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Volume 5, Number 1—February 1999

Campylobacter jejuni—An Emerging Foodborne Pathogen

Sean F. Altekruse*, Norman J. Stern†, Patricia I. Fields‡, and David L. Swerdlow‡
Author affiliations: *U.S. Food and Drug Administration, Blacksburg, Virginia, USA;; †U.S. Department of Agriculture, Athens, Georgia, USA;; ‡Centers for Disease Control and Prevention, Atlanta, Georgia, USA

Cite This Article


Campylobacter jejuni is the most commonly reported bacterial cause of foodborne infection in the United States. Adding to the human and economic costs are chronic sequelae associated with C. jejuni infection—Guillian-Barré syndrome and reactive arthritis. In addition, an increasing proportion of human infections caused by C. jejuni are resistant to antimicrobial therapy. Mishandling of raw poultry and consumption of undercooked poultry are the major risk factors for human campylobacteriosis. Efforts to prevent human illness are needed throughout each link in the food chain.


Figure 1

Thumbnail of Cases of Campylobacter and other foodborne infections by month of specimen collection; Centers for Disease Control and Prevention/U.S. Department of Agriculture/Food and Drug Administration Collaborating Sites Foodborne Disease Active Surveillance Network, 1996.

Figure 1. Cases of Campylobacter and other foodborne infections by month of specimen collection; Centers for Disease Control and Prevention/U.S. Department of Agriculture/Food and Drug Administration Collaborating Sites Foodborne Disease Active Surveillance Network,...

Awareness of the public health implications of Campylobacter infections has evolved over more than a century (1). 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 (1). 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 (1). The development of selective growth media in the 1970s permitted more laboratories to test stool specimens for Campylobacter. Soon Campylobacter spp. were established as common human pathogens. Campylobacter jejuni infections are now the leading cause of bacterial gastroenteritis reported in the United States (2). In 1996, 46% of laboratory-confirmed cases of bacterial gastroenteritis reported in the Centers for Disease Control and Prevention/U.S. Department of Agriculture/Food and Drug Administration Collaborating Sites Foodborne Disease Active Surveillance Network were caused by Campylobacter species. Campylobacteriosis was followed in prevalence by salmonellosis (28%), shigellosis (17%), and Escherichia coli O157 infection (5%) (Figure 1).

Disease Prevalence

In the United States, an estimated 2.1 to 2.4 million cases of human campylobacter- iosis (illnesses ranging from loose stools to dysentery) occur each year (2). Commonly reported symptoms of patients with laboratory-confirmed infections (a small subset of all cases) include diarrhea, fever, and abdominal cramping. In one study, approximately half of the patients with laboratory-confirmed campylobacter- iosis reported a history of bloody diarrhea (3). Less frequently, C. jejuni infections produce bacteremia, septic arthritis, and other extraintestinal symptoms (4). The incidence of campylobacteriosis in HIV-infected patients is higher than in the general population. For example, in Los Angeles County between 1983 and 1987, the reported incidence of campylobacteriosis in patients with AIDS was 519 cases per 100,000 population, 39 times higher than the rate in the general population. (5). Common complications of campylobacteriosis in HIV-infected patients are recurrent infection and infection with antimicrobial-resistant strains (6). Deaths from C. jejuni infection are rare and occur primarily in infants, the elderly, and patients with underlying illnesses (2).

Sequelae to Infection

Guillain-Barré syndrome (GBS), a demyelating disorder resulting in acute neuromuscular paralysis, is a serious sequela of Campylobacter infection (7). An estimated one case of GBS occurs for every 1,000 cases of campylobacteriosis (7). Up to 40% of patients with the syndrome have evidence of recent Campylobacter infection (7). Approximately 20% of patients with GBS are left with some disability, and approximately 5% die despite advances in respiratory care. Campylobacteriosis is also associated with Reiter syndrome, a reactive arthropathy. In approximately 1% of patients with campylobacteriosis, the sterile postinfection process occurs 7 to 10 days after onset of diarrhea (8). Multiple joints can be affected, particularly the knee joint. Pain and incapacitation can last for months or become chronic.

