References: Blaser 2005):

C fetus
C jejuni
C coli
C lari
C sputorum
C hyointestinalis

C jejuni and C coli account for about 99% of US cases of campylobacteriosis (see References: CDC 2005: Campylobacter infections) and 95% of the species isolated from clinical samples in the United Kingdom (see References: Snelling 2005).
C jejuni accounts for most of the enteric disease, while C fetus is the species most often responsible for extraintestinal infections.

Key Microbiological Characteristics

The key microbiologic characteristics of Campylobacter include (see References: Nachamkin 2003):

Curved, S-shaped or spiral rods, although some species (such as C hominis) form straight rods
Between 0.2 to 0.9 microns wide and 0.5 to 5 microns long
Gram negative, non-spore-forming rods that may form spherical or coccoid bodies in old cultures or cultures exposed to air for prolonged periods
Motile and usually move by a single polar unsheathed flagellum at one or both ends (although they may lack flagella)
Microaerobic with a respiratory-type metabolism, but some strains grow aerobically or anaerobically
Catalase- and oxidase-positive; hippurate hydrolysis distinguishes C jejuni (positive) from other species (negative)
Relatively small genome of about 1.6 to 1.7 million base pairs (bp) (see References: Blaser 2005, Snelling 2005)

Campylobacter species have a relatively high minimum growth temperature (>30°C) and, therefore, generally do not multiply in the environment or in most foods (see References: Snelling 2005).

Pathogenesis

Virulence Factors

Campylobacter organisms enter the host intestine after passing through the stomach's acid barrier and colonize the mucus blanket that covers the epithelial layer of the distal ileum and colon. The organisms then penetrate the mucus layer covering the intestinal cells by using their polar flagella and corkscrew movements (see References: Snelling 2005).
Outer membrane adhesion proteins CadF and PEB1 are involved in adherence and invasion (see References: Blaser 2005).
Adhesion and invasion are dependent on both flagella motility and flagella expression. Experiments reveal that mutants of flaA, the primary structural gene for flagella, are unable to colonize 3-day-old chicks and cannot invade human intestinal cells in culture (see References: Snelling 2005).
Major outer membrane lipo-oligosaccharides and lipopolysaccharides are involved in serum resistance, endotoxicity, and adhesion.
The superoxide dismutase protein SodB is the main component of the C jejuni superoxide stress defense (see References: Snelling 2005).
The Campylobacter genome contains several heat-shock proteins (GroELS, DnaJ, DanK, and Lon) and also two negative regulators of the heat shock response (see References: Murphy 2006).
Campylobacter organisms contain several two-component signal transduction regulators, three of which are involved in colonization (see References: Murphy 2006).
The tetracycline resistance plasmid pVir is a likely virulence factor. The plasmid contains components of a type 4 secretion system known to be important for virulence of several other bacterial pathogens. The pVir plasmid was identified in 18 (17%) of 104 C jejuni clinical isolates in a small study and was significantly associated with the presence of bloody diarrhea; however, isolates from some patients with bloody diarrhea did not contain the pVir plasmid, suggesting that other virulence determinants are involved (see References: Tracz 2005).
Campylobacter may induce disease in humans via a cytolethal distending toxin (CDT)-induced host cell death and the ensuing inflammatory responses. CDT causes cell cycle arrest and is involved with interleukin-8 production and release (see References: Blaser 2005, Snelling 2005).
C jejuni has been shown to induce intestinal epithelial cells to secrete chemokines, which are essential in activation of the host inflammatory response (see References: Hu 2005).
C jejuni mutants with decreased motility due to paralyzed flagella manifest reduced adhesion and no invasion, indicating that other adhesins are involved in the subsequent internalization (see References: Snelling 2005).
Campylobacter organisms appear to produce extracellular toxins and classic enterotoxins, although these toxins tend to be present at low concentrations and their role in producing diarrhea is unclear (see References: Blaser 2005).

Disease Process

The disease process for gastrointestinal illness occurs via several steps:

Oral ingestion
Passage through the stomach
Multiplication in human bile
Colonization of the jejunum, ileum, and colon
Epithelial cell changes and diarrhea
Diffuse bloody, edematous, exudative enteritis in severely affected patients, apparent on microscopic examination (see References: Blaser 2005)

Localized or systemic infections can occur after gastrointestinal infection.

After colonization, cellular infiltration occurs via a multifactorial process.
Localized infections can occur as a result of direct spread from the intestine and include infections such as cholecystitis, pancreatitis, peritonitis, and mesenteric adenitis (see References: Allos 2001).
Bacteremia also can occur and several patterns have been noted (see References: Blaser 2005).

Transient bacteremia in the normal host, which is generally benign.
Sustained bacteremia or deep infection in a normal host, which usually is associated with acute enteritis.
Sustained bacteremia in an immunocompromised host, which often occurs in the absence of acute enteritis. Bacteremia and sepsis are more likely to occur in immunocompromised or impaired patients.
Bacteremia can lead to infections at sites distant from the intestines (eg, meningitis, endocarditis).

Postinfectious complications also have been noted (see References: Blaser 2005).

Reactive arthritis may develop several weeks after infection and is associated with the HLA-B27 histocompatibility antigens (see References: Hannu 2002).
Guillain Barre syndrome (GBS), which likely results from an autoimmune-mediated process affecting host nerve tissue, occurs at an incidence of about 1.17/1,000 person years for patients with Campylobacter infection, which is a rate 77 times higher than the rate in the general population (see References: Tam 2006). Some Campylobacter strains possess outer membrane lipopolysaccharides (LPSs) which closely resemble human gangliosides; this feature may be important in the pathogenesis of postinfectious GBS (see References: Nachamkin 1998).

Epidemiology

General Information

Campylobacteriosis is a worldwide zoonosis. Organisms commonly are found as commensal organisms in the gastrointestinal tracts in all types of fowl, wild and domesticated cattle, domestic dogs and cats, rodents, and many other animals (see table below). Campylobacter acquisition by animals occurs early in life and may lead to disease and death, but most animals become lifelong carriers (see References: Blaser 2005, Nachamkin 2003).
C jejuni and C coli are the Campylobacter species most commonly associated with diarrheal diseases in humans and are clinically indistinguishable (see References: Nachamkin 2003).
C jejuni occurs year-round in the United States and in developed countries, with the incidence showing a sharp peak in summer and early fall (see References: Blaser 2005). C fetus infection has a similar seasonal variation, but the peak is less marked.
In tropical countries, more human-to-human transmission is suspected and asymptomatic carriage in healthy persons is common; infections are especially common in the first five years of life (see References: Blaser 2005, Murphy 2006). C jejuni is an important cause of travelers’ diarrhea.
The infectious dose of C jejuni is considered to be relatively low; human feeding studies suggest that as few as 400 to 500 bacteria may cause illness, although for some individuals greater numbers of organisms are required (see References: FDA: Campylobacter jejuni).

