Selected content from the Animal Health and Production Compendium (© CAB International 2013). Distributed under license by African Union – Interafrican Bureau for Animal Resources.
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Identity Pathogen/s Overview Distribution Hosts/Species Affected Host Animals Systems Affected Epidemiology Impact: Economic Zoonoses and Food Safety Pathology Diagnosis Disease Course Disease Treatment Table Disease Treatment Vaccines Prevention and Control References Links to Websites OIE Reference Experts and Laboratories
Preferred Scientific Name
International Common Names
avian campylobacter infection, avian vibrionic hepatitis, avian vibrionic hepatitis, campylobacter jejuni infection, vh, campylobacter diarrhea in calves, campylobacter diarrhea in pigs, campylobacter fetus in calves, campylobacter fetus in sheep and goats, campylobacter fetus infertility and abortion in cattle, campylobacter jejuni in sheep and goats, campylobacter, arcobacter mastitis in cows, campylobacteriosis, colitis in weaned lambs due to campylobacter, enteric campylobacteriosis, enzootic abortion, enzootic infertility, ovine genital campylobacteriosis, swine proliferative enteritis
Campylobacter fetus subsp. fetus
Campylobacter fetus subsp. venerealis
The genus Campylobacter contains several species, which were formerly classified in the genus Vibrio. Most members of this genus are pathogenic inhabitants of the reproductive tract, such as C. fetus and C. jejuni, or the gastrointestinal tract, such as C. jejuni, C. coli, C. hyointestinalis, C. mucosalis and C. laridis of cattle, sheep, goats, pigs, horses, dogs, cats, rabbits, ferrets, hamsters and mink. Humans, as well as many other domestic and wild bird and animal species, including non-human primates, are also affected. Campylobacter species are commonly present in the intestinal tract of both healthy and diseased animals and birds, and are often found in their manure. The organisms are associated with infections of either the gastrointestinal tract or the genital tract resulting in abortion and female infertility. Although Campylobacter jejuni rarely causes fatal disease in animals, it is one of the leading causes of foodborne diseases in humans. The common signs of campylobacteriosis in humans are diarrhoea and cramps. Faecal contamination of poultry skin, meat, milk and water are all sources of campylobacteriosis in humans. Asymptomatic human carriers can also contaminate foods during processing. Numerous on-farm reservoirs and unknown modes of transmission make reduction of farm animal contamination difficult.
The increasing recognition of Campylobacter species as human pathogens has reinforced the importance of this genus in veterinary medicine and resulted in accelerated studies of their taxonomy. As a consequence, the scheme for the classification of Campylobacter organisms has been modified several times since its inception in 1963, when the genus comprised only two species. Taxa that were once assigned to Campylobacter presently belong to one of over 50 species and six genera. Vandamme et al. (1991) introduced a new taxonomic position of the genus Campylobacter within a new ribosomal RNA (rRNA) superfamily VI that is distinct from other rRNA superfamilies within the Gram-negative bacterial group. The taxonomic diversity of the group is matched by the diverse habitats in which they may be found, and by the wide range of diseases that they are associated with. Campylobacter organisms of significance in animal and human health include C. fetus (which has two subspecies, C. fetus subsp venerealis, and C. fetus subsp fetus), C. jejuni, C. coli, C. lari, C. mucosalis, C. hyointestinalis, C. sputorum, C. upsaliensis, C. curvus and C. rectus. Other previously named campylobacters associated with animal and human infections have been transferred to the new genera Arcobacter and Helicobacter.
Members of the genus Campylobacter are recognized as the most common human gastroenteric pathogens throughout much of the developed world and other temperate countries. Reports of campylobacteriosis in the UK and other countries have been increasing, with 61,713 human cases of Campylobacter infectious intestinal disease reported to the UK Communicable Disease Surveillance Centre in 1999, and it is believed that only half of incidents are reported. The contamination rates, identification of common pathogenic serotypes and extended survival of Campylobacter in surface waters illustrate the significance of threats associated with Campylobacter organisms (Thomas et al., 1999).
The US national surveillance on Campylobacter in poultry farms, which included four major producers in Alabama, Arkansas, California and Georgia, representing modern commercial conditions in the USA, showed that 87.5% of the flocks were Campylobacter-positive during the 6- to 8-week rearing period. Even in some of the Campylobacter-negative flocks, contamination of the rearing environment was positive for Campylobacter (Stern et al., 2001). Center for Disease Prevention estimated 2.4M people per year are affected in the USA.