Both GBS and Reiter syndrome are thought to be autoimmune responses stimulated by infection. Many patients with Reiter syndrome carry the HLA B27 antigenic marker (8). The pathogenesis of GBS (9) and Reiter syndrome is not completely understood.

Treatment of C. jejuni Infections

Supportive measures, particularly fluid and electrolyte replacement, are the principal therapies for most patients with campylobacteriosis (10). Severely dehydrated patients should receive rapid volume expansion with intravenous fluids. For most other patients, oral rehydration is indicated. Although Campylobacter infections are usually self limiting, antibiotic therapy may be prudent for patients who have high fever, bloody diarrhea, or more than eight stools in 24 hours; immunosuppressed patients, patients with bloodstream infections, and those whose symptoms worsen or persist for more than 1 week from the time of diagnosis. When indicated, antimicrobial therapy soon after the onset of symptoms can reduce the median duration of illness from approximately 10 days to 5 days. When treatment is delayed (e.g., until C. jejuni infection is confirmed by a medical laboratory), therapy may not be successful (10). Ease of administration, lack of serious toxicity, and high degree of efficacy make erythromycin the drug of choice for C. jejuni infection; however, other antimicrobial agents, particularly the quinolones and newer macrolides including azithromycin, are also used.

Antimicrobial Resistance

The increasing rate of human infections caused by antimicrobial-resistant strains of C. jejuni makes clinical management of cases of campylobacteriosis more difficult (11,12). Antimicrobial resistance can prolong illness and compromise treatment of patients with bacteremia. The rate of antimicrobial-resistant enteric infections is highest in the developing world, where the use of antimicrobial drugs in humans and animals is relatively unrestricted. A 1994 study found that most clinical isolates of C. jejuni from U.S. troops in Thailand were resistant to ciprofloxacin. Additionally, nearly one third of isolates from U.S. troops located in Hat Yai were resistant to azithromycin (11). In the industrialized world, the emergence of fluoroquinolone-resistant strains of C. jejuni illustrates the need for prudent antimicrobial use in food-animal production (12). Experimental evidence demonstrates that fluoroquinolone-susceptible C. jejuni readily become drug-resistant in chickens when these drugs are administered (13). After flouroquinolone use in poultry was approved in Europe, resistant C. jejuni strains emerged rapidly in humans during the early 1990s (12). Similarly, within 2 years of the 1995 approval of fluoroquinolone use for poultry in the United States, the number of domestically acquired human cases of ciprofloxacin-resistant campylobacteriosis doubled in Minnesota (14). In a 1997 study conducted in Minnesota, 12 (20%) of 60 C. jejuni isolates obtained from chicken purchased in grocery stores were ciprofloxacin-resistant (14).


The pathogenesis of C. jejuni infection involves both host- and pathogen-specific factors. The health and age of the host (2) and C. jejuni-specific humoral immunity from previous exposure (15) influence clinical outcome after infection. In a volunteer study, C. jejuni infection occurred after ingestion of as few as 800 organisms (16). Rates of infection increased with the ingested dose. Rates of illness appeared to increase when inocula were ingested in a suspension buffered to reduce gastric acidity (16).

Figure 2

Thumbnail of Scanning electron microscope image of Campylobacter jejuni, illustrating its corkscrew appearance and bipolar flagella. Source: Virginia-Maryland Regional College of Veterinary Medicine, Blacksburg, Virginia.

Figure 2. Scanning electron microscope image of Campylobacter jejuni, illustrating its corkscrew appearance and bipolar flagella. Source: Virginia-Maryland Regional College of Veterinary Medicine, Blacksburg, Virginia.

Many pathogen-specific virulence determinants may contribute to the pathogenesis of C. jejuni infection, but none has a proven role (17). Suspected determinants of pathogenicity include chemotaxis, motility, and flagella, which are required for attachment and colonization of the gut epithelium (Figure 2) (17). Once colonization occurs, other possible virulence determinants are iron acquisition, host cell invasion, toxin production, inflammation and active secretion, and epithelial disruption with leakage of serosal fluid (17).