Reservoirs

The main reservoirs for Campylobacter are animals, especially poultry. Humans may also carry the bacteria.

Reservoirs for Campylobacter
Reservoir	Species
Humans	C jejuni, C sputorum bv sputorum, C concisus, C curvus, C rectus, C showae, C gracilis
Cattle	C jejuni, C fetus subsp fetus or C fetus subsp venerealis, C hyointestinalis, C sputorum bv paraureolyticus and faecalis
Sheep	C fetus, C sputorum bv faecalis
Pigs	C coli, C hyointestinalis, C mucosalis
Birds	C jejuni, C coli, C lari
Domestic pets	C jejuni, C lari, C upsaliensis (dogs in particular), C hyointestinalis, C helveticus
Abbreviation: bv, biovar; subsp, subspecies. Adapted from Nachamkin 2003 (see References).

Modes of Transmission

The major mode of transmission is foodborne, usually from ingestion of contaminated products of animal origin (most commonly undercooked meats and unpasteurized milk) (see References: AAP 2003, Friedman 2004).

The single most important source of human Campylobacter infection in the United States and other developed countries is infected chicken (see References: Friedman 2004).
Commercially raised poultry is almost always colonized with C jejuni, and consumption of undercooked poultry is estimated to be responsible for 50% to 70% of sporadic Campylobacter infections in developed countries (see References Altekruse 1999; Evans 2003, Kassenborg 2004, Moore 2006). Moreover, a recent study from Denmark showed that eating fresh (not previously frozen) chicken was the factor most significantly associated with illness (see References: Wingstrand 2006).
Meat often becomes contaminated with intestinal contents during slaughter. Slaughterhouse procedures and/or hygiene can subsequently amplify contamination (see References: Blaser 2005; CDC 2005: Campylobacter infections).
A number of studies have demonstrated that raw milk consumption is associated with Campylobacter infection. Consumption of raw milk was implicated as the source of infection in 30 out of 80 outbreaks of campylobacteriosis reported to CDC between 1973 and 1992 (see References: Altekruse 1999).
Outbreaks from infected food handlers rarely are reported, owing to the fact that Campylobacter organisms do not survive well or multiply on foods that are exposed to oxygen (see References: Olsen 2001).

Waterborne transmission also has been reported as a source for a number of outbreaks and for sporadic cases. Untreated or improperly treated surface water and water from malfunctioning municipal water systems are the most common sources (see References: Samuel 2004). Bottled water was significantly associated with illness in one report, but the validity of this finding has not been confirmed (see References: Evans 2003).
Fecal-oral transmission has been noted; examples include contact with animal feces and handling diapers of infected infants (see References: Blaser 2005, Olsen 2001).
Bloodborne transmission through blood transfusion has been reported (see References: Pepersack 1979) and perinatal or in utero transmission has been identified (see References: Vesikari 1981).
Some researchers have suggested that flies could be a source for sporadic Campylobacter infections in humans or could transmit the pathogen in broiler chicken flocks (see References: Hald 2004, Nichols 2005).

Incidence of Disease

Domestic

The Centers for Disease Control and Prevention (CDC) estimates the number of US cases is about 1 million per year or 0.5% of the general population, although the actual incidence of Campylobacter infections is not known (see References: CDC 2005: Campylobacter infections). The prevalence of infection in healthy individuals in the US is thought to be very low (less than 1%) (see References: Blaser 2005).
In 2005, Campylobacter was the second leading cause of laboratory-confirmed cases of foodborne infection in the United States, with an estimated incidence of 12.72 cases per 100,000 population (5,655 of 16,614 infections in FoodNet surveillance areas) (see References: CDC 2006). This incidence approaches the 12.30 goal of the Healthy People 2010 objectives and represents a decrease from the 2004 figure of 12.9 (see References: CDC 2005: Preliminary FoodNet data, 2004). The overall incidence has shown continuous decline; most of the decline occurred before 2001 with small increments since then (see References: Samuel 2004, CDC 2006)
In 2003, nine US deaths were confirmed to be caused by Campylobacter. CDC estimates that mortality rate for the campylobacteriosis in the United States is about 24 per 10,000 culture-confirmed cases and that about 124 people die each year from Campylobacter infections (see References: CDC 2003; CDC 2005: Campylobacter infections).
All ages are affected, but peak incidence occurs in children younger than 1 year of age and in persons between the ages of 15 and 29. The incidence of Campylobacter infections during 1996 to 1998 in the US among children <5 years of age was estimated at 43.4 per 100,000 (see References: Koehler 2006). Males may have a higher incidence than females up to age 45, and after that the gender-specific rates are similar.
Bacteremia is noted in less than 1% of patients with C jejuni infections (see References: Blaser 2005).

Global

Campylobacter infections rank as the most common bacterial cause of diarrhea in most industrialized and developing countries, with an estimated 400 million cases per year worldwide (see References: Girard 2006). The World Health Organization and other national public health agencies are coordinating activities to strengthen disease surveillance and to determine the burden of acute gastroenteritis (see References: Flint 2005).
Estimates for the campylobacteriosis in general populations in developing and developed countries are similar, about 90 per 100,000 population (see References: Coker 2002), but incidence rates vary from about 12.9 per 100,000 in the United States to 60 to 90 per 100,000 in northern European countries (see References: Coker 2002).
The epidemiology of Campylobacter infection in developing countries is markedly different than that in developed countries. C jejuni is often isolated from healthy individuals, and infection is very common in children (see References: Coker 2002). In developing countries, Campylobacter enteritis has no seasonal preference, unlike in developed countries where epidemics tend to occur in summer and autumn (see References: Alterkuse 1999).
Community-based studies in developing countries have provided estimates of campylobacteriosis at 40,000 to 60,000 cases per 100,000 children less than age 5, compared with a rate of 300 per 100,000 children for developed countries (see References: Coker 2002).
In developing countries, C jejuni often is isolated from the stool of healthy people, especially during the first 5 years of life. Infections in children up to age 2 are symptomatic, while those occurring later in early childhood are usually asymptomatic. Such a pattern of may contribute to patterns of Campylobacter isolation from adults (see References: Blaser 2005, Nachamkin 2003).
Isolation rates of Campylobacter among symptomatic children in developing countries range from 5.5% to 18% (see References: Coker 2002).
Investigators suspect that human-to-human transmission may be more common in developing than in developed countries, since older children and adults may be asymptomatic carriers (see References: Blaser 2005, Coker 2002). Differences observed between developed and developing countries' infection-to-illness ratios may be due to differences in age- or exposure-related immunity of the populations rather than to differences in isolates (see References: Blaser 2005).
Campylobacter species other than C jejuni and C coli (eg, C upsaliensis, C concisis) may be more common in developing countries. More than 50% of Campylobacter infections in a Cape Town, South Africa, hospital were species other than C jejuni and C coli (see References: Coker 2002).

