Campylobacter infection and Campylobacter excretion in turkeys

Five turkey poults at an age of 27 days were infected with Campylobacter jejuni strain. Additional five poults were infected by contact. Turkeys infected by contact and artificially were necropsied 1 and 3 months later, respectively. The histological examination of the liver revealed degenerative changes in contact birds and a proliferation of the connective tissue and bile-ducts in two of the oral infected poults. Campylobacter spp. were excreted daily during the first two weeks and afterwards with interruptions of several days. The excretion lasted until the end of the experiment between day 86 and 98. The excretion period, which is prolonged compared with that of chickens may be of particular importance under aspects of epizootiology and food hygiene.     

Campylobacter infection in domestic dogs

Campylobacter jejuni, a recently recognised human enteric pathogen, was recovered from the faeces of 21.7 per cent of domestic dogs with diarrhoea as compared with only 3.1 per cent of normal healthy dogs. The recovery rate from non-diarrhoeic, but unhealthy, domestic dogs was 6.7 per cent. The differences in the incidence of C jejuni between breeds was not statistically significant. The majority of isolations were from puppies between birth and six months old. The incidence of C jejuni in domestic dogs did not appear to be sex specific. Domestic canine infections with C jejuni could possibly be an important source of human infection, especially to those in close contact.     

Campylobacter jejuni infection in broiler chickens

Day-old, straight-run broiler chickens were procured from a hatchery located in the Pacific Northwest. The chickens were subdivided individually into nine groups of 20 chickens. The chickens were tagged, housed in isolation chambers on wire, fed commercial broiler feed, and given water ad libitum. Three isolates of Campylobacter jejuni of poultry origin and one of human origin were tested in this study. Various C. jejuni cultures were inoculated into 9-day-old chickens by crop gavage. Four groups of 20 chickens were inoculated at a dose level of 0.5 ml of 1 x 10(2) colony-forming units (CFU)/ml. The other four groups were inoculated with 0.5 ml of 1 X 10(4) CFU/ml. One group of 20 chickens was kept as an uninoculated control group. Four randomly selected chickens from each of the inoculated and uninoculated groups were necropsied at 5, 12, and 19 days postinoculation (DPI). The C. jejuni was cultured and enumerated from a composite of the upper and midintestine and the cecum. Body weights of all chicken groups at 7 days of age and at 5, 12, and 19 DPI were measured and statistically analyzed. No significant differences were present in the mean body weights (MBWs) of 7-day-old, 5 DPI, and 12 DPI male and female broiler chickens inoculated with C. jejuni at both dose levels compared with uninoculated controls. Differences in MBWs of the male and female broilers at 19 DPI were observed in some of the groups. Results of the C. jejuni culture enumeration mean (CEM) of composite intestine samples at 5 DPI from all inoculated chicken groups, irrespective of the dose level, ranged from (2.5 +/- 5.0) x 10(2) to (2.8 +/- 4.8) x 10(5) CFU/g (mean +/- SD). Results of cecum C. jejuni CEM at 5 DPI inoculated at both dose levels ranged from (2.5 +/- 5.0) x 10(6) to (1 +/- 0.0) x 10(7) CFU/g in all treatment groups irrespective of the dose level. CEM results from the composite intestine samples at 12 and 19 DPI increased by 1 log unit, or sometimes more. Results of cecum C. jejuni CEM at 5 DPI inoculated at both dose levels ranged from (2.5 +/- 5.0) x 10(6) to (1 +/- 0.0) x 10(7) CFU/g in all treatment groups irrespective of the dose level. Increases of 2-5 log units in C. jejuni CEM was present in chicken groups inoculated with 1 X 10(2) CFU of C. jejuni, and a 2- to 3-log increase was present in groups inoculated with a higher dose level of C. jejuni at 12 DPI. The results of C. jejuni CEM from cecal samples at 19 DPI were similar to chicken groups at 12 DPI. Campylobacterjejuni was not isolated from the uninoculated control chickens at 5, 12, and 19 DPI. Clinical signs of illness or gross pathologic lesions were not present in any of the chicken groups during this study. No lesions were present on histopathologic evaluations in C. jejuni-inoculated chickens or uninoculated control chickens.     

