Campylobacteriosis as a clinical disease is not common in poultry and other birds. Campylobacteriosis is a significant enterocolitis of people, frequently acquired through consumption of undercooked poultry meat contaminated with Campylobacter jejuni. It is the leading bacterial cause of sporadic enteritis in developed countries. The organism colonizes the intestine of chickens, turkeys, and waterfowl but is generally nonpathogenic in birds. It can also be acquired from handling backyard poultry as well as diarrheic companion animals and from contaminated water.
Columbae and domestic and free-living Galliformes and Anseriformes birds are natural reservoirs of the human pathogenic Campylobacter species (C jejuni, C coli, and C lari) and other poorly defined Campylobacter species. Many commercial broiler and turkey flocks harbor C jejuni, although the prevalence can vary from 0% to 100% depending on season (lowest in fall and winter and highest in summer) and age of the birds. C jejuni has been found in all areas of commercial poultry production.
Some strains of C jejuni have been reported to cause enteritis and death in newly hatched chicks and poults; but administering isolates of C jejuni to chickens has not reproduced the syndrome. However a new species of Campylobacter, C hepaticus, has been identified as the cause of spotty liver disease in layer chickens. Key signs, in addition to multifocal necrotic hepatitis, include egg production losses and increased flock mortality. Diagnosis is based on signs and detection of the pathogen by culture. However, culture of the organism is difficult because it is susceptible to a number of the antimicrobials used in common Campylobacter enrichment media and selective agar.
C jejuni is the predominant species associated with foodborne infection derived from poultry, but C coli and C lari have also been implicated in some cases and can also be recovered from the intestinal tract of birds.
C hepaticus is the species associated with spotty liver disease of layers and breeder chickens and may be the etiological agent of the disease formerly known as avian vibrionic hepatitis.
Environmental contamination with bird droppings is probably the most common source of infection for dissemination of both C jejuni and C hepaticus. But some species of Campylobacter can be transmitted vertically, either on the surface of eggs or by transovarial transmission.
Insects, fomites, and contaminated water and feed can transmit Campylobacter to young birds. Commercial poultry litter can remain infective for long periods, subject to at least a 10% moisture level and neutral pH. Nonchlorinated water derived from a dam, river, or shallow well should be regarded as a possible source. Rats, mice, wild birds, darkling beetles, and houseflies can be a transmission source for flocks; equipment and footwear contaminated with feces from an infected source may also serve as a vehicle of transmission. Young chicks and poults are easily colonized when exposed to C jejuni and can excrete the organism in the feces for their lifetimes.
Once C jejuni has been introduced into the environment, rapid transmission within the flock occurs, with subsequent colonization of a high proportion of exposed breeders, commercial-meat, or laying-strain poultry. It has been isolated from the reproductive tracts of hens and roosters, suggesting vertically transmission in some cases. Therefore, biosecurity may not be adequate to control transmission of Campylobacter until it has been eradicated from parent flocks.
Birds challenged with C hepaticus exhibit focal hepatic necrosis in varying degrees of severity. Infected layer flocks exhibit spotty livers, increased mortality rates approaching 15%, and decreased egg production. Death can occur rapidly, suggesting the involvement of acute septicemia/toxemia.
Birds challenged with C jejuni generally do not exhibit clinical disease. Many birds are colonized with Campylobacter species early in life with no associated clinical signs or pathology. Some studies have reported that challenged chicks may exhibit distention of the jejunum, disseminated hemorrhagic enteritis, and in some cases, focal hepatic necrosis. However, infected flocks seldom exhibit these lesions, increased mortality rates, or decreased feed conversion.
Detection of Campylobacter species can be done by culture or PCR.
C jejuni surveillance of flocks is best performed by collecting cecal droppings into sterile laboratory sampling bags and packing them on ice.
C hepaticus specimens should consist of whole livers packed on ice. Samples of bile or liver can be collected using swabs, then placed in Cary-Blair transport medium.
Enrichment culture followed by isolation on selective agar medium facilitates detection of Campylobacter.
There are no reliable serologic tests for Campylobacter in avian spp. Detection of colonized birds can be done by culture of fecal samples. Diagnosis of spotty liver disease is done by clinical presentation and culture of C hepaticus from liver lesions.