Survival in the Environment

Survival of C. jejuni outside the gut is poor, and replication does not occur readily (17). C. jejuni grows best at 37°C to 42°C (18), the approximate body temperature of the chicken (41°C to 42°C). C. jejuni grows best in a low oxygen or microaerophilic environment, such as an atmosphere of 5% O2, 10% CO2, and 85% N2. The organism is sensitive to freezing, drying, acidic conditions (pH < 5.0), and salinity.

Sample Collection and Transport

If possible, stool specimens should be chilled (not frozen) and submitted to a laboratory within 24 hours of collection. Storing specimens in deep, airtight containers minimizes exposure to oxygen and desiccation. If a specimen cannot be processed within 24 hours or is likely to contain small numbers of organisms, a rectal swab placed in a specimen transport medium (e.g., Cary-Blair) should be used. Individual laboratories can provide guidance on specimen handling procedures (18).

Numerous procedures are available for recovering C. jejuni from clinical specimens (18). Direct plating is cost-effective for testing large numbers of specimens; however, testing sensitivity may be reduced. Preenrichment (raising the temperature from 36°C to 42°C over several hours), filtration, or both are used in some laboratories to improve recovery of stressed C. jejuni organisms from specimens (e.g., stored foods or swabs exposed to oxygen) (19). Isolation can be facilitated by using selective media containing antimicrobial agents, oxygen quenching agents, or a low oxygen atmosphere, thus decreasing the number of colonies that must be screened (18,19).

Subtyping of Isolates

No standard subtyping technique has been established for C. jejuni. Soon after the organism was described, two serologic methods were developed, the heat-stable or somatic O antigen (20) and the heat-labile antigen schemes (21). These typing schemes are labor intensive, and their use is limited almost exclusively to reference laboratories. Many different DNA-based subtyping schemes have been developed, including pulsed-field gel electrophoresis (PFGE) and randomly amplified polymorphic DNA (RAPD) analysis (22). Various typing schemes have been developed on the basis of the sequence of flaA, encoding flagellin (23); however, recent evidence suggests that this locus may not be representative of the entire genome (24).

Transmission to Humans

Most cases of human campylobacteriosis are sporadic. Outbreaks have different epidemiologic characteristics from sporadic infections (2). Many outbreaks occur during the spring and autumn (2). Consumption of raw milk was implicated as the source of infection in 30 of the 80 outbreaks of human campylobacteriosis reported to CDC between 1973 and 1992. Outbreaks caused by drinking raw milk often involve farm visits (e.g., school field trips) during the temperate seasons. In contrast, sporadic Campylobacter isolates peak during the summer months (Figure 1). A series of case-control studies identified some risk factors for sporadic campylobacteriosis, particularly handling raw poultry (25,26) and eating undercooked poultry (27-31) (Table). Other risk factors accounting for a smaller proportion of sporadic illnesses include drinking untreated water (29); traveling abroad (25); eating barbequed pork (28) or sausage (27); drinking raw milk (29,32) or milk from bird-pecked bottles (33); and contact with dogs (27) and cats (29,31), particularly juvenile pets or pets with diarrhea (25,34). Person-to-person transmission is uncommon (25,32). Overlap is reported between serotypes of C. jejuni found in humans, poultry, and cattle, indicating that foods of animal origin may play a major role in transmitting C. jejuni to humans (35).

Epidemiologic studies of laboratory-confirmed cases of sporadic campylobacteriosis
Date Population Location Foods associated with illness Animal contacts Ref.
Cases Controls
52 103 1989-1990 Residents of three counties Norway Poultry, sausage Dogs 27
218 526 1982-1983 HMO patients Washington State Undercooked chicken Animals with diarrhea 30, 34
29 42 1990 Residents of Manchester England Bottled milka 33
45 45 1983-1984 University students Georgia Chicken Cats 31
53 106 1982-1983 Rural children Iowa Raw milk 32
40 80 1981 Residents of Denver Ft. Collins Colorado Untreated water, raw milk, undercooked chicken Cats 29
54 54 1982 Residents of Rotterdam Netherlands Chicken, pork, barbequed foods 28
10 15 1982 Residents of Larimer County Colorado Preparing chicken 26
55 14 1980 Residents of Göteborg Sweden Preparing chicken Kitten dog with diarrhea 25

aBottle tops pecked by wild birds.