Experimental infection of dogs with Campylobacter jejuni

Three groups of conventional puppies were inoculated orally with Campylobacter jejuni biotype 2 which had been isolated from the small intestine of a dog with enteritis. Mild enteric disease was observed in one group. There was superficial intestinal colonization by the organism but penetration of intestinal epithelial cells was not apparent. C jejuni was isolated from the blood and viscera of inoculated dogs which showed no histological evidence of disease.     

Porcine intestinal epithelial responses to Campylobacter infection

Campylobacter infection is estimated to cause diarrhoea in 1% of the population of developed countries every year, but our understanding of this disease has been hampered by a lack of a suitable animal model. Colostrum-deprived piglets have been suggested as models since they produce similar clinical signs to humans when infected but little information currently exists regarding the response of this species to Campylobacter at cellular and molecular level. This study shows that intestinal epithelial cells from both species respond in a similar manner to Campylobacter infection regarding invasion, induction of innate immune response and effect on barrier function.     

Campylobacter infection in a closed dog breeding colony

Most dogs in a closed breeding unit were shown to be asymptomatic excretors of campylobacter organisms by eight weeks old. Increasing serum antibody levels, which were correlated with the excretion of organisms, were demonstrated in the puppies and serum antibodies were also demonstrated in adult dogs. The significance of these findings with respect to the pathogenicity of campylobacter in dogs and their zoonotic implications are discussed.     

Chronic diarrhea associated with Campylobacter jejuni infection in a cat

Campylobacter jejuni was isolated from a cat with chronic diarrhea. The diarrheic cat and another cat (which previously had diarrhea) in the same household had bactericidal antibody titers to the C jejuni. Clinical response to antibiotic therapy and not recovering Campylobacter sp from normal feces after treatment also supported the diagnosis of Campylobacter-associated diarrhea. Although the owner had a protracted episode of diarrhea, C jejuni was not isolated from the owner's feces, nor was a bactericidal antibody detected in the owner's serum.     

Risk factors for Campylobacter infection in Norwegian cats and dogs

Rectal swabs from healthy cats and dogs, and from dogs and cats with clinical diarrhoea were collected approximately every third month from May 2000 to June 2001 from six small-animal practices throughout Norway. A questionnaire was filled in for each animal. Of the 301 healthy cats sampled, 54 (18%) were positive for Campylobacter, compared to 5 out of 31 (16%) cats with diarrhoea. Campylobacter jejuni was isolated from 11 (3%), C. upsaliensis from 42 (13%) and C. coli from 2 (0.6%) of the cats sampled. Isolates from four cats (1%) could not be specified. Of the 529 healthy dogs, 124 (23%) were positive for Campylobacter, compared to 18 of 66 (27%) dogs with diarrhoea. C. jejuni was isolated from 20 (3%) and C. upsaliensis from 117 (20%) of the dogs sampled. Isolates from five dogs (0.8%) could not be specified. Eighteen out of the 20 investigated C. upsaliensis samples were resistant to streptomycin. The clinically healthy animals were included in the analysis to identify factors associated with Campylobacter prevalence. The cat model had low classification ability. The dog-data model indicated increased odds of infection with Campylobacter for dogs ≤1 year, and in dogs sampled during the spring. No difference was observed between the prevalence of Campylobacter infections in cats and dogs with diarrhoea and healthy animals.     

