What is Campylobacter bacteria?

Campylobacter (camp-UH-low-back-ter) is a genus of bacteria that is among the most common causes of bacterial infections in humans worldwide. [1, 5, 6] The name means “curved rod,” deriving from the Greek campylos (curved) and baktron (rod). [5, 22] It has been noted that there “is wide diversity in the genus. The species are metabolically and genetically different to the extent that one can question whether one genus is adequate to house all of the species.” [22]

Of its many species, Campylobacter jejuni (juh-JUNE-eye) is considered one of the most important from both a microbiological and public health perspective. The history of this species of bacteria has been summarized as follows:

Awareness of the public health implications of Campylobacter infections has evolved over more than a century. In 1886, Escherich observed organisms resembling campylobacters in stool samples of children with diarrhea. In 1913, McFaydean and Stockman identified campylobacters (called related Vibrio) in fetal tissues of aborted sheep. In 1957, King described the isolation of related Vibrio from blood samples of children with diarrhea, and in 1972, clinical microbiologists in Belgium first isolated campylobacters from stool samples of patients with diarrhea. The development of selective growth media in the 1970s permitted more laboratories to test stool specimens for Campylobacter. Soon Campylobacter [species] were established as common human pathogens. [1]

Campylobacter jejuni is a gram-negative, microaerophilic, thermophilic rod that grows best at 42°C (107°F) and low oxygen concentrations. [5, 22] These characteristics are adaptations for growth in its normal habitat—the intestines of warm-blooded birds and mammals. [1, 5] Several closely related species with similar characteristics, C. coli, C. fetus, and C. upsalienis, may also cause disease in humans, but are responsible for less than 1% of human infections annually. [1, 5, 12] “Campylobacters multiply more slowly than do the usual bacteria of the enteric flora and therefore cannot be isolated from fecal specimens unless selective techniques are used.” [5] Campylobacter is the most commonly isolated bacterial pathogen from persons suffering diarrheal illnesses, and C. jejuni is the most commonly isolated of the species. [28]

The Incidence of Campylobacter Infections

From the time of its initial discovery, through the ensuing period of investigation and study, Campylobacter jejuni has come to be understood as one of the leading causes of bacterial gastroenteritis. [1, 5, 7] In the United States, these bacteria are the most common cause of bacterial foodborne illness, ahead of Salmonella—the second most common cause. [1, 10, 25] According to the CDC, based on data collected through its Foodborne Disease Active Surveillance Network (or FoodNet),

Campylobacter is one of the most common causes of diarrheal illness in the United States. The vast majority of cases occur as isolated, sporadic events, not as part of recognized outbreaks. Active surveillance through FoodNet indicates that about 13 cases are diagnosed each year for each 100,000 persons in the population. Many more cases go undiagnosed or unreported, and campylo-bacteriosis is estimated to affect over 2.4 million persons every year, or 0.8% of the population. [12]

In 2006, 5,712 confirmed cases of Campylobacter infection were reported to the CDC through FoodNet. [10] Three years later, in 2009, there were 6,033 confirmed cases of Campylobacter infections, which represented an incidence rate of 13.02 cases for every 100,000 persons in the United States. [11] The 2009 numbers represented a reported 30% decrease in the number of infections compared to the 1996—1998 rates of infection. Although the nature and degree of underreporting is subject to dispute, all agree that the confirmed cases represent just the tip of the iceberg. Indeed, one study estimates the annual incidence rate for Campylobacter to be around 1,000 cases per 100,000 persons. [6] As early as 1990, it was noted that annual reports to the CDC of Campylobacter infections was as high as 10,000 lab-confirmed cases. [15] 

The Prevalence of Campylobacter in Food and Elsewhere

Although most cases of Campylobacter infection in humans are sporadic, a substantial number of outbreaks—30 outbreaks by one report, and 50 by another—have been linked to the consumption of unpasteurized (raw) milk. [1, 5] Since 1992, food remains the most common vehicle for the spread of Campylobacter, and chicken is the most common food implicated. [5, 25, 28] As one authority points out, “commercially raised poultry is nearly always colonized with C. jejuni, slaughterhouse procedures amplify contamination, and chicken and turkey in supermarkets, ready for consumers to take home, frequently is contaminated.” [5] Similarly, prominent USDA researchers have noted:

Most retail chicken is contaminated with C. jejuni; one study reported an isolation rate of 98% for retail chicken meat. C. jejuni counts often exceed 103 per 100 g. Skin and giblets have particularly high levels of contamination. In one study, 12% of raw milk samples from dairy farms in eastern Tennessee were contaminated with C. jejuni. Raw milk is presumed to be contaminated by bovine feces; however, direct contamination of milk as a consequence of mastitis also occurs. Campylobacters are also found in red meat. In one study, C. jejuni was present in 5% of raw ground beef and in 40% of veal specimens. [1]

Since 1998, the publisher of Consumer Reports magazine has conducted surveys and tested chicken at retail for Salmonella and Campylobacter. While the first study identified Campylobacter in 63% of more than 1000 chickens obtained in grocery stores, a 2009 study found only a 1% improvement, with 62% of the 382 chickens tested positive for Campylobacter. [14] A USDA Baseline Data Collection Program done in 1994 documented Campylobacter contamination on 88.2% of broiler-chicken carcasses [30]. Subsequent USDA data collection has shown an estimated 46.7% prevalence of Campylobacter in chicken [31], and 1.46% in turkeys. [32] Campylobacter is also prevalent in wild birds of all kinds. [1, 5]

As already noted, contamination occurs during slaughter and processing when meat comes into contact with animal feces. Consequently,

Slaughter and processing provide opportunities for reducing C. jejuni counts on food-animal carcasses. Bacterial counts on carcasses can increase during slaughter and processing steps. In one study, up to a 1,000-fold increase in bacterial counts on carcasses was reported during transportation to slaughter. In studies of chickens and turkeys at slaughter, bacterial counts increased by approximately 10- to 100-fold during defeathering and reached the highest level after evisceration. However, bacterial counts on carcasses decline during other slaughter and processing steps. In one study, forced-air chilling of swine carcasses caused a 100-fold reduction in carcass contamination. In Texas turkey plants, scalding reduced carcass counts to near or below detectable levels. Adding sodium chloride or trisodium phosphate to the chiller water in the presence of an electrical current reduced C. jejuni contamination of chiller water by 2 log10 units. In a slaughter plant in England, use of chlorinated sprays and maintenance of clean working surfaces resulted in a 10- to 100-fold decrease in carcass contamination. In another study, lactic acid spraying of swine carcasses reduced counts by at least 50% to often undetectable levels. A radiation dose of 2.5 KGy reduced C. jejuni levels on retail poultry by 10 log10 units. [1]

Further, with poultry, contamination levels peak during the summer months [1, 5, 28], and this seasonal pattern is reflected in the number of reported Campylobacter infections. [5, 28]

Transmission of and Infection with Campylobacter

Most Campylobacter infections in humans are caused by the consumption of contaminated food or water. [5]  Direct contact with infected animals, including pets, is also a well-documented means of disease-transmission. [1, 6] Although not common, person-to-person transmission can also occur. [5, 6] Males and females appear to be equally affected, although the prevalence of infection in otherwise healthy people is quite low. [5] Population-based studies show that the peak incidence of infection is in children one year of age and under, and in persons between 15 and 29 years of age. [26] Incidence of Campylobacter infection in HIV-positive individuals is higher than in the general population. [1, 5]

The infective dose—that is, the amount of bacteria that must be ingested to cause illness—is relatively small. [5, 28]  Ingestion of as few as 500 organisms, an amount that can be found in one drop of chicken juice, has been shown to cause human infection. [5, 12, 28]  Despite this low infectious dose, and the ubiquity of Campylobacter in the environment, most cases of Campylobacter infection occur as isolated, sporadic events, and are not usually part of large outbreaks. [1, 26] But, very large outbreaks (greater than 1,000 illnesses) have been documented, most often from consumption of contaminated milk or unchlorinated water supplies. [1, 5, 6, 28]