In a nationwide survey in Denmark (Nielsen et al., 1997), the isolation rate of thermophilic campylobacters at abattoirs was 36% in broilers, 47% in cattle and 46% in pigs. C. jejuni accounted for 83-91% of isolates from broilers and cattle, whereas 95% of isolates from pigs were C. coli.
The high prevalence of Campylobacter infection is not limited to livestock animals and humans. Campylobacter is also a common pathogen in cats and dogs as well as in wild birds. Abate et al. (1999) in his study isolated Campylobacter organisms from 65% of adult cats, 50% of puppies, 44% of wild birds and 42% of captive animals.
The introduction of an infected bull can rapidly spread C. fetus subsp venearalis through the herd as the bull mates with each cow. Similarly, the introduction of an infected cow may lead to infection of the bull at first mating, and consequently to rapid spread of the infection to the rest of herd. Direct transfer from animal to animal can occur, but this is uncommon. In herds in which artificial insemination is used in reproduction, C. fetus infection is rare. [More details on factors associated with husbandry systems are provided in the section on Disease Prevention and Control.]
|Alectoris rufa (red-legged partridge)||Domesticated host, Wild host|
|Bos indicus (zebu)||Domesticated host, Experimental settings, Wild host|
|Bos taurus (cattle)||Domesticated host, Experimental settings, Wild host|
|Camelus dromedarius (dromedary camel)||Domesticated host|
|Capra hircus (goats)||Domesticated host, Wild host|
|Gallus gallus domesticus (chickens)||Domesticated host, Wild host|
|Ovis aries (sheep)||Domesticated host, Wild host|
|Perdix perdix (grey partridge)||Domesticated host, Wild host|
|Sus scrofa (pigs)||Domesticated host, Wild host|
Digestive - Large Ruminants
Digestive - Pigs
Digestive - Poultry
Digestive - Small Ruminants
Reproductive - Large Ruminants
Reproductive - Small Ruminants
The genus Campylobacter contains several bacteria that are pathogenic to domestic and wild animals. C. fetus subsp venerealis is the cause of a specific venereal disease of cattle, which is transmitted either by coitus or in the course of artificial insemination. Infection of bulls is usually asymptomatic and can be eliminated spontaneously. Passive transfer of infection by the bull is unlikely. The infection in cows is characterized by temporary infertility and prolonged oestrous cycle. C. fetus subsp venerealis has a marked tropism for chorionic epithelium, and causes embryonic death and induces endometritis.
C. fetus subsp fetus, also known as C. fetus subsp intestinalis, causes abortion in ewes. However, this is not a venereal disease since infection is acquired by the oral route. Birds can contribute to spreading of this infection. C. fetus subsp fetus infection occasionally causes abortion in cows, but the incidence is much lower than in sheep. C. fetus subsp fetus infection can also cause abortion in horses, and enteritis in cattle, sheep, pigs and horses similar to that caused by C. jejuni.
C. jejuni, also known as C. fetus subsp jejuni or Vibrio jejuni, is a normal inhabitant of the intestinal tract of cattle, sheep, goats, dogs, cats, rabbits and many species of birds. However, C. jejuni, as well as C. laridis and C. upsaliensis are also important causes of enteritis and diarrhoea in humans, dogs, cats, cattle, foals, rabbits, ferrets, hamsters and mink. C. jejuni is also a recognized cause of late abortion and stillbirths in sheep and goats, and may also cause mastitis in cattle.
C. mucosalis (formerly C. sputorum subsp mucosalis), C. hyointestinalis and Campylobacter-like organisms (CPO) all have been recovered from pigs with swine proliferative enteritis (SPE). This is a complex disease of the lower small intestine and occasionally of the caecum and colon. SPE includes porcine intestinal adenomatosis, proliferative ileitis, terminal ileitis, necrotic enteritis and haemorrhagic enteritis.
C. coli does not appear to be an important pathogen, although it had been considered the cause of winter dysentery in cattle, which is now believed to be caused by coronavirus, and swine dysentery, which is in fact caused by Treponema hyodysenteriae.