Risk Factors for Infection

Numerous studies of outbreak investigations and sporadic cases have shown that eating undercooked chicken is the primary risk factor for infection (see References: Friedman 2004, Samuel 2004, Stern 2006).

Thorough cooking kills Campylobacter, although consumers should be aware that certain methods of cooking (such as fondue or barbequing) may not cook the meat completely at adequate temperatures to kill the bacteria (see References: CDC 2005: Campylobacter infections).
A recent study of risk factors for sporadic cases in the United States found that the highest population attributable fraction (PAF) (24%) was related to eating chicken prepared at a restaurant. Eating nonpoultry meats in a restaurant also had a high PAF (21%), whereas eating chicken prepared at home was not associated with illness.

Improper handling of raw meats, particularly poultry also has been shown to be a risk factor. Foods can be cross-contaminated during preparation or recontaminated afterward (eg, getting juice from raw chicken on other foods, placing cooked food on plates that held raw chicken, transferring bacteria from raw food to mouth) (see References: CDC 2005: Campylobacter infections; Moore 2005). In situations where vegetables have been implicated (such as salad) as a source of infection, cross-contamination from raw chicken during preparation has been suspected (see References: CDC 1998, Evans MR 2003).
Homosexual men have been shown in the past to be at increased risk for Campylobacter infection (see References: Gaudreau 2003, Quinn 1984). A recent analysis, however, suggests that the rate of infection for homosexual men is similar to the rate for heterosexual men of a similar age (see References: Allos 2001).
HIV-infected patients have been shown to be at increased risk of infection (see References: Sorvillo 1991).
Additional risk factors include:

Drinking or swimming in contaminated water (see References: Clark 2003, Kuusi 2005, Schonberg-Norio 2004)
Occupational exposure to cattle, sheep, and other farm animals, and direct contact with infected animals (eg, domestic pets, especially young dogs and cats with diarrhea, rodents, and birds) (see References: CDC 2005: Compendium)
Laboratory or other work that involves contact with excreta of infected individuals (see References: AAP 2003)
Travel to foreign countries (see References: Kassenborg 2004, Freedman 2006)

Examples of Key Outbreaks

Most recent outbreaks of campylobacteriosis are small, usually involving fewer than 50 people. However, several larger outbreaks are notable:

Southwestern Oklahoma 1996: Fourteen cases of C jejuni infection occurred between Aug 16 and 20 among 25 patrons who ate at a local restaurant and were available for interviews. Lettuce and lasagna were statistically associated with the illness. Inspection of the restaurant indicated that the countertop surface area was too small to separate raw poultry and other foods adequately during preparation. The lettuce and lasagna were probably cross-contaminated with C jejuni from raw chicken through unwashed or inadequately washed workers' hands, cooking utensils, and/or kitchen countertops (see References: CDC 1998).
Finland 1998: An estimated 2,700 cases of campylobacteriosis occurred in a large outbreak of gastrointestinal illness in one municipality. Repair work on a water main was implicated as the source of outbreak (see References: Kuusi 2005).
Walkerton, Ontario, Canada 1985, 2000: Outbreaks arose from contamination of well water by agriculture waste runoff. The 2000 outbreak was associated with Campylobacter and Escherichia coli O157:H7. A total of 532 stool specimens were tested; samples from 116 patients were positive for Campylobacter and 11 were positive for E coli O157:H7. Manure specimens from animals on 11 of 13 farms tested in the area revealed several serotypes of C jejuni and E coli, with the former the most common and the agent most often responsible for human cases. The outbreak occurred after heavy spring runoff contaminated municipal wells; bacteria entered the Walkerton municipal water supply from neighboring farms. Campylobacter and E coli organisms swept into the wells were distributed through the town's water supply. One farm was implicated as the major source of the outbreak strains (see References: Clark 2003).
Sawyer County, Wisconsin 2001: Gastrointestinal illness associated with C jejuni occurred in 75 persons. All of them had drunk unpasteurized milk from a local dairy farm. Of the 75 patients, 29 provided stool samples, and 28 specimens (93%) grew C jejuni. PFGE was done on 21 isolates; the DNA patterns were indistinguishable. The milk was from a grade A organic farm that provided unpasteurized milk samples at community events and to persons who toured the farm. The farm also distributed unpasteurized milk through a cow-leasing program (unpasteurized milk cannot be sold legally to consumers in Wisconsin). Customers paid a lease fee for a share in a cow; the milk from the leased animals was stored and customers picked up or had the milk delivered. Samples of C jejuni from the farm milk matched the outbreak strain and the farm was ordered to divert all milk to a processor for pasteurization (see References: CDC 2002).
Madrid, Spain 2003: C jejuni was found to be responsible for 81 cases of enteritis among 253 students in a school. All the cases occurred in school children, and all had eaten at the school. Infection was traced to custard made with ultra-high-temperature milk that had been cross-contaminated with bacteria from raw chicken prepared the previous day in the same kitchen. Inspection revealed that the food preparation areas for uncooked meats and ready-to-eat foods were not separate (see References: Jimenez 2005).
Finland 2005: Six members of a farm family acquired long-lasting (5-month duration) campylobacteriosis, two of whom had had several episodes of diarrhea within the previous 5 months. Identical strains of C jejuni were isolated from human and bovine feces and bulk milk samples on the farm. The probable source of infection was incompletely sealed rubber liners fitted to a milking machine, which allowed fecal material to contaminate milk in holding tanks (see References: Schildt 2006).