Symptoms of Campylobacter infection

Not all Campylobacter infections cause the infected person to fall ill or develop symptoms. [5] The lack of symptoms can be the result of two things—the relative susceptibility (or immunity) of the person infected, and the dose of organisms that reach the small intestines. [5, 28] When a person is infected and develops symptoms, the illness is called campylobacteriosis. [12, 28]

The amount of time from infection to the onset of symptoms—typically referred to as the incubation period—can vary to a significant degree.  According to one authoritative text, “the incubation period varies from 1 to 7 days, a characteristic that is probably inversely related to the dose ingested.” [5]  Others note that the “incubation period is 1 to 10 days, with most cases occurring 3 to 5 days after exposure.” [28] Most agree, however, that incubation periods of greater than 7 days are not uncommon. [1, 5, 6, 26, 28]

Diarrhea is the most consistent and prominent manifestation of campylobacteriosis, and is often bloody. [1, 6, 9] As one article summarizes,

Campylobacteriosis symptoms can range from diarrhea and lethargy that lasts a day to severe diarrhea and abdominal pain (and occasionally fever) that lasts for several weeks.  Diarrhea and abdominal pain are the most common symptoms and the vast majority of cases are mild.  [Two researchers] report that abdominal pain from campylobacteriosis can be so strong that it has been misdiagnosed as originating from appendicitis and has led to unnecessary appendectomy… [28]

Although most cases of campylobacteriosis are self-limiting, up to 20% have a prolonged illness (longer than 1 week) or a relapse [5], and 2% to 10% may be followed by chronic sequelae. [6, 15] Other typical symptoms of C. jejuni infection include fever, nausea, vomiting, abdominal pain, headache, and muscle pain. [1, 15] Such infections can also be severe and life-threatening. [5, 6]  Death is more common when other diseases (e.g., cancer, liver disease, and immuno-deficiency diseases) are present. [1, 5, 28] One often-cited study estimates that 200 to 730 persons dies as a result of Campylobacter infections each year. [8, 26]

The illness usually lasts no more than one week; however, severe cases may persist for up to three weeks, and roughly 25% of individuals experience symptom relapse. [5, 15, 28] In most cases, the worst of the illness, which is to say the most intense and painful of the symptoms, lasts 24-48 hours, before then taking a week to fully resolve. [6]

Complications of Campylobacter infection

For those persons who suffer a Campylobacter infection that does not resolve on its own, the complications (or sequelae) can be many. [5] The complications can include septicemia (bacterial pathogens in the blood, also known as bacteremia), meningitis, inflammation of the gall bladder (cholecystitis), urinary tract infections, and appendicitis. [1, 6, 28].

Guillain-Barré Syndrome (GBS)

“Each year, there are an estimated 2,628 to 9,575 people who develop GBS in the United States.” [8] A sizeable percentage of persons who suffer Campylobacter infections develop GBS. [1, 8, 28]  Since the vaccination programs have eliminated polio in the United States, GBS is the leading cause of acute neuromuscular paralysis. [8] Over time, the paralysis is to some extent typically reversible; nonetheless, approximately 20% of patients with GBS are left disabled, and approximately 5% die. [1, 28]

An estimated one case of GBS occurs for every 1,000 Campylobacter infections. [1] Along these same lines, researchers estimate that between 20% and 40% of all GBS cases are caused by Campylobacter infections. [28] Indeed, up to 40% of GBS patients have evidence of recent Campylobacter infection. [1, 23] “Assuming that 20 to 40 percent of all patients with GBS have prior Campylobacter infections, there are an estimated 526 to 3, 830 new patients diagnosed with Campylobacter-associated GBS each year in the United States.” [8]

GBS occurs when an infected person’s immune system makes antibodies against components of Campylobacter, and these antibodies attack components of the body’s nerve cells because they are chemically similar to bacterial components. [1, 2, 8] Miller Fisher Syndrome is another, related neurological syndrome that can follow campylobacteriosis, and is also caused by a triggered immune-response. [2] Overall, there is no one factor that appears to cause a greater percentage of GBS cases other than Campylobacter infections. [8]

The annual cost of Campylobacter-associated GBS in the United States is estimated to be between $0.2 to $1.8 billion (in 1995 dollars). [8]