Sequential spread of Campylobacter infection in a multipen broiler house

Generally, colonization with Campylobacter jejuni is first detected in broilers 2-3 wk after hatching. Once introduced into a flock, this infection spreads very rapidly. The sources and routes of transmission of C. jejuni in broilers remain debatable. In this study, the spread of infection was monitored in a commercial multipen broiler house in which birds were contained in discrete groups and sampled sequentially. Colonization was monitored in two broiler flocks up to slaughter. Serotyping and fla typing methods were applied to differentiate all the C. jejuni strains isolated. In flock 1, colonization was first detected at 32 days of age in birds located at the rear of the house. By 40 days, nearly all the birds were infected with the same strain (fla type 1.9). However, at 46 days of age, a second strain (fla type 3.7) was detected in some of the birds. These birds were also located toward the rear of the house. In flock 2, infection was detected at 5 wk of age. This infection was once again first detected in birds located at the rear of the house. In this flock, only a single fla type (1.1) was isolated throughout. A survey of the broiler house relative to the location of first point of infection indicated the use of an entrance door unprotected by boot dips. However, securing this door during the second flock study did not prevent infection.     

Occurrence of Campylobacter spp. in young gulls, duration of Campylobacter infection and reinfection by contact.

Two groups of three week old Herring Gulls (Larus argentatus) were held to observe the carrier state with Campylobacter. All 27 birds of group I excreted Campylobacter jejuni biotype III when they were caught from their colony. Four weeks later all but one were negative, indicating that the carrier state lasts until about the seventh week of life, with self-elimination if infection with another Campylobacter species is prevented by housing in a closed environment as in this study. Only one bird became reinfected one year later when gulls from group I were brought into contact with gulls from group II, consisting of ten freshly caught gulls, four of which were infected with the same biotype of Campylobacter, indicating that there might be some kind of immunity protection against infection with the same biotype of Campylobacter spp.     

Risk factors for Campylobacter spp. infection in Senegalese broiler-chicken flocks

Our objective was to identify the risk factors for Campylobacter infection in Senegalese broiler flocks. Seventy broiler farms were studied around Dakar from January 2000 to December 2001 around Dakar. A questionnaire was administered to the farmers, and samples of fresh droppings were taken to assess the flocks' Campylobacter status. About 63% of the flocks were infected by Campylobacter spp.; Campylobacter jejuni was the most-prevalent species (P < 0.05). An elevated risk of Campylobacter infection was associated with other animals (mainly laying hens, cattle and sheep) being bred in the farm, the farm staff not wearing their work clothing exclusively in the poultry houses, uncemented poultry-house floors and the use of cartons that transport chicks from the hatchery to the farm as feed plates (rather than specifically designed feed plates). Alternatively, thorough cleaning and disinfection of poultry-house surroundings and manure disposal outside the farm were associated with decreased flock risk.     

Feed can be a source of Campylobacter jejuni infection in broilers

1. The aim was to determine the importance of a contaminated diet as a possible cause of Campylobacter jejuni infection in broilers.

2. This study evaluated the viability of C. jejuni in both starter and finisher diets and the interference from other mesophilic bacteria in this viability.

3. Starter and finisher samples of broiler diet were deliberately contaminated with 3 or 5 log CFU·g^?1 of C. jejuni (NCTC 11351) and then maintained at two different storage temperatures (25°C or 37°C) for 3 or 5 d.

4. C. jejuni survived during this period and, when inoculated at 10³ CFU·g^?1, multiplied with greater proliferation at a storage temperature of 37°C. There was no relationship between the amount of mesophilic bacteria and C. jejuni viability.

5. This study highlights the importance of the diet in the epidemiology of C. jejuni in broilers.     

Experimental infection of the mouse mammary gland with Campylobacter coli.

Campylobacter coli strains of bovine and avian origin were inoculated into the mammary gland of mice. A bovine strain isolated from a case of mastitis produced gross and histological changes in most of the glands; one bovine and one avian faecal isolate did not. Histologically, lesions were characterised by neutrophil infiltration in the alveolar spaces and necrosis and oedema in the interalveolar tissue. On bacteriological examination, the bovine mastitis strain could be isolated from most of the glands, but neither of the faecal strains. The mouse, therefore, appears to provide a convenient model for studying campylobacter mastitis.     