In the United States, infants have the highest age-specific Campylobacter isolation rate, approximately 14 per 100,000 person years. As children get older, isolation rates decline to approximately 4 per 100,000 person years for young adolescents. A notable feature of the epidemiology of human campylobacteriosis is the high isolation rate among young adults, approximately 8 per 100,000 person years. Among middle-aged and older adults, the isolation rate is < 3 per 100,000 person years (2). The peak isolation rate in neonates and infants is attributed in part to susceptibility on first exposure and to the low threshold for seeking medical care for infants (2). The high rate of infection during early adulthood, which is pronounced among men, is thought to reflect poor food-handling practices in a population that, until recently, relied on others to prepare meals (2).


The ecology of C. jejuni involves wildlife reservoirs, particularly wild birds. Species that carry C. jejuni include migratory birds—ranes, ducks, geese (36), and seagulls (37). The organism is also found in other wild and domestic bird species, as well as in rodents (38). Insects can carry the organism on their exoskeleton (39).

The intestines of poultry are easily colonized with C. jejuni. Day-old chicks can be colonized with as few as 35 organisms (40). Most chickens in commercial operations are colonized by 4 weeks (41,42). Vertical transmission (i.e., from breeder flocks to progeny) has been suggested in one study but is not widely accepted (43). Reservoirs in the poultry environment include beetles (39), unchlorinated drinking water (44), and farm workers (41,42,45). Feeds are an unlikely source of campylobacters since they are dry and campylobacters are sensitive to drying.

C. jejuni is a commensal organism of the intestinal tract of cattle (46). Young animals are more often colonized than older animals, and feedlot cattle are more likely than grazing animals to carry campylobacters (47). In one study, colonization of dairy herds was associated with drinking unchlorinated water (48).

Campylobacters are found in natural water sources throughout the year. The presence of campylobacters is not clearly correlated with indicator organisms for fecal contamination (e.g., E. coli) (49). In temperate regions, organism recovery rates are highest during the cold season (49,50). Survival in cold water is important in the life cycle of campylobacters. In one study, serotypes found in water were similar to those found in humans (50). When stressed, campylobacters enter a "viable but nonculturable state," characterized by uptake of amino acids and maintenance of an intact outer membrane but inability to grow on selective media; such organisms, however, can be transmitted to animals (51). Additionally, unchlorinated drinking water can introduce campylobacters into the farm environment (44,48).

Campylobacter in the Food Supply

C. jejuni is found in many foods of animal origin. Surveys of raw agricultural products support epidemiologic evidence implicating poultry, meat, and raw milk as sources of human infection. Most retail chicken is contaminated with C. jejuni; one study reported an isolation rate of 98% for retail chicken meat (52). 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 (53). Raw milk is presumed to be contaminated by bovine feces; however, direct contamination of milk as a consequence of mastitis also occurs (54). 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 (55).

Control of Campylobacter Infection

On the Farm

Control of Campylobacter contamination on the farm may reduce contamination of carcasses, poultry, and red meat products at the retail level (27). Epidemiologic studies indicate that strict hygiene reduces intestinal carriage in food-producing animals (41,42,45). In field studies, poultry flocks that drank chlorinated water had lower intestinal colonization rates than poultry that drank unchlorinated water (42,44). Experimentally, treatment of chicks with commensal bacteria (56) and immunization of older birds (57) reduced C. jejuni colonization. Because intestinal colonization with campylobacters readily occurs in poultry flocks, even strict measures may not eliminate intestinal carriage by food-producing animals (39,41).

At Processing

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 (58). In studies of chickens (59) and turkeys (60) 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 (61). In Texas turkey plants, scalding reduced carcass counts to near or below detectable levels (60). 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 (62). 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 (63). In another study, lactic acid spraying of swine carcasses reduced counts by at least 50% to often undetectable levels (64). A radiation dose of 2.5 KGy reduced C. jejuni levels on retail poultry by 10 log10 units (65).