Reactive Arthritis

Another chronic condition that may be associated with Campylobacter infection is a condition formerly known as Reiter’s syndrome, a form of reactive arthritis. [1, 6, 28] “Multiple joints can be affected, particularly the knee joint. Pain and incapacitation can last for months or become chronic.” [1] Reactive Arthritis is a complication that is strongly associated with a particular genetic make-up—that is, persons who have the human lymphocyte antigen B27 (HLA-B27) are most susceptible. [1, 5] Most often, the symptoms of reactive arthritis can occur up to several weeks after infections. [5]

Diagnosis of a Campylobacter Infection

Diagnosis of infection is usually based on the isolation of Campylobacter jejuni from a stool culture. [1, 7] A diagnosis can also be established by the direct examination of a stool sample using contrast microscopy or Gram’s strain. [5, 6] This direct examination provides for a rapid presumptive diagnosis that must still be confirmed by stool culture. [5]

Stool samples should be chilled, but not frozen, for transportation to the testing-lab. [1] Labs now routinely perform culture-procedures on stool specimens that are specifically designed to promote the growth and identification of Campylobacter jejuni and the other species of Campylobacter. [1, 11, 12] Only a small percentage of persons suffering from Campylobacter infections both present for medical care and have their infections culture-confirmed. [5, 12, 26] In the study of one Campylobacter outbreak, only 5.4% of the outbreak cases visited a physician. [28] It is estimated that 12,700 to 13,230 cases are hospitalized each year. [26, 28]

Many persons submit samples for culturing after they have started antibiotics, which may make it even more difficult for a lab to grow Campylobacter.  [5] Blood cultures are often not performed and in most cases the blood stream is not infected. [1, 5]

Treatment of a Campylobacter Infection

Patients with Campylobacter infection should drink plenty of fluids as long as the diarrhea lasts in order to maintain hydration. [5] Dehydration is a common consequence of the diarrhea that infection causes, and, when severe, requires the administration of intravenous fluids. [5] For those not severely dehydrated, taking fluids by mouth works well, especially fluids that contain glucose and electrolytes—e.g., Gatorade or Pedialyte. [5, 12]

Campylobacteriosis is usually a self-limited illness, with fewer than half of patients seen for medical care being good candidates for treatment with antibiotics. [5] But for those patients with a high fever, bloody diarrhea, or stools more frequent than eight times per day, antibiotic-treatment is deemed a “prudent course.” [5] When indicated, such treatment with antibiotics can reduce the average duration of the illness from ten to five days. [1]

In more severe cases of gastroenteritis, antibiotics are often begun before culture results are known.  Macrolide antibiotics (erythromycin, clarithromycin, or azithromycin) are the most effective agents for Campylobacter jejuni.  [5, 6] Fluoroquinolone antibiotics (ciprofloxacin, levofloxacin, gatifloxacin, or moxifloxacin) can also be used, but resistance to this class has been rising, at least in part due to the use of this class of antimicrobial in poultry feed. [1, 25]

Antimicrobial Resistance in Bacteria 

Antimicrobial resistance in bacteria is an emerging and increasing threat to human health. [1, 4] Physicians are increasingly aware that antimicrobial resistance is increasing in foodborne pathogens and that, as a result, patients who are prescribed antibiotics are at increased risk for acquiring antimicrobial-resistant foodborne infections. [1] Indeed, “increased frequency of treatment failures for acute illness and increased severity of infection may be manifested by prolonged duration of illness, increased frequency of bloodstream infections, increased hospitalization or increased mortality.” [3]

The use of antimicrobial agents in the feed of food animals is estimated by the FDA to be over 100 million pounds per year. [4] Estimates range from 36%  to 70% of all antibiotics produced in the United States are used in a food animal feed or in prophylactic treatment to prevent animal disease. [3, 4, 18] In 2002, the Minnesota Medical Association published an article by David Wallinga, M.D., M.P.H. who wrote:

According to the [Union of Concerned Scientists], 70 percent of all the antimicrobials used in the United States for all purposes—or about 24.6 million pounds annually—are fed to poultry, swine, and beef cattle for nontherapeutic purposes, in the absence of disease. Over half are “medically important” antimicrobials; identical or so closely related to human medicines that resistance to the animal drug can confer resistance to the similar human drug. Penicillin, tetracycline, macrolides, streptogramins, and sulfonamides are prominent examples. [33]

Moreover, the National Antimicrobial Resistance Monitoring System (NARMS) has reported that Campylobacter has been recovered from 47% of chicken breasts tested in recent studies. [34] According to the report of findings,

Antimicrobial resistance among these foodborne bacteria is not uncommon and often associated with the use of antimicrobial agents in food animals.  Retail food represents a point of exposure close to the consumer, and when combined with data from slaughter plants and on-farm studies, may provide an indication of the prevalence of resistance in foodborne pathogens. [34].

By way of further example, especially given that Salmonella is so often found co-present with Campylobacter in raw poultry, Ceftriaxone-resistant Salmonella has also been reported. [18] As such, the emergence of multidrug-resistant Salmonella Typhimurium in the United States is another example of a drug-resistant bacteria spreading from animals to humans. [19]

The use of antibiotics in feed for food animals, on animals prophylactically to prevent disease, and the use of antibiotics in humans unnecessarily must be reduced. [1, 25] European countries have reduced the use of antibiotics in animal feed and have seen a corresponding reduction in antibiotic-resistant illnesses in humans. [1, 4]

The Economic Impact of Campylobacter Infections

The USDA Economic Research Service (ERS) published its first comprehensive cost estimates for sixteen foodborne bacterial pathogens in 1989. [24]  Five years later, it was estimated that the medical costs and productivity losses that Campylobacter infections caused each year ran from $907 million to over $1 billion, based on an estimate of 2.1 million cases and between 120-360 deaths. [15] Using a different kind of economic analysis, this same 1996 study estimated that the average cost of each Campylobacter infection to be $920, with this estimate based on a much lower incidence and death rate. [15]

In 1996, ERS updated the cost-estimates for six bacterial pathogens, including Campylobacter. [28] ERS continued to use cost-of-illness (COI) methodology for nonfatal illnesses, but adopted two different health valuation methodologies for premature deaths: the individualized human capital approach and the willingness-to-pay (WTP) approach. This report concluded as follows:

We assumed that 55-70 percent of all estimated human illness cases of Campylobacter in the United States are foodborne (1,375,000 to 1,750,000 cases).  Estimates of those who do not visit a physician range from 1,293,765 to 1,646,239 cases annually.  A low of 74,250 and a high of 94,500 visit a physician. The number of hospitalized cases (including those who died) ranges from 6,985 to 9,261. Foodborne deaths caused by Campylobacter range from 110 to 511 annually. Given our assumption that 55-70 percent of all U.S. campylobacteriosis cases are attributed to food, estimated costs of foodborne campylobacteriosis range from $0.6-$1.0 billion annually.

ERS updated the cost-estimates for four pathogens (Campylobacter, Salmonella, E. coli O157:H7, and Listeria monocytogenes) again in 2000. The 2000 estimates were based on newly released estimates of annual foodborne illnesses by the CDC, and put the total cost in the United States for these four pathogens at $6.5 billion a year. More recently, in 2007, it was estimated that the annual costs of all foodborne disease in the United States was $1.4 trillion. [8]

Real Life Impacts of Campylobacter Infection

Because the illnesses caused by the ingestion of Campylobacter bacteria range from mild to severe, the real life impacts of Campylobacter infection vary from person to person.

While anyone can become ill with Campylobacter infection, very young children, the elderly, and persons with compromised immune systems are most likely to develop severe illness.

  • An estimated 1 in 1,000 patients with Campylobacter infection develop a rare disease called Guillain-Barre syndrome, or GBS. GBS typically sets in several weeks after acute Campylobacter  During GBS, a person’s immune system attacks the body’s nerves, resulting in paralysis that can last for several weeks or years.  According to the CDC, as many as 40% of Guillain-Barre syndrome cases in the U.S. may be triggered by Campylobacter infection.[12]
  • An unknown percentage of patients with Campylobacter infections develop reactive arthritis.