Clinical Features

Clinical Features of Campylobacter Gastrointestinal Illness and Complications
	Gastrointestinal Illness	Complications
		Guillain Barre Syndrome (GBS)	Reactive Arthritis	Hemolytic-Uremic Syndrome (HUS)
Incubation period	1-7 days	5 -21 days after episode of diarrhea	7-10 days after onset of diarrhea	Sudden appearance, usually several days after illness onset
Presenting features	—Diarrhea, malaise, fever and abdominal pain (cramping) are common. —Diarrhea may be bloody and associated with vomiting and nausea. —Watery secretory diarrhea (>10 stools per day) may be seen in children. —Inflammatory diarrhea symptoms are indistinguishable from those caused by Escherichia coli, Salmonella, and Shigella species.	—Muscular weakness, which usually begins as symmetric weakness in the legs and progresses to the arms, is the hallmark. —Deep tendon responses are lost. —Mild sensory loss often is present. —More than 50% with severe disease have weakness of facial and oral musculature.	—Musculoskeletal symptoms develop about 12 days after positive stool culture and arthritis develops in the next few weeks. —Other features include low-grade fever and conjunctivitis. —About 50% of cases involve multiple joints; knee and proximal interphalangeal joints are most often affected. —Joint involvement is asymmetric or polyarticular and mainly in the large joints of the extremities. —Mucocutaneous lesions may be present. —Hyperketotoic skin lesions in palms and soles and around nails are noted in some patients.	—Fever is present. —Illness manifests as a triad of renal insufficiency, hemolytic anemia and thrombocytopenia. —CNS signs, such as confusion and coma, may also be present.
Laboratory features	—Darkfield or phase contrast microscopy of fresh fecal specimens reveals darting motility of the organism. —Gram stain of stool reveals Vibrio forms (slim, short, curved rods). —Red blood cells and neutrophils are present in stool in about 75% of patients. —Most laboratory evaluations are within normal limits. —Peripheral white blood count is usually normal; left shift may occur. —AAT; ESR may be slightly elevated.	—Protein levels often are increased in the CSF. —67% of patients have slow nerve conduction velocities and evidence of segmental demyelination at onset. —Some patients have serum antibodies to GM1 ganglioside.	—63% to 96% of patients have HLA-B27 histocompatibility antigens.	—Evidence of hemolytic anemia, including fragmented erythrocytes on blood smear, is usually present. —Other findings include elevated LDH levels, severe thrombocytopenia, and elevated serum creatinine and BUN.
Duration of illness	—Typically lasts 1 week. —Mild episodes subside within 7 days in 60%-70%. —Illness lasts for 2 weeks in 20%-30%, and persists for longer periods in 5%-10%. —Relapses occur in about 25% of patients.	—Most patients improve considerably after a period of months. —Residual effects may require retraining, orthopedic appliances, or surgery.	—Often resolves in 3 to 4 months. —Up to 50% of patients experience transient or prolonged recurrences of arthritis or the components of the syndrome for several years.	—Duration of illness generally is several weeks and recovery may require a prolonged period.
Complications:	—Complications are relatively rare. —Reactive arthritis, HUS, septicemia, and GBS are the most serious complications. —Rare complications include meningitis, endocarditis; septic abortion, erythema nodosum, hepatitis, intestinal nephritis, and immunoglobulin A nephropathy, and very rarely, toxic megacolon with massive bleeding. —Underlying conditions that increase the risk of Campylobacter-associated bacteremia include: hypogamma-globulinemia, HIV infection, pregnancy, malignancy, diabetes mellitus, alcoholism, asplenism, and others (see References: Olesen 2005).	—About 10% of patients experience chronic relapsing polyneuropathy. —5% of patients die despite respiratory care. —20% have some permanent disability.	Joint deformity, ankylosis, sacroiliits, or spondylitis may occur with chronic or recurrent disease.	If untreated, the disorder can be fatal.
Incidence rates for complications, case-fatality rates (CFRs)	—Symptomatic infection-associated mortality rate in the US is estimated at 24 per 10,000 culture-confirmed cases or 200 deaths per year. —Infection with C fetus is of concern to patients who are immunocompromised, women who are pregnant, and neonates. —Patients who are immunocompromised and neonates have high mortality rates.	—GBS is a life-threatening condition. —About 1 in 2,000 to 1 in 5,000 Campylobacter infections are followed by GBS. —Infection is most likely to occur after infection with Penner serotype O:19 in the US and Japan, O:11 in Germany, O:41 in South Africa. —Campylobacter accounts for about 30% of GBS cases in US. —GBS is more likely to follow asymptomatic infection. —GBS occurring after C jejuni infection may be more severe and likely to cause irreversible neurologic damage.	—About 1% of patients who have a Campylobacter infection manifest the disorder. —Affected Finnish patients had an incidence of reactive arthritis (10%) associated with HLA-B27 about equal to the Finnish general population (14%) but much lower than that reported in studies of other populations (80%-90%).	The CFR for Campylobacter-associated HUS has not been well studied. (The CFR for HUS in general is 5% to 15%.)
Abbreviations: AAT, alanine aminotransferase; BUN, blood urea nitrogen; CSF, cerebral spinal fluid; ESR, erythrocyte sedimentation rate; LDH, lactate dehydrogenase. Data from Allos 1998, Allos 2004, Alterkuse 1999, Blaser 2005, Hannu 2002 Hannu 2005, Sivadon-Tardy 2006, Tam 2006 (see References).

Differential Diagnosis

Infectious agents to consider in differential diagnosis are:

Shigella
Enteroinvasive Escherichia coli
E coli O157:H7
Salmonella
Yersinia enterocolitica
Aeromonas spp
Vibrio parahemolyticus
Pleisomonas shigelloides
Clostridium difficile
Clostridium perfringens

Other conditions in the differential diagnosis include:

Inflammatory bowel disease
Pseudomembranous enterocolitis secondary to Clostridium difficile toxin
Intussusception (infants and young children)
Acute abdomen
Acute appendicitis

Laboratory Diagnosis

Specimen Collection and Transport

Fecal specimens are the preferred sample for isolating Campylobacter (see References: AAP 2003, Nachamkin 2003, and Thompson 2003).

Collect whole stool in a sterile container (10 mL liquid, 1 marble-sized piece of whole fresh stool).
Samples should be stored at 4°C until processed, preferably within 2 hours of collection. When possible, test within 48 hours after collection; otherwise freeze samples at -70°C.
Stool cultures should not be routinely ordered on patients who have been in the hospital for 3 or more days because of potential nosocomial infections with other organisms and antibiotic-induced overgrowth of Clostridium difficile.
Transport media such as Cary-Bair, modified Stuart medium, or alkaline peptone water with thioglycolate and cystine can be used; buffered glycerol-saline should not be used as a transport medium for samples to be tested for Campylobacter.
Store a portion of each specimen at less than –15°C for PCR testing.