Campylobacter is recognized as an important zoonotic pathogen of worldwide economic significance. Campylobacteriosis in cattle can cause sporadic abortions, temporary or permanent sterility, irregular heats due to early embryonic death, and disruption of the breeding regime. This can lead to heavy economic losses as the animals are out of production for months and repeatedly return to service period. In sheep, heavy losses from epizootic abortion caused by C. fetus can occur during the lambing season. Swine proliferative enteritis (SPE) occurs worldwide and causes severe economic losses in recently weaned pigs.
The economic losses of campylobacteriosis in humans are even higher. Scott et al. (2000) estimated the annual economic cost of all foodborne infectious diseases in New Zealand. Campylobacteriosis was shown to account for most of these costs. It was found that the 119,320 reported episodes of all food poisonings (3241 per 100,000 population) cost an estimated $55.1 million ($462 per case). Direct medical costs were estimated at $2.1 million, direct non-medical costs at $0.2 million, indirect costs of lost productivity were $48.1 million, and the cost of loss of life was $4.7 million. These findings implied that an estimated $55 million could be required for preventing foodborne infectious diseases and that efforts should focus on lowering the incidence of campylobacteriosis since this disease accounted for the majority of foodborne diseases.
Lindqvist (1999) examined the incidence of food poisoning in Uppsala, Sweden between February 1998 and January 1999. There were 268 reported incidents of food poisoning, affecting 515 people. It is believed that these cases represented around 10% of the total number of instances in Uppsala (total population, 186,000). The most common causes of food poisoning were Campylobacter and calicivirus. The financial cost of food poisoning was estimated to be Skr2164 per person.
Animal-derived foods, excretions and by-products are the most common sources of infection for humans. C. jejuni has been found in milk, poultry products and in faeces of pigs, dogs and cats. Humans usually become infected after ingesting contaminated animal products, particularly chicken meat. Contamination of water sources by human or animal excrement can also be a source.
C. jejuni is the most commonly reported bacterial cause of foodborne infection in the USA and other countries. Adding to the human and economic costs are chronic sequelae associated with C. jejuni infection such as Guillain-Barre syndrome and reactive arthritis (Altekruse et al., 1999). In addition, increasing proportions of human infections caused by C. jejuni are resistant to antimicrobial therapy. Contamination of raw poultry and consumption of undercooked poultry are the major risk factors for human campylobacteriosis. Efforts to prevent Campylobacter infections in humans throughout each link in the food chain are needed.
Postmortem findings in animals that die due to Campylobacter infections are variable. C. fetus subsp venerealis lesions in cattle are usually subtle. In ewes, C. fetus subsp fetus localizes in the pregnant uterus and, after a brief bacteraemia, results in abortions during late pregnancy, stillbirth, or birth of weak lambs, which usually die soon after birth. Immunity follows abortion, but certain ewes may carry the organism in the gastrointestinal tract. Cattle are also susceptible to C. fetus subsp fetus and late abortions may occur, but the incidence is much lower than it is in sheep. Abortion caused by C. fetus subsp fetus is also seen in horses. This pathogen may also cause enteritis similar to that caused by C. jejuni in cattle, sheep, pigs and horses. Campylobacter jejuni has also been shown to cause abortion in sheep with lesions similar to those caused by C. fetus subsp fetus. Lesions are found most often in the placenta but may also occur in the foetus. However, autolytic changes usually preclude adequate pathological study. The bacteria first localize in the hilar zone of the placentomes, resulting in vascular damage and thrombosis of small vessels, causing separation of the chorion with formation of haematomas. Subsequent invasion of the chorion and chronic capillaries leads to necrosis at this site and invasion of the foetus. Both hypoxia from placental damage and foetal invasion contribute to foetal death. The placenta, particularly cotyledons are oedematous and contain foci of necrosis. The foetus is oedematous and often macerated. In some, relatively specific lesions are present in the form of focal diffuse necrotic, grey foci, 1 to 2 mm in diameter.