C. jejuni, first identified as a human diarrheal pathogen in 1973, is the most frequently diagnosed bacterial cause of human gastroenteritis in the United States. Sequelae including GBS and reactive arthritis are increasingly recognized, adding to the human and economic cost of illness from human campylobacteriosis. The emergence of fluoroquinolone-resistant infections in Europe and the United States, temporally associated with the approval of fluoroquinolone use in veterinary medicine, is also a public health concern. The consumption of undercooked poultry and cross-contamination of other foods with drippings from raw poultry are leading risk factors for human campylobacteriosis. Reinforcing hygienic practices at each link in the food chain—from producer to consumer—is critical in preventing the disease.

Dr. Altekruse is a Public Health Service Epidemiology Fellow with the Food and Drug Administration, Center for Veterinary Medicine. His current research interest is antimicrobial-resistant foodborne pathogens.



  1. Kist  M. The historical background of Campylobacter infection: new aspects. In: Pearson AD, editor. Proceedings of the 3rd International Workshop on Campylobacter Infections; Ottawa;1985 Jul 7-10. London: Public Health Laboratory Service;1985. p.23-7.
  2. Tauxe  RV. Epidemiology of Campylobacter jejuni infections in the United States and other industrial nations. In: Nachamkin I, Blaser MJ, Tompkins LS, editors. Campylobacter jejuni: current and future trends. Washington: American Society for Microbiology; 1992. p. 9-12.
  3. Blaser  MJ, Wells  JG, Feldman  RA, Pollard  RA, Allen  JR. the Collaborative Diarrheal Disease Study Group. Campylobacter enteritis in the United States: a multicenter study. Ann Intern Med. 1983;98:3605.PubMedGoogle Scholar
  4. Peterson  MC. Clinical aspects of Campylobacter jejuni infections in adults. West J Med. 1994;161:14852.PubMedGoogle Scholar
  5. Sorvillo  FJ, Lieb  LE, Waterman  SH. Incidence of campylobacteriosis among patients with AIDS in Los Angeles County. J Acquir Immune Defic Syndr Hum Retrovirol. 1991;4:598602.
  6. Perlman  DJ, Ampel  NM, Schifman  RB, Cohn  DL, Patton  CM, Aguirre  ML, Persistent Campylobacter jejuni infections in patients infected with the human immunodeficiency virus (HIV). Ann Intern Med. 1988;108:5406.PubMedGoogle Scholar
  7. Allos  BM. Association between Campylobacter infection and Guillain-Barré syndrome. J Infect Dis. 1997;176:S1258. DOIPubMedGoogle Scholar
  8. Peterson  MC. Rheumatic manifestations of Campylobacter jejuni and C. fetus infections in adults. Scand J Rheumatol. 1994;23:16770. DOIPubMedGoogle Scholar
  9. Shoenfeld  Y, George  J, Peter  JB. Guillain-Barré as an autoimmune disease. Int Arch Allergy Immunol. 1996;109:31826. DOIPubMedGoogle Scholar
  10. Blaser  MJ. Campylobacter species. In: Principles and practice of infectious diseases. Mandell GL, Douglas RG, Bennett JE, editors. 3rd ed. New York: Churchill Livingstone, 1990;194:1649-58.
  11. Murphy  GS Jr, Echeverria  P, Jackson  LR, Arness  MK, LeBron  C, Pitarangsi  C. Ciprofloxacin- and azithromycin-resistant Campylobacter causing traveler's diarrhea in U.S. troops deployed to Thailand in 1994. Clin Infect Dis. 1996;22:8689.PubMedGoogle Scholar
  12. Piddock  LJV. Quinolone resistance and Campylobacter spp. Antimicrob Agents Chemother. 1995;36:8918. DOIGoogle Scholar
  13. Jacobs-Reitsma  WF, Kan  CA, Bolder  NM. The induction of quinolone resistance in Campylobacter bacteria in broilers by quinolone treatment. In: Campylobacters, helicobacters, and related organisms. Newell DG, Ketley JM, Feldman RA, editors. New York: Plenum Press; 1996. p. 307-11.