Standard Diagnostic Tests

Presumptive diagnosis can be made by direct examination with phase-contrast microscopy and darkfield microscopy of fresh stool samples. Organisms exhibit a characteristic darting movement.
Campylobacter can be detected on Gram stain that employs carbol-fuchsin or 0.1% basic fuchsin counterstain for stool smears or pure cultures. Gram stain has a sensitivity of 66% to 94% and specificity of 95%, and staining reveals Vibrio forms (slim, short, curved rods) (see References: Nachamkin 2003).
C jejuni and C coli are usually cultured from stool samples, but selective media for culturing them may not permit growth of C fetus or atypical Campylobacter species. Identification of the latter species usually requires media without antibiotics and incubation at 37°C. Routine media are adequate for isolation of Campylobacter from normally sterile sites such as blood, body fluids, and tissues (see References: AAP 2003).
Laboratory identification of C jejuni and C coli in stool specimens requires culturing on selective media, microaerophilic conditions (5% oxygen, 10% carbon dioxide, and 85% nitrogen), and incubation temperature of 42°C (for C jejuni).
Selective media used for culture include blood-free media such as charcoal cefoperazone deoxycholate agar (CCDA), charcoal-based selective medium (CSM), and blood-containing media, such as Campy-CVA medium and Skirrow medium. The optimal method for obtaining the highest yield of Campylobacter from stool samples employs a combination of media including either CCDA or CSM. Most of the selective media have one or more antimicrobial agents to inhibit enteric bacterial flora (see References: Nachamkin 2003).
Filtration methods and antimicrobial agents to inhibit normal colonic flora will aid detection of Campylobacter species other than C jejuni and C coli except for C upsaliensis, C hyointestinalis, and C fetus, which are susceptible to antimicrobials in selective media (see References: AAP 2003).
Campylobacter species may have different appearances that depend on the media used for plating:

In general, colonies appear gray, flat, irregular, and spreading on the media.
They do not produce hemolysis on blood agar.

Enzyme immunoassay and PCR (see References: On 2003) can be used to detect Campylobacter species in stool samples, but these techniques are not standardized or widely available.

Antimicrobial Susceptibility

Most Campylobacter infections are self-limiting, but indiscriminant antibiotic use in humans and antibiotic use in animals has resulted in growing levels of antibiotic resistance (see References: Ge 2003, Gupta 2004, Iovine 2004).
Erythromycin has low rates of resistance, making it the optimal drug for treatment of campylobacteriosis (see References: Allos 2001).
Increasing resistance to antibiotics for C jejuni can make clinical management more difficult, prolong illness, and compromise treatment of patients who have bacteremia (see References: Engberg 2001, Nelson 2004).
Macrolides and fluoroquinolones represent first- and second-line drugs for treatment of campylobacteriosis enteritis, so multidrug resistance among Campylobacter species is highly undesirable. Cultural practices, unhygienic conditions, and widespread availability of drugs in developing countries have contributed to increased antibiotic resistance (see References: Okeke 1999). Widespread use of antibiotics such as fluoroquinolones in animal husbandry in the US and other Western countries during the 1990s has increased antibiotic resistance in poultry and subsequently in isolates from human infections (see References: Evans 2003, Ge 2003, Iovine 2004, Price 2005).
In the United States, fluoroquinolone resistance among chickens has been shown to be related to fluoroquinolone-resistant infections in humans (see References: Price 2005). Resistance to other drugs also has been noted. Rates of ciprofloxacin-resistant Campylobacter isolated from humans were found to be 13% in 1997 and 19% in 2001; erythromycin resistance was 2% in 1997 and 2001. In 1999, ciprofloxacin-resistant Campylobacter was isolated from 10% of 180 chicken products purchased from grocery stores in the United States (see References: Gupta 2004).
In September 2005, concern about increasing resistance to Campylobacter in chickens prompted the US Food and Drug Administration to prohibit distribution or use of enrofloxacin, a fluoroquinolone used in poultry, to arrest the increase in resistance among commercial flocks (see References: FDA 2005, Price 2005). New research suggested that fluoroquinolone resistance may persist in commercial poultry environments without any selection pressure (ie, without fluoroquinolone use) and such resistant strains contaminate a larger portion of foods than previously reported (see References: Price 2005).
Most studies report a greater frequency of antibiotic resistance for C coli than for C jejuni (0% to 68.4% versus 0% to 11%). Erythromycin resistance rates are stable and low in Japan, Canada, and Finland but rising in Thailand and Sweden (see References: Engberg, 2001). In Finland, reduced susceptibilities to fluoroquinolones and doxycycline were detected almost exclusively among isolates from patients who had traveled abroad (see References: Schonberg-Norio 2006).
Worldwide, fluoroquinolone resistance is increasing for Campylobacter strains (see References: Allos 2001, Engberg 2001, Molbak 2005). In some Asian countries, such as Thailand, resistance rates to tetracycline and ampicillin are sufficiently high that the agents no longer have a role in treatment of Campylobacter or noncholera diarrhea (see References: Engeberg 2001, Coker 2002).
Primary resistance in Asian and European countries coincided with the addition of enrofloxacin to animal feed (eg, feed for broiler chickens). The basis for most resistance in C jejuni stems from a mutation in the gyrA gene (see References: Altekruse 1999, Allos 2001, Norstrom 2006). Restriction of antibiotic use in food-producing animals has kept resistance rates low in Australia and recent prohibition of enrofloxacin in the United States may help address resistance. European countries also have restricted usage (see References: Price 2005, Unicomb 2006).
Despite cessation of fluoroquinolone use in commercial flocks, resistance persists, fueled by resistant strains' ability to grow faster than nonresistant strains and crowd them out (see References: Price 2005).

Alternative Identification Techniques

Enrichment broths can be used in instances where low numbers of organisms are expected, for example, with delayed transport to the laboratory. They also can be useful in the acute stage when concentration of organisms may be low, for example, in investigation of Guillain-Barre syndrome after Campylobacter infection (see References: Nachamkin 2003).
Campylobacter species can be detected with enzyme-linked immunoassays or polymerase chain reaction (PCR), but these are not widely available (see References: AAP 2003).
DNA probes and PCR assays are mainly research tools and are not routinely performed. Multiplex PCR methods that target multiple genes may hold promise for routine diagnostic laboratory detection of C jejuni and C coli (see References: Persson 2005).

Serologic Testing

Serologic testing is useful for epidemiologic investigations but is not recommended for routine diagnosis.