How can I prevent the spread of Campylobacter food poisoning?

Campylobacter jejuni grows poorly on properly refrigerated foods, but does survive refrigeration and will grow if contaminated foods are left out at room temperature. [1, 7] The bacterium is sensitive to heat and other common disinfection procedures; pasteurization of milk, adequate cooking of meat and poultry, and chlorination or ozonation of water will destroy this organism. [1, 5, 12] Infection control measures at all stages of food processing may help to decrease the incidence of Campylobacter infections, but the single most important and reliable step is to adequately cook all poultry products. [17, 27]

The most reliable method to ensure this is to use a digital food thermometer. [17] Document that the thickest part of the chicken, turkey, duck or goose (the center of the breast) reaches 180°F or higher, as recommended by the U.S. Food and Drug Administration. [14, 17] The FDA and its Model Food Code recommends at least 165°F for stuffing, 170°F for ground poultry products, and that thighs and wings be cooked until juices run clear. [17, 27]

Most cases of campylobacteriosis are sporadic or involve small family groups, although some common-source outbreaks involving many people have been traced to contaminated water or milk. [1,5, 26] Other sources of Campylobacter include children prior to toilet training, especially in childcare settings [20], and intimate contact with other infected individuals. [5]  C. jejuni is commonly present in the gastrointestinal tract of healthy cattle, pigs, chickens, turkeys, ducks, and geese, and direct animal exposure can lead to infection. [1] Pets that may carry Campylobacter include birds, cats, dogs, hamsters, and turtles. [1, 5, 16] The organism is also occasionally isolated from streams, lakes and ponds. [1]

There are a large number of control measures of import that are available to consumers and foodservice personnel to prevent the transmission of Campylobacter. [17, 21, 27] These control measures include the following:

  • Choose the coolest part of the vehicle (generally the trunk in winter and cab in summer) to transport meat and poultry home from the market.
  • Defrost meat and poultry in the refrigerator. Place the item on a low shelf, on a wide pan, lined with paper towel; ensure that drippings do not land on foods below. If there is not enough time to defrost in the refrigerator, then use the microwave.
  • Do not cook stuffing actually inside the bird.
  • Rapidly cool leftovers.
  • Never leave food out at room temperature (either during preparation or after cooking) for more than 2 hours.
  • Avoid raw milk and products made from raw milk. Drink only pasteurized milk products.
  • Wash hands thoroughly using soap and water, concentrate on fingertips and nail creases, and dry completely with a disposable paper towel at the following times:
    • after contact with pets, especially puppies, or farm animals. [16]
    • before and after preparing food, especially poultry.
    • after changing diapers or having contact with an individual with an intestinal infection.
    • children on arrival home from school or day-care.
  • Wash fruits and vegetables carefully, particularly if they are eaten raw. If possible, vegetables and fruits should be peeled.
  • Use pasteurized eggs.