  14. Smith  KE, Besser  JM, Leano  F, Bender  J, Wicklund  J, Johnson  B, Fluoroquinolone-resistant Campylobacter isolated from humans and poultry in Minnesota [abstract]. Program of the 1st International Conference on Emerging Infectious Diseases; Atlanta, Georgia; 1998 Mar 7-10. Atlanta: Centers for Disease Control and Prevention;1998.
  15. Blaser  MJ, Sazie  E, Williams  LP Jr. The influence of immunity on raw milk-associated Campylobacter infection. JAMA. 1987;257:436. DOIPubMedGoogle Scholar
  16. Black  RE, Levine  MM, Clements  ML, Hughes  TP, Blaser  MJ. Experimental Campylobacter jejuni infection in humans. J Infect Dis. 1988;157:4729.PubMedGoogle Scholar
  17. Ketley  JM. Pathogenesis of enteric infection by Campylobacter. Microbiology. 1997;143:521. DOIPubMedGoogle Scholar
  18. Nachamkin  I. Campylobacter and Arcobacter. In: Manual of clinical microbiology. 6th ed. Washington: ASM Press; 1995. p. 483-91.
  19. Humphrey  TJ. An appraisal of the efficacy of pre-enrichment for the isolation of Campylobacter jejuni from water and food. J Appl Bacteriol. 1989;66:11926.PubMedGoogle Scholar
  20. Penner  JL, Hennessy  JN, Congi  RV. Serotyping of Campylobacter jejuni and Campylobacter coli on the basis of thermostable antigens. Eur J Clin Microbiol Infect Dis. 1983;2:37883. DOIGoogle Scholar
  21. Lior  H, Woodward  DL, Edgar  JA, Laroche  LJ, Gill  P. Serotyping of Campylobacter jejuni by slide agglutination based on heat-labile antigenic factors. J Clin Microbiol. 1982;15:7618.PubMedGoogle Scholar
  22. Hilton  AC, Mortiboy  D, Banks  JG, Penn  CW. RAPD analysis of environmental, food and clinical isolates of Campylobacter spp. FEMS Immunol Med Microbiol. 1997;18:11924. DOIPubMedGoogle Scholar
  23. Meinersmann  RJ, Helsel  LO, Fields  PI, Hiett  KL. Discrimination of Campylobacter jejuni isolates by fla gene sequencing. J Clin Microbiol. 1997;35:28104.PubMedGoogle Scholar
  24. Harrington  CS, Thomson-Carter  FM, Carter  PE. Evidence for recombination in the flagellin locus of Campylobacter jejuni: implications for the flagellin gene typing scheme. J Clin Microbiol. 1997;35:238692.PubMedGoogle Scholar
  25. Norkrans  G, Svedhem  Å. Epidemiologic aspects of Campylobacter jejuni enteritis. Journal of Hygiene (Cambridge). 1982;89:16370. DOIGoogle Scholar
  26. Hopkins  RS, Scott  AS. Handling raw chicken as a source for sporadic Campylobacter jejuni infections [letter]. J Infect Dis. 1983;148:770.PubMedGoogle Scholar
  27. Kapperud  G, Skjerve  E, Bean  NH, Ostroff  SM, Lassen  J. Risk factors for sporadic Campylobacter infections: results of a case-control study in southeastern Norway. J Clin Microbiol. 1992;30:311721.PubMedGoogle Scholar
  28. Oosterom  J, den Uyl  CH, Bänffer  JRJ, Huisman  J. Epidemiologic investigations on Campylobacter jejuni in households with primary infection. Journal of Hygiene (Cambridge). 1984;92:32532. DOIGoogle Scholar
  29. Hopkins  RS, Olmsted  R, Istre  GR. Endemic Campylobacter jejuni infection in Colorado: identified risk factors. Am J Public Health. 1984;74:24950. DOIPubMedGoogle Scholar
  30. Harris  NV, Weiss  NS, Nolan  CM. The role of poultry and meats in the etiology of Campylobacter jejuni/coli enteritis. Am J Public Health. 1986;76:40711. DOIPubMedGoogle Scholar
  31. Deming  MS, Tauxe  RV, Blake  PA. Campylobacter enteritis at a university from eating chickens and from cats. Am J Epidemiol. 1987;126:52634.PubMedGoogle Scholar