Campylobacter colonization in poultry: sources of infection and modes of transmission

Since its recognition as a human pathogen in the early 1970s, Campylobacter jejuni has now emerged as the leading bacterial cause of food-borne gastroenteritis in developed countries. Poultry, particularly chickens, account for the majority of human infections caused by Campylobacter. Reduction or elimination of this pathogen in the poultry reservoir is an essential step in minimizing the public health problem; however, farm-based intervention measures are still not available because of the lack of understanding of the ecological aspects of C. jejuni on poultry farms. Although Campylobacter is highly prevalent in poultry production systems, how poultry flocks become infected with this organism is still unknown. Many investigations indicate that horizontal transmission from environmental sources is the primary route of flock infections by Campylobacter. However, some recent studies also suggest the possibility of vertical transmission from breeder to progeny flocks. The transmission of the organism is not well understood, but it is likely to be through both vertical and horizontal transmission and may be affected by the immune status of the poultry host and the environmental conditions in the production system. Intervention strategies for Campylobacter infection in poultry should consider the complex nature of its transmission and may require the use of multiple approaches that target different segments of the poultry production system.     

Campylobacter

Species within the genus, Campylobacter, have emerged over the last three decades as significant clinical pathogens, particularly of human public health concern, where the majority of acute bacterial enteritis in the Western world is due to these organisms. Of particular concern are the species, C. jejuni and C. coli, which are responsible for most of these gastrointestinal-related infections. Although these organisms have already emerged as causative agents of zoonoses, several aspects of their epidemiology and pathophysiology are only beginning to emerge. Trends in increasing antibiotic resistance are beginning to emerge with oral antibiotics, which may be the drug of choice for when it is necessary to intervene chemotherapeutically. This review wishes to examine (i) emerging clinical aspects of the disease, such as Guillain Barre syndrome (GBS), (ii) the association between these organisms and poultry as a natural host, (iii) environmental aspects of Campylobacter epidemiology, (iv) the emergence of atypical campylobacters (v) emerging trends in antibiotic resistance, (vi) adoption of modern methods for the detection of campylobacters.     

Colonization strategy of Campylobacter jejuni results in persistent infection of the chicken gut

Although poultry meat is now recognized as the main source of Campylobacter jejuni gastroenteritis, little is known about the strategy used by the bacterium to colonize the chicken intestinal tract. In this study, the mechanism of C. jejuni colonization in chickens was studied using four human and four poultry isolates of C. jejuni. The C. jejuni strains were able to invade chicken primary cecal epithelial crypt cells in a predominantly microtubule-dependent way (five out of eight strains). Invasion of cecal epithelial cells was not accompanied by necrosis or apoptosis in the cell cultures, nor by intestinal inflammation in a cecal loop model. C. jejuni from human origin displayed a similar invasive profile compared to the poultry isolates. Invasiveness of the strains in vitro correlated with the magnitude of spleen colonization in C. jejuni inoculated chicks. The C. jejuni bacteria that invaded the epithelial cells were not able to proliferate intracellularly, but quickly evaded from the cells. In contrast, the C. jejuni strains were capable of replication in chicken intestinal mucus. These findings suggest a novel colonization mechanism by escaping rapid mucosal clearance through short-term epithelial invasion and evasion, combined with fast replication in the mucus.     