C. mucosalis (formerly C. sputorum subsp mucosalis) and C. hyointestinalis have been recovered from pigs with swine proliferative enteritis (SPE). This complex disease includes intestinal adenomatosis, proliferative ileitis, terminal ileitis, necrotic enteritis and haemorrhagic enteritis. Campylobacter organisms are isolated regularly from the apical cytoplasm of crypt and glandular epithelial cells. The proliferative lesions commence in the epithelium of crypts and glands, where hypertrophied cells with larger than normal vesicular nuclei can be seen. Hyperplasia leads to crowding of cells, development of a pseudostratified appearance, and elongated crypts and branching glands, which may extend into the submucosa. Individual glands may assume a dysplastic appearance. Villi overlying such areas become atrophic and fused. Crypts contain neutrophils and mononuclear cells, and there is extensive mononuclear inflammation in the mucosa and submucosa. The terminal ileum is most severely affected. Necrotic enteritis and haemorrhagic enteritis are characterized by either extensive necrosis or necrosis accompanied by haemorrhage of an adenomatous mucosa. In either circumstance there is an extensive polymorphonuclear inflammatory response to the necrotic tissue in these conditions.
The course of Campylobacter infection, clinical signs and postmortem findings depend on many factors, particularly on the pathogenic species, host animal and age of affected animals. Campylobacter spp can be found in both healthy and diarrhoeic animals and in many cases Campylobacter infections may be inapparent. In one study, diarrhoea in pigs due to this agent did not affect performance and treatment was not required (Straw, 1990). However, the most common clinical manifestations of campylobacteriosis are abortion and gastroenteritis.
C. jejuni is a recognized cause of abortion in late pregnancy and stillbirths in sheep and goats, which must be differentiated from that caused by C. fetus subsp fetus by identification of the pathogen in the stomach contents of aborted fetus. C. jejuni can also cause mastitis in cattle. Similar Campylobacter organisms have been recovered from aborted puppies. In most cases, C. jejuni lesions are not specific, consisting of stunting and fusion of villi, dilation of crypts and crypt abscesses, mild cellular infiltration of the mucosa. Occasionally ulceration and haemorrhages can be seen. Most severe lesions are found in the proximal small intestine, but can also affect the entire small intestine and colon. Comma-shaped organisms can be seen on the surface of the epithelium and within the lamina propria using silver staining. Other lesions include necrotizing and suppurative placentitis and fetal bronchopneumonia. Large numbers of C. jejuni organisms can be cultured from placental and foetal tissue. C. jejuni has also been isolated from cows with mastitis (Gudmundson and Chirino-Trejo, 1993) and from a flock of lambs with severe diarrhoea and high mortality (Stansfield et al., 1986). C. jejuni and C. coli can cause diarrhoea with occasional blood and mucosa in experimental calves. Most healthy animals also carry the organisms. Demonstration of a rising antibody titre is probably the best way to make the diagnosis in such cases.
Diagnosis of C. jejuni infection in chickens can be made on the basis of disease history, lesions, and isolation of the organism. In affected birds, the most specific lesion is an enlarged, discoloured liver with small yellowish foci, but this lesion is observed in less than 10% of cases. The most suitable serological tests for diagnosis of this infection are agglutination and complement fixation.
C. fetus subsp. venerealis lesions in cattle are usually subtle and may include subacute, diffuse mucopurulent endometritis. Lymphocytic infiltrates, often in the form of small nodules, may be found in the uterine mucosa, cervix and vagina. Placental necrosis along with neutrophilic and lymphocytic placentitis may provide evidence of infection. Diagnosis is usually possible from the herd history, as it is rare in herds where artificial insemination is used in reproduction. Campylobacter organisms may be visible in tissue sections of the placenta and can be specifically identified with immunological staining techniques. C. spitorum subsp bubulus is a common commensal of the male and female genital tract of cattle and must be differentiated from the pathogenic species. Diagnosis is by culture or titres.
In general, Campylobacter organisms can be isolated from affected intestinal samples, stomach content, smegma or vaginal fluid on selective media containing antimicrobial agents such as polymyxin B or trimethoprim. Immunodiagnosis is unsuitable for diagnosing intestinal Campylobacter infections; however, enzyme-linked immunosorbent assays (ELISA) have been used in epidemiological studies. Antibodies against C. fetus can be detected in the cervicovaginal mucus by using an agglutination test or ELISA.
Cattle appear to be resistant to Campylobacter fetus subsp fetus up to the age of 12 months. All other cattle are susceptible, but 2- to 3-year-old cows are mainly affected. Natural resistance against venereal vibriosis occurs in about 10% of cows. After Campylobacter infection, animals develop convalescent immunity (following recovery from infection). If animals are not re-infected, specific serum IgG, IgM and IgA antibodies remove Campylobacter pathogens from the reproductive tract within a year of infection. Convalescent immunity disappears