  32. Schmid  GP, Schaefer  RE, Plikaytis  BD, Schaefer  JR, Bryner  JH, Wintermeyer  LA, A one-year study of endemic campylobacteriosis in a midwestern city: association with consumption of raw milk. J Infect Dis. 1987;156:21822.PubMedGoogle Scholar
  33. Lighton  LL, Kaczmarski  EB, Jones  DM. A study of risk factors for Campylobacter infection in spring. Public Health. 1991;105:199203. DOIPubMedGoogle Scholar
  34. Saaed  AM, Harris  NV, DiGiacomo  RF. The role of exposure to animals in the etiology of Campylobacter jejuni/coli enteritis. Am J Epidemiol. 1993;137:10814.PubMedGoogle Scholar
  35. Nielsen  EM, Engberg  J, Madsen  M. Distribution of serotypes of Campylobacter jejuni and C. coli from Danish patients, poultry, cattle, and swine. FEMS Immunol Med Microbiol. 1997;19:4756.PubMedGoogle Scholar
  36. Luetchefeld  NA, Blaser  MJ, Reller  LB, Wang  WL. Isolation of Campylobacter fetus subsp. jejuni from migratory waterfowl. J Clin Microbiol. 1980;12:4068.PubMedGoogle Scholar
  37. Glunder  G, Neumann  U, Braune  S. Occurrence of Campylobacter spp. in young gulls, duration of Campylobacter infection and reinfection by contact. [Series B]. Journal of Veterinary Medicine. 1992;39:11922. DOIGoogle Scholar
  38. Cabrita  J, Rodrigues  J, Braganca  F, Morgado  C, Pires  I, Goncalves  AP. Prevalence, biotypes, plasmid profile and antimicrobial resistance of Campylobacter isolated from wild and domestic animals from northeast Portugal. J Appl Bacteriol. 1992;73:27985.PubMedGoogle Scholar
  39. Jacobs-Reitsma  WF, van de Giessen  AW, Bolder  NM, Mulder  RWAW. Epidemiology of Campylobacter spp. at two Dutch broiler farms. Epidemiol Infect. 1995;114:41321. DOIPubMedGoogle Scholar
  40. Kaino  K, Hayashidani  H, Kaneko  K, Ogawa  M. Intestinal colonization of Campylobacter jejuni in chickens. Japanese Journal of Veterinary Science. 1988;50:48994.PubMedGoogle Scholar
  41. Humphrey  TJ, Henley  A, Lanning  DG. The colonization of broiler chickens with Campylobacter jejuni; some epidemiologic investigations. Epidemiol Infect. 1993;110:6017. DOIPubMedGoogle Scholar
  42. Kapperud  G, Skjerve  E, Vik  L, Hauge  K, Lysaker  A, Aalmen  I, Epidemiological investigation of risk factors for Campylobacter colonization in Norwegian broiler flocks. Epidemiol Infect. 1993;111:4555. DOIGoogle Scholar
  43. Pearson  AD, Greenwood  MH, Feltham  RK, Healing  TD, Donaldson  J, Jones  DM, Microbial ecology of Campylobacter jejuni in a United Kingdom chicken supply chain: intermittent common source, vertical transmission, and amplification by flock propagation. Appl Environ Microbiol. 1996;62:461420.PubMedGoogle Scholar
  44. Pearson  AD, Greenwood  M, Healing  TD, Rollins  D, Shahamat  M, Donaldson  J, Colonization of broiler chickens by waterborne Campylobacter jejuni. Appl Environ Microbiol. 1993;59:98796.PubMedGoogle Scholar
  45. Kazwala  RR, Collins  JD, Hannan  J, Crinion  RAP, O'Mahony  H. Factors responsible for the introduction and spread of Campylobacter jejuni infection in commercial poultry production. Vet Rec. 1990;126:3056.PubMedGoogle Scholar
  46. Fricker  CR, Park  RWA. A two year study of the distribution of thermophilic campylobacters in human, environmental and food samples from the Reading area with particular reference to toxin production and heat stable serotype. J Appl Bacteriol. 1989;66:47790.PubMedGoogle Scholar
  47. Giacoboni  GI, Itoh  K, Hirayama  K, Takahashi  E, Mitsuoka  T. Comparison of fecal Campylobacter in calves and cattle of different ages and areas in Japan. J Vet Med Sci. 1993;55:5559.PubMedGoogle Scholar