Campylobacter jejuni infection in the ferret: an animal model of human campylobacteriosis

Campylobacter infection in weanling ferrets (Mustela putorius furo) was studied as an animal model for enteric campylobacteriosis in persons. The screening of fecal cultures on selective campylobacter media showed that Campylobacter jejuni/coli was not present in the normal enteric flora. Intragastric feeding of a mixture of cat feed and 2.5 X 10(8) C jejuni isolated from ferrets with naturally occurring proliferative colitis was accomplished. All ferrets (n = 8) became infected on 3 days after they were inoculated, and at 5 to 7 days, they had bile-tinged, liquid feces with excessive mucus and blood. Ferrets gradually recovered from the diarrhea, and feces were normal 10 to 14 days after inoculation was done. Feces contained C jejuni at 14, 23, 28, 39, 46, 60, 91, 101, 109 and 144 days. In the second experiment, weanling ferrets initially were treated with 10% sodium bicarbonate, and 1 X 10(10) C jejuni organisms were administered in the cat feed. Diarrhea with fecal leukocytes and occult blood with occasional mucus appeared in almost all of the 21 ferrets from days 4 through 7. Campylobacter jejuni was isolated from the blood of 11 ferrets between 3 hours and 14 days after they were inoculated. Campylobacter jejuni bactericidal antibodies were present in serum samples at 14 days, with titers of 1:16 to 1:32. Intestinal lesions including cellular infiltration with mononuclear and polymorphonuclear leukocytes were in the lamina propria of the pyloric mucosa and small intestine of infected and control ferrets. The colon of 3 infected ferrets had small focal infiltrates of neutrophils on the lamina propria; one ferret had perivascular cuffing.(ABSTRACT TRUNCATED AT 250 WORDS)     

Epidemiologic features of Campylobacter infection among cats in the upper midwestern United States

OBJECTIVE: To describe the epidemiologic features of Campylobacter infection among cats in the Minneapolis-Saint Paul metropolitan area. DESIGN: Prevalence survey. ANIMALS: 152 cats examined at 3 private veterinary clinics and an animal humane society. PROCEDURES: Fecal samples were submitted for bacterial culture for Campylobacter spp. To determine the duration of Campylobacter carriage, follow-up fecal samples were collected from cats with positive Campylobacter culture results. RESULTS: Campylobacter organisms were cultured from 37 of the 152 (24%) fecal samples. Campylobacter isolates were identified as Campylobacter upsaliensis (29 cats), Campylobacter jejuni (2), and Campylobacter coli (1); species of the remaining 5 isolates could not be determined. Campylobacter organisms were isolated from 36 of the 122 (30%) cats that were < or = 1 year old but from only 1 of the 30 (3%) cats that were > 1 year old, and shedding was more common during the summer and fall months. No association between Campylobacter shedding and clinical signs of disease was identified. For 4 of 13 cats from which follow-up fecal samples were obtained, duration of Campylobacter carriage could not be determined because Campylobacter organisms were isolated from all follow-up samples. For the remaining 9 cats, median duration of Campylobacter carriage was 44 days. CONCLUSIONS AND CLINICAL RELEVANCE: C. upsaliensis can commonly be isolated from the feces of overtly healthy kittens in the Midwest United States. Because carriage may be prolonged, veterinarians should encourage good hand hygiene among owners of cats, especially among owners with new kittens in their household.     

Epidemiology of ovine Campylobacter infection determined by numerical analysis of electrophoretic protein profiles

The relationship of 50 Campylobacter strains isolated from aborted ovine foetuses, and the faeces of sheep, cattle and chickens were determined by numerical analysis of electrophoretic (SDS-PAGE) protein profiles. Comparison of protein patterns by numerical methods revealed differences between C. fetus ssp. fetus, C. jejuni, and C. coli strains as well as heterogeneity among isolates from different outbreaks. Isolates from each farm produced a distinct cluster and flocks from different locations were found to be infected with relatively different strains. In most cases, protein patterns of ovine foetal isolates were very similar to those of ovine faecal isolates. Ovine isolates of C. fetus ssp. fetus, C. jejuni and C. coli gave similar protein patterns to the corresponding Campylobacter species isolated from cattle or chicken, on the same farm. Thus, it was concluded that certain protein types of ovine Campylobacter strains were more likely associated with local areas, and Campylobacter strains causing ovine abortions are distributed in the environment more widely than assumed to date.