  1. Altekruse, Sean et al., “Campylobacter jejuni—An Emerging Foodborne Pathogen,” EMERGING INFECTIOUS DISEASES, Vol. 5, No. 1, pp. 28-35 (Jan.-Mar. 1999), online at http://www.cdc.gov/ncidod/eid/vol5no1/pdf/altekruse.pdf
  2. Ang, C.W., et al., “Guillain-Barre syndrome and Miller Fisher syndrome-associated Campylobacter jejuni lipopolysaccharides induce anti-GM1 and anti-GQ1b antibodies in rabbits,” INFECTION AND IMMUNITY, Vol. 69, No. 4, pp. 2462-69 (April 2001).
  3. Angulo, F.J., et al., “Antimicrobial Use in Agriculture: Controlling the Transfer of Antimicrobial Resistance to Humans,” SEMINARS IN PEDIATRIC INFECTIOUS DISEASES, Vol. 15, No. 2, pp. 78-85 (April 2004).
  4. Angulo, F.J., et al., “Evidence of an Association Between Use of Anti-microbial Agents in Food Animals and Anti-microbial Resistance Among Bacteria Isolated from Humans and the Human Health Consequences of Such Resistance, JOURNAL OF VETERINARY MEDICINE, Series-B, Vol. 51, Issue 8-9, pp. 374-79 (Oct. 2004).
  5. Blaser, Martin J., “Campylobacter jejuni and Related Species,” in Mandell, Douglas, And Bennett’s PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES, Fifth Edition, Chap. 204, pp. 2276-85 (2000, Mandell, Bennett, and Dolan, Editors)
  6. Blaser, M.J., “Epidemiologic and Clinical Features of Campylobacter jejuni Infections,” THE JOURNAL OF INFECTIOUS DISEASES, Vol. 176, Supplement 2, pp. S103-05 (1997) online at http://jid.oxfordjournals.org/content/176/Supplement_2/S103.long
  7. Blaser, M.J. and Reller, L.B., “Campylobacter Enteritis,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 305, pp. 1444-52 (Dec. 10, 1981).
  8. Buzby, Jean and Roberts, Tonya, “The Economics of Enteric Infections: Human Foodborne Disease Costs, GASTROENTEROLOGY, 136, No. 6, pp. 1851-62 (May 2009).
  9. CDC, “Preliminary FoodNet data on the incidence of foodborne illnesses – Selected sites, United States, 1999,” MORBIDITY AND MORTALITY WEEKLY REPORT, Vol. 49, No. 10, pp. 201-03 (March 17, 2000) at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm4910a1.htm
  10. CDC, “Preliminary FoodNet Data on the Incidence of Infection with Pathogens Transmitted Commonly through Food—10 States, 2006,” MORBIDITY AND MORTALITY WEEKLY REPORT, Vol. 56, No. 14, pp. 336-9 (April 13, 2007), available online at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5614a4.htm
  11. CDC, “Preliminary FoodNet Data on the Incidence of Infection with Pathogens Transmitted Commonly through Food—10 States, 2009,” MORBIDITY AND MORTALITY WEEKLY REPORT, Vol. 59, No. 14, pp. 418-22 (April 16, 2010) available online at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5914a2.htm
  12. CDC, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, “Campylobacter—General Information and Frequently Asked Questions,” (last updated: July 20, 2010), available at http://www.cdc.gov/nczved/divisions/dfbmd/diseases/campylobacter/
  13. CDC, SALMONELLA SURVEILLANCE: ANNUAL SUMMARY: 2005 (2007) available online at http://www.cdc.gov/ncidod/dbmd/phlisdata/salmtab/2005/SalmonellaIntroduction2005.pdf
  14. Consumers Union, “How Safe is that Chicken?” CONSUMER REPORTS (Jan. 2010), online at http://www.consumerreports.org/cro/magazine-archive/2010/january/food/chicken-safety/overview/chicken-safety-ov.htm
  15. Council for Agriculture, Science and Technology (CAST), “Foodborne Pathogens: Risks and Consequences: Task Force Report No.122,” pp. 1-87 (Sept. 1994) download at http://www.cast-science.org/publications/index.cfm/foodborne_pathogens_risks_and_consequences?show=product&productID=2852
  16. Fang, G, et al., “Enteric infections associated with exposure to animals or animal products,” INFECTIOUS DISEASE CLINICS OF NORTH AMERICA Vol. 5, pp. 681-701 (1991).
  17. FDA, “Safe Food Handling: What You Need to Know,” (Last Updated: 06/23/2011), online at http://www.fda.gov/Food/ResourcesForYou/Consumers/ucm255180.htm