C jejuni can be cultured on many different commercially available media, but the strategy includes a broth enrichment followed by isolation on selective agar. Thermophilic Campylobacter spp should be cultured at 42°C under humid, microaerophilic conditions (85% nitrogen, 10% carbon dioxide, and 5% oxygen) for 48 hours. Some strains require a hydrogen-enriched atmosphere (5%). Campylobacter spp can be identified by biochemical testing or by PCR. Nalidixic acid sensitivity is no longer reliable because of the increasing prevalence of fluoroquinolone-resistant C jejuni. The Penner or Lior serotyping schemes can be used to classify C jejuni, and pulsed-field gel analysis can distinguish various C jejuni isolates.
C hepaticus samples should consist of liver or bile swabs; culture of feces or cecal droppings is not definitive for diagnosis. Cultivation can be challenging because commercial enrichment broths and selective agar contain cefoperazone, which is inhibitory to many C hepaticus strains. Swabs of bile can be cultured directly onto Brucella blood agar and incubated in microaerophilic conditions at 42°C. Livers can be enriched in modified Preston broth, incubated at 37°C in microaerophilic conditions for 7 days, then isolated on Brucella blood agar. The selective filtration method can also be used for contaminated organ samples: a 1/10 diluted sample is allowed to penetrate a sterile filter (0.45 mcm pores) placed on the surface of a blood agar plate. After the liquid is absorbed into the plate, the filter is removed and incubated microaerophilically. Identification can be done by biochemical testing or PCR.
Because C jejuni is not found as a specific pathogen under commercial conditions, treatment of poultry flocks is not a consideration. If C jejuni is considered a problem in companion bird aviaries or in exotic species, antibiotics such as erythromycin should not be administered in drinking water in an attempt to eradicate it. Because of the zoonotic risk associated with C jejuni and its ability to rapidly develop antibiotic resistance, antibiotics should be used with caution in companion birds. Fluoroquinolones and erythromycins are the classes of antimicrobials used to treat people for campylobacteriosis.
Preharvest prevention of Campylobacter infection in commercial poultry is based on strict biosecurity, decontamination of housing between successive flocks, exclusion of rodents and wild birds, and insect eradication. Chlorination of drinking water to 2 ppm and operation of farms on a strict “all-in/all-out” basis occasionally reduces the prevalence of infection. Innovative methods of prevention, such as competitive exclusion, bacteriophage therapy, bacteriocins, and the use of vaccines, are under intensive investigation. Withholding feed from broilers and turkeys for at least 12 hours before slaughter and thorough decontamination of transport coops and modules reduce fecal contamination and lower the level of C jejuni introduced into processing plants.
C jejuni is a major source of foodborne enteritis in people; contaminated, undercooked poultry is responsible for a majority of cases. The condition was recognized in the mid-1970s, and the significance of the organism has become apparent with improved methods of isolation and identification. Nonchlorinated ground water, unpasteurized milk, young diarrheic pets, and contaminated beef and pork products are also responsible for infection of people.
In commercial poultry processing, improved washing of carcasses, use of counter-flow mechanical advances in scalding, elimination of immersion chillers, and reduction in manual handling by installation of advanced automated equipment has reduced C jejuni contamination on poultry meat. Chemical disinfectants in the washes, such as chlorine, peracetic acid with hydrogen peroxide; trisodium phosphate, glutaraldehyde, and succinic acid; and organic compounds such as lactic and acetic acids may effectively also reduce C jejuni on poultry carcasses in the processing plant. Some research indicates that bacteriophages and bacteriocins may also be useful. However, the regulations regarding chemical or biological sanitizers that can be used in processing plants and the performance standards for Campylobacter in the plant are currently in flux.
Concurrent measures in food preparation, hygienic storage, handling, and preparation are necessary to prevent contamination of prepared foods, work surfaces, and utensils by raw poultry and other meats. The risk of foodborne C jejuni infection can be reduced through cooking of poultry to achieve a core temperature of 74°C for 1 minute.
Campylobacter infection does not commonly cause clinical disease in birds, but it is a significant cause of enteritis in humans, frequently acquired through consumption of undercooked C jejuni-contaminated poultry meat and other foods.
Many Campylobacter species colonize the intestine of poultry and waterfowl but are generally nonpathogenic to birds.
The exception is C hepaticus, the causative agent of spotty liver disease in layer chickens.