Two major serotyping schemes are used worldwide. The Lior system detects heat-labile (HL, flagellar) antigens and the Penner system identifies heat stable (O, somatic) antigens.
Based on uncharacterized bacterial surface antigens and in some serotypes, flagellar antigens, Lior system serotyping can detect more than 100 serotypes of C jejuni, C coli, and C lari (see References: Nachamkin 2003).
Somatic serotyping detects 60 types of C jejuni and C coli. This system detects a Campylobacter capsular polysaccharide.
Serum IgG, IgM, and IgA levels rise during Campylobacter infection, with IgA appearing in the serum during the first few weeks and then decreasing rapidly. Serum antibody assays vary in sensitivity and specificity for detecting Campylobacter infections, and tests appear to be population-dependent.
Some patients who have Campylobacter infection may have false positive Legionella antibody test results.

Treatment

Treatment of diarrhea usually consists of oral fluid and electrolyte replacement. Patients who are severely dehydrated should have rapid volume expansion with intravenous solutions of electrolytes in water (see References: AAP 2003, Blaser 2005, CDC 2003, CDC 2004).
Antibiotics can be used in patients with high fever, bloody diarrhea, or more than eight stools per day; those whose symptoms have not diminished after several days of illness, worsened over time, or exceeded 1 week in duration; and those who are immunocompromised (see table below). C jejuni and C coli have variable susceptibilities to selected antimicrobial agents (see References: CDC 2003, CDC 2004, Nachamkin 2003).
Extensive quinolone use in animals and humans has increased Campylobacter resistance and has limited the utility of these drugs for empiric treatment of acute diarrheal illness (see References: Blaser 2005). Clarithromycin or azithromycin may shorten the duration of illness and decrease Campylobacter excretion, but growing resistance to macrolides is a concern (see References: Kuschner 1995, Engberg 2001).
Use of antimotility agents may prolong duration of symptoms and has been associated with fatalities (see References: Smith 1985).
For systemic infections, the following points should be kept in mind:

Endovascular infections from C fetus are treated with gentamicin or ampicillin for at least 4 weeks. Imipenem or meropenem are other alternatives (see References: Blaser 2005, Tremblay 2003).
Central nervous system infections should be treated with ampicillin, imipenem, or chloramphenicol for 2 to 3 weeks.
Patients with other serious infections also should receive parenteral gentamicin or another aminoglycoside, amipicillin, or imipenem for at least 2 weeks.

Drugs Used for Treating Campylobacter Infections*
Drug	Dosage for Adults	Dosage for Children
Macrolides
—Erythromycin stearate (drug of choice)†	250 mg PO qid or 500 my PO bid x 5-7 days	30-50 mg/kg/day in divided doses PO x 5-7 days
—Azithromycin	500 mg PO on day 1; 250 mg on days 2-5	Not recommended for children <16 yr
—Clarithromycin	250 mg PO x 12 hr for 5 days	Safe dosages not established
Quinolones
—Ciprofloxacin	500 mg PO bid for 5 days	Safe dosages not established
—Ofloxacin	200-400 mg PO every 12 hr x 5 days	Safe dosages not established
Nitrofurantoins
—Furazolidone	100 mg PO qid x 5 days	1.25 mg/kg PO qid for 5 days
Alternatives
—Clindamycin	150-300 mg PO x 6 hrs for 5 days	2-4 mg/kg every 6 hr for 5 days
—Tetracylcine	250-500 mg PO qid	6-12 mg/kg PO qid for children <8 yr
Abbreviations: PO, by mouth; bid, twice a day; tid, three times a day; qid, four times a day. Amoxicillin or ticarcillin plus clavulinic acid (but not sulbactam or tazobactam) may be effective (see References: Lachance 1993); most isolates are not susceptible to cephalosporins and penicillins (see References: Nachamkin 2003). †Telithromycin, a new drug, can also be used, but it offers no advantage over erythromycin (see References: Schonberg-Norio 2006). In developing countries, Campylobacter* species, especially C coli, are more likely to be resistant to erythromycin and tetracycline (see References: Smith 1985). Adapted from AAP 2003, Allos 2004, Blaser 2005, Nachamkin 2003 (see References).

Vaccines

Studies in developing countries of natural immunity in children who have been infected multiple times suggests that development of a vaccine for Campylobacter is possible, but lack of an animal model of virulence has hindered research (see References: Prendergast 2005).
Several antigens may serve as possible vaccine candidates owing to their ability to protect against disease. These include a 62 kDa flagellin protein, a 45 kDa major outer membrane protein, and a group of low-molecular mass proteins known as PEB proteins (see References: Walker 2005).
A major stumbling block to vaccine development is finding proteins that provide cross-protection against the species associated with human disease (see References: Walker 2005, Girard 2006).
A whole-cell vaccine tested in an animal model showed that cross protection among some of the major serotypes of Campylobacter responsible for human disease is possible, although it is not yet ready for use in humans (see References: Burr 2005).

Travel Implications

C jejuni and other Campylobacter species are important causes of diarrheal illness among travelers (see References: Freedman 2006).
Cautionary measures for travel include:

Eat only thoroughly cooked foods prepared in facilities that practice safe food handling techniques.
Consume pasteurized milk and milk products.
Drink bottled beverages or beverages made with water that has been boiled 5 minutes or local municipal water that has been adequately treated with chlorine or other appropriate disinfectant.
Avoid eating raw or undercooked meat and seafood.
Avoid eating raw fruits (eg, oranges, bananas, avocados) and vegetables unless the traveler peels them.
Avoid eating foods or drinking beverages purchased from street vendors or other establishments where unhygienic conditions are present.
Avoid drinking water (including ice in beverages) from sources where there is any question about the quality of the water supply, including tap water. Safe beverages include bottled carbonated beverages, hot tea or coffee, beer, wine, and water boiled or appropriately treated with iodine or chlorine.
To reduce the spread of infection, ensure that infected persons (especially children) wash their hands carefully and frequently with soap and water and do not prepare or handle food items.

Disease Prevention and Control

Prevention Measures

Food Safety Inspection Service (FSIS) guidelines are in place to minimize foodborne illnesses, and action plans have been developed for meat and poultry, fresh produce, and prepared foods. Information resources have been developed for consumers (see References: CFSAN 2004).
Because of the high levels of contamination among poultry flocks, eliminating Campylobacter may not be a viable strategy for control. Possible ways of reducing Campylobacter among chickens may include limiting use of antibiotics to minimize resistance, disinfecting animal food and water, treating manure, and isolating contagious and ill birds (see References: Adkin 2006, Norstrom 2006, Wingstrand 2006).
Proper hygienic practices for handling and preparing poultry include:

Use proper hand hygiene after handling raw poultry.
Wash cutting boards and utensils with soap and water after contact with raw poultry.
Use separate cutting boards for foods of animal origin and other foods.
Do not allow juices from raw poultry to contact other foods.
Cook poultry until juices run clear and the inside is cooked to 170°F (77°C) for breast meat and 180° (82°C) for thigh meat.