  18. Fey, PD, et al., “Ceftriaxone-resistant Salmonella infection acquired by a child from cattle,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 342, pp. 1242–49 (April 27, 2000), online http://www.nejm.org/doi/full/10.1056/NEJM200004273421703
  19. Glynn, MK, et al., “Emergence of multidrug-resistant Salmonella enterica serotype typhimurium DT104 infections in the United States,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 338, pp. 1333-38 (May 7, 1998) http://www.nejm.org/doi/full/10.1056/NEJM199805073381901
  20. Goossens, H, et al., “Investigation of an outbreak of Campylobacter upsaliensis in day care centers in Brussels: Analysis of relationships among isolates by phenotypic and genotypic typing methods,” JOURNAL OF INFECTIOUS DISEASES, Vol. 172, pp.1298-305 (Nov. 1995).
  21. Minnesota Department of Health (MDH), “Preventing Campylobacteriosis,” online at http://www.health.state.mn.us/divs/idepc/diseases/campylobacteriosis/prevention.html
  22. Penner, J.L., “Genus of Campylobacter: a Decade of Progress,” CLINICAL MICROBIOLOGY REVIEWS, Vol. 1, No. 2, pp. 157-72 (April 1988) at http://cmr.asm.org/cgi/reprint/1/2/157
  23. Rees, JH, et al., “Campylobacter jejuni infection and Guillain-Barré syndrome,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 333, pp. 1374-79 (Nov. 23, 1995) available at http://www.nejm.org/doi/full/10.1056/NEJM199511233332102
  24. Roberts, T, “Human Illness Costs of Foodborne Bacteria,” AMERICAN JOURNAL OF AGRICULTURE ECONOMICS, Vol. 71, No. 2, pp. 468-474 (1989).
  25. Smith, KE, et al., “Quinolone-resistant Campylobacter jejuni infections in Minnesota, 1992-1998,” NEW ENGLAND JOURNAL OF MEDICINE, Vol. 340, pp. 1525-32 (May 20, 1999) online at http://www.nejm.org/doi/full/10.1056/NEJM199905203402001
  26. Tauxe, Robert, “Epidemiology of Campylobacter jejuni infections in the United States and other industrial nations,” in CAMPYLOBACTER JEJUNI: CURRENT AND FUTURE TRENDS, pp. 9-12, (Nachamkin, Blaser, and Tompkins, Eds., 1992).
  27. University of Florida, IFIS Extension, “Preventing Foodborne Illness: Campylobacteriosis,” Food Science and Human Nutrition Department, Florida Cooperative Extension Service, (Jan. 2003) online at http://edis.ifas.ufl.edu/fs098
  28. USDA Economic Research Service, “Bacterial Foodborne Disease—Medical Costs and Productivity Losses,” AER-741, August 1996 (authors: Jean C. Buzby, et al.) online at http://www.ers.usda.gov/Publications/AER741/
  29. USDA Economic Research Service, “Estimated Annual Costs of Campylobacter-Associated Guillain-Barré Syndrome,” AER-756, July 1997 (authors: Jean C. Buzby, et al.) online at http://www.ers.usda.gov/publications/aer756/AER756.PDf
  30. USDA Food Safety and Inspection Service (FSIS), NATIONWIDE BROILER CHICKEN MICROBIOLOGICAL BASELINE DATA COLLECTION PROGRAM, July 1994—July 1995, (April 1996), online at http://www.fsis.usda.gov/OPHS/baseline/broiler1.pdf
  31. USDA Food Safety and Inspection Service (FSIS), THE NATIONWIDE MICROBIOLOGICAL BASELINE DATA COLLECTION PROGRAM: YOUNG CHICKEN SURVEY, July 2007—June 2008, at http://www.fsis.usda.gov/PDF/Baseline_Data_Young_Chicken_2007-2008.pdf
  32. USDA Food Safety and Inspection Service (FSIS), THE NATIONWIDE MICROBIOLOGICAL BASELINE DATA COLLECTION PROGRAM: YOUNG TURKEY SURVEY, Aug. 2008—July 2009, at http://www.fsis.usda.gov/PDF/Baseline_Data_Young_Turkey_2008-2009.pdf
  33. Wallinga, D, “Antimicrobial Use in Animal Feed:  An Ecological and Public Health Problem,” MINNESOTA MEDICINE, Vol. 85, No. 10 pp. 12-16 (Oct. 2002).
  34. White, David, National Antimicrobial Resistance Monitoring System (NARMS), Meetings for Expert Reviews on the NARMS Program, June 23-24, 2005, Rockville, MD, TRANSCRIPT, http://www.fda.gov/AnimalVeterinary/SafetyHealth/AntimicrobialResistance/NationalAntimicrobialResistanceMonitoringSystem/ucm143994.htm