  48. Humphrey  TJ, Beckett  P. Campylobacter jejuni in dairy cows and raw milk. Epidemiol Infect. 1987;98:2639. DOIPubMedGoogle Scholar
  49. Carter  AM, Pacha  RE, Clark  GW, Williams  EA. Seasonal occurrence of Campylobacter spp. and their correlation with standard indicator bacteria. Appl Environ Microbiol. 1987;53:5236.PubMedGoogle Scholar
  50. Bolton  FJ, Coates  D, Hutchinson  DN, Godfree  AF. A study of thermophilic campylobacters in a river system. J Appl Bacteriol. 1987;62:16776.PubMedGoogle Scholar
  51. Stern  N, Jones  D, Wesley  I, Rollins  D. Colonization of chicks by non-culturable Campylobacter spp. Lett Appl Microbiol. 1994;18:3336. DOIGoogle Scholar
  52. Stern  NJ, Line  JE. Comparison of three methods for recovery of Campylobacter spp. from broiler carcasses. J Food Prot. 1992;55:6636.
  53. Rohrbach  BW, Draughon  FA, Davidson  PM, Oliver  SP. Prevalence of Listeria monocytogenes, Campylobacter jejuni, Yersinia enterocolitica, and Salmonella in bulk tank milk: risk factors and risk of human exposure. J Food Prot. 1992;55:937.
  54. Hudson  PJ, Vogt  RL, Brondum  J, Patton  CM. Isolation of Campylobacter jejuni from milk during an outbreak of campylobacteriosis. J Infect Dis. 1984;150:789.PubMedGoogle Scholar
  55. Lammerding  AM, Garcia  MM, Mann  ED, Robinson  Y, Dorward  WJ, Truscott  RB, Prevalence of Salmonella and thermophilic Campylobacter in fresh pork, beef, veal, and poultry in Canada. J Food Prot. 1988;51:4752.
  56. Stern  NJ. Mucosal competitive exclusion to diminish colonization of chickens by Campylobacter jejuni. Poult Sci. 1994;73:4027.PubMedGoogle Scholar
  57. Widders  PR, Perry  R, Muir  WI, Husband  AJ, Long  KA. Immunization of chickens to reduce intestinal colonization with Campylobacter jejuni. Br Poult Sci. 1996;37:7658. DOIPubMedGoogle Scholar
  58. Stern  NJ, Clavero  MRS, Bailey  JS, Cox  NA, Robach  MC. Campylobacter spp. in broilers on the farm and after transport. Poult Sci. 1995;74:93741.PubMedGoogle Scholar
  59. Izat  AL, Gardner  FA, Denton  JH, Golan  FA. Incidence and levels of Campylobacter jejuni in broiler processing. Poult Sci. 1988;67:156872.PubMedGoogle Scholar
  60. Acuff  GR, Vanderzant  C, Hanna  MO, Ehlers  JG, Golan  FA, Gardner  FA. Prevalence of Campylobacter jejuni in turkey carcasses during further processing of turkey products. J Food Prot. 1986;49:7127.
  61. Oosterom  J, De Wilde  GJA, De Boer  E, De Blaauw  LH, Karman  H. Survival of Campylobacter jejuni during poultry processing and pig slaughtering. J Food Prot. 1983;46:7026.
  62. Li  YB, Walker  JT, Slavik  MF, Wang  H. Electrical treatment of poultry chiller water to destroy Campylobacter jejuni. J Food Prot. 1995;58:13304.
  63. Mead  GC, Hudson  WR, Hinton  MH. Effect of changes in processing to improve hygiene control on contamination of poultry carcasses with Campylobacter. Epidemiol Infect. 1995;115:495500. DOIPubMedGoogle Scholar
  64. Epling  LK, Carpenter  JA, Blankenship  LC. Prevalence of Campylobacter spp. and Salmonella spp. on pork carcasses and the reduction effected by spraying with lactic acid. J Food Prot. 1993;56:5367, 540.
  65. Patterson  MF. Sensitivity of Campylobacter spp. to irradiation in poultry meat. Lett Appl Microbiol. 1995;20:33840. DOIPubMedGoogle Scholar




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DOI: 10.3201/eid0501.990104

Table of Contents – Volume 5, Number 1—February 1999

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