Critical food safety measures for individuals include:

Do not drink unpasteurized milk or eat products made from it, such as cheese and butter.
Drink only treated (chlorinated) water.
Make certain that persons who have diarrhea, especially children, wash their hands carefully before meals.
Wash hands after contact with animals or feces of animals (especially dogs and cats with diarrhea).

Guidelines for preventing disease associated with animals in public settings have also been issued that also include a section on disinfectants and their properties (see References: CDC 2005: Compendium).
Irradiation can eliminate bacteria in some foods.

Steps to Decrease Community Transmission

Appropriate hand hygiene is the most important factor in decreasing transmission of campylobacteriosis.
Symptomatic people should be excluded from food handling, care of patients in hospitals, care of people in long-term care facilities, and child-care centers.
Infected food handlers and hospital employees who are asymptomatic can work if they practice appropriate personal hygiene, including handwashing.
General measures for interrupting enteric transmission in child-care centers are recommended (see References: AAP 2003) and include:

Antimicrobial treatment or prophylaxis
Immunization (when appropriate)
Exclusion of ill or infected children from the facility
Provision of alternative care at a separate site
Cohorting to provide care
Limiting new admissions
Closing the facility (rarely used)

Infants and children with symptomatic C jejuni infection who are in diapers should be withheld from child care or cared for in a separate area until diarrhea has subsided.

Infection Control Measures in Healthcare Settings

Patients with Campylobacter infections should be managed with Standard Precautions (see References: CDC/HICPAC 1996).
According to CDC and the Hospital Infection Control Practices Advisory Committee (HICPAC), Contact Precautions should be added when caring for diapered or incontinent children younger than age 6 for the duration of illness (see References: CDC/HICPAC 1996):

Place the patient in a private room or if a private room is not available, place in a room with a patient who has an active infection with the same pathogen. When a patient is not available and cohorting is not possible, at least 3 feet of spatial separation should be maintained between the infected patient and other patients and visitors.
Gloves should be worn when entering the room and removed before leaving the room; hands should be washed with an antimicrobial agent or waterless handwashing agent immediately after removing gloves, and clean hands should not touch potentially contaminated items or environmental surfaces.
Gowns should be worn when entering the room if clothing will have substantial contact with the patient, environmental surfaces, or items in the room; the gown should be removed before leaving the patient's environment.
Patient transport should be limited to essential purposes only; if the patient is transported out of the room, precautions should be maintained.
Noncritical patient-care equipment should be dedicated whenever possible. If equipment cannot be dedicated, then it should be adequately cleaned and disinfected between uses.

Information for Businesses

Consumption of undercooked poultry and handling of raw poultry are the main risk factors for human Campylobacter infection; many serotypes of C jejuni isolated from chicken carcasses are frequently linked to human cases of campylobacteriosis (see References: Allos 2001, Keener 2004, Kramer 2000).

Pathogen Reduction Strategies

The US Department of Agriculture's Food Safety and Inspection Service (FSIS) implemented the Pathogen Reduction Hazard Analysis and Critical Control Point (HACCP) Systems, Final Rule in 1996 (see References: CFSAN 1996). The rule sought to reduce the risk of foodborne illnesses associated with consumption of meat and poultry products.
Pathogen-specific performance standards for raw products allow direct measures of progress in controlling and reducing pathogens (see References: Keener 2004), and FSIS strategies have been successful in reducing the incidence of E coli, Salmonella, and Listeria.
HACCP plans for plants and managers have been published in the United States (see References: CFSAN 2006: A manual for voluntary use; CFSAN 2006: A regulator's manual) and Europe (see References: Van Schothorst 2004), but these do not address Campylobacter specifically. Recent work suggests that measures that have been successful for Salmonella should work for Campylobacter, a more susceptible organism (see References: NACMCF 2006).
Campylobacter has been a target area in the Healthy People 2010 report (see References: CFSAN 2004), and the FSIS is preparing for studies on Campylobacter in poultry (see References: NACMCF 2005: Analytical utility of Campylobacter methodologies; NACMCF 2006: Responses to questions).
FSIS baseline testing in 1994-1995 estimated the prevalence of Campylobacter on raw chicken carcasses to be 88%, but concerns about methodology used in collecting the 1999-2000 data held up publication of new data and provided impetus for a new baseline study (see References: CFSAN 2004; FSIS 2006: Microbiology baseline data, FSIS 2006: NACMCF 2004-2006 Subcommittee).
The FSIS may implement a Campylobacter performance standard in the near future. They are seeking advice on proposed methodology for studying Campylobacter in poultry. Input will be used for initiating a nationwide baseline study to determine the prevalence and numbers of Campylobacter species in broiler carcasses at federally-inspected establishments as a basis for developing risk management strategies to reduce human exposure to Campylobacter (see References: FSIS 2006; NACMCF 2005: Analytical utility of Campylobacter methodologies; NACMCF 2006: Responses to questions).

The proposed study will focus on thermophilic species (those that grow between 37ºC and 42ºC) responsible for most of the laboratory-confirmed Campylobacter infections (C jejuni and C coli) (see References: NACMCF 2005).
Although other Campylobacter species occasionally are noted as causes of human illness, they are uncommon and require specialized growth conditions (see References: Keener 2004, NACMCF 2005).

Methods for Reducing Campylobacter in Poultry

Campylobacter is a commensal organism in many birds, including those grown commercially, as well as many other animals. Chicken internal organs, particularly the ceca, can be colonized to very high levels without causing symptoms (see References: Alterkuse 1999). Once an infection becomes established in a poultry house, entire flocks can be colonized (see References: Rivoal 2005).
Poultry processing can permit cross-contamination at many points, but contamination can be reduced with HACCP procedures. No control measure, however, has completely eliminated Campylobacter (see References: Keener 2004, Oyarzabal 2005).
Strategies at the animal production stage include (see References: Allos 2001, Altekruse 1999):

Limiting animal consumption of antibiotics (this strategy has been implemented to attempt to reduce development of fluoroquinolone-resistant species [see References: FDA 2005, Ge 2003, Price 2005])
Disinfection of animal food and water
Treatment of manure
Isolation of contagiously ill animals
Irradiation of foods of animal origin
Introduction of competing microbial populations into newly hatched chicks
Chlorination of poultry drinking water
Vaccination
Selective breeding of poultry for resistance to pathogens
Improving animal husbandry and hygiene practices

Several methods for reducing contamination in processing plants are in place (see References: Keener 2004, Oyarzabal 2004) and include:

Multiple modifications to procedures during scalding, defeathering, and evisceration to minimize cross-contamination.
Carcass washing (the degree of effectiveness depends on water volume, water pressure, and chlorine levels [see References: Oyarzabal 2005])
Carcass chillers (reduce growth of bacteria, but Campylobacter numbers remain high, and normal chilling may not be effective in reducing numbers) (see References: Oyarzabal 2005)
Processing aids: Results vary depending on the method, conditions, and type employed (see References: Keener 2004, Oyarzabal 2004); agents used to wash or prepare carcasses include:

Water (used as a rinse)
Organic acids (various acids are effective for removing Salmonella and C jejuni)
Chlorine (up to 50 parts per million [ppm] available chlorine added to rinse water)
Chlorine dioxide (the FDA has approved the use of up to 3 ppm residual chlorine dioxide in poultry process water)
Trisodium phosphate (effective, but phosphate content of waste water is a major limitation)
Acidified sodium chlorite (when used as a postchill dip, reduced Campylobacter to less that 0.2 log CFU/mL of carcass rinse; its effect may be indirectly increased by the chilling process) (see References: Oyarzabal 2004)
Irradiation: (effective but different Campylobacter species and strains exhibit significantly different sensitivities to radiation) (see References: Patterson 1995)

Online reprocessing (removes gross contamination from carcasses, but some bacteria remain after treatment)
Post-processing decontamination

Carcasses can be treated after inspection and processing, but levels of contamination of retail poultry remain high despite interventions made at the processing plant (see References: Smith 1999)
Post-chill counts of 0.5 to 1 log CFU/mL of carcass rinse (about 4,000 CFU per carcass) are still common (see References: Oyarzabal 2005)

Additional efforts to design more efficient and effective systems are needed to obtain better results (see References: Keener 2004)

The poultry industry is making progress in reducing levels of Campylobacter among poultry.

In the past 10 years, the US poultry industry has reduced Campylobacter contamination of processed broilers by more than 10-fold (see References: Stern 2006). The high levels of Campylobacter among poultry and the heavy bacterial burden in flocks make the reducing the organism levels a challenge, although measures taken have caused infections from Campylobacter to decline in recent years (see References: Samuel 2004).
Among 4,200 samples from 13 poultry processing complexes in the US taken during a 13-month period, 74% of carcass rinses yielded no countable Campylobacter cells. Campylobacter species were isolated from about 3.6% of all commercially processed broiler carcasses at more than 10,000 CFU per carcass, a fact that suggests the next incremental reduction may need to occur during animal production (see References: Stern 2006).

Analysis of published studies produced a ranking of measures used in Campylobacter control and may serve as the basis for additional research on the most effective control measures (see References: Adkin 2006). The analysis found that major sources of Campylobacter on farms include a depopulation event, another house on-farm, on-farm staff, and other animals on farm. Factors associated with increased risk included the depopulation schedule (staggered slaughter) and multiple houses on farm.

Information for Consumers

The ideal way to control the number of human Campylobacter infections would be to limit contamination of poultry flocks, but because this tactic is difficult to accomplish, safe handling methods are important for consumers (see References: Adkin 2006, Stern 2006).
Campylobacter affects many people in the US and other countries and nonadherence to safe handling measures can lead to infection. In the US, about 50% to 70% of Campylobacter cases are believed to arise from consuming undercooked poultry and poultry products (see References: Keener 2004), and improper handling methods contributed to the first major outbreak of Campylobacter associated with chicken in Denmark (see References: Mazick 2006).
In experimental studies, combined prerefrigeration and freezing methods reduced cell counts on chicken skin and ground chicken, but C jejuni survived storage at 4ºC and -20ºC in both products. Such results indicate that either method alone or in combination is no substitute for safe handling and proper cooking (see References: Bhaduri 2004).
Experimental studies of handling techniques reveal that large numbers of bacteria can be transferred from chicken by improper handling and hygiene practices in domestic kitchens (see References: Kusumaningrum 2004, Luber 2006, Moore 2003).

Quantitative assessment of Campylobacter numbers revealed considerable bacterial transfer to ready-to-eat food in poultry handling experiments that simulated several kitchen preparation scenarios. The mean transfer rates from hands or kitchen utensils to ready-to-eat foods were 2.9% for chicken legs and 3.8% for breast filets. Transfer rates were higher in chicken samples that had greater numbers of bacteria (see References: Luber 2006).
Studies of quantitative transfer of Campylobacter from stainless steel preparation surfaces to prepared foods showed mean transfer rates of 42.5% to cucumber slices (see References: Kusumaningrum 2004), up to 38% for dry lettuce, and as much as 27% for wet lettuce (see References: Moore 2003).

Basic food safety

Consumers should avoid contaminating food and can follow procedures in the kitchen to prevent foodborne illnesses (see References: FSIS 2002; PFSE 2006: Safe food handling; PFSE 2006: Fight Bac!).
Basic food safety suggestions include :

Clean: Wash hands often.
Separate: Don’t cross contaminate. Separate raw, cooked, and ready to eat foods while shopping, preparing, or storing. Never place cooked food on a plate that previously held raw meat, poultry, or seafood.
Cook: Cook food to proper temperature. Use a food thermometer to be sure (see References: FSIS 2006: Thermy).
Chill: Refrigerate promptly. Refrigerate or freeze perishables, prepared foods, and leftovers within 2 hours. Never store uncooked foods on the shelf above prepared foods because the juice may drip into and contaminate the cooked food.

Downloadable handouts and guidelines for food safety are available on fact sheets (see References: FSIS 2006: Food safety education; FSIS 2002: Safe food handling; WHO 2004; WHO 2005).

Handling and Cooking Poultry

Consumers should be careful when handling and preparing chicken. One drop of raw chicken juice can contain 500 Camplylobacter organisms (an amount approximately that of an infective dose). Simply failing to wash hands after handling chicken, then touching or preparing other items can cross-contaminate food and preparation surfaces and lead to infection (see References: Allos 2001).
Chicken should be cooked to a minimum internal temperature of 165ºF (73.8ºC), and current recommendations suggest using a meat thermometer to measure internal temperature (see References: FSIS 2006: Is it done yet?; FSIS 2006: Thermy).
Some cuts may have to be cooked to higher temperatures—170ºF (76.7ºC) for breast meat and 180ºF (82.2ºC) for whole thigh meat—to eliminate pinkness and ensure meat is done (See References: NACMCF 2006).
Downloadable information about poultry, preservation methods, handling, safe cooking, and storage are available at:

New consumer guidelines for cooking poultry are currently being developed and should offer more detailed instructions in the future (see References: NACMCF 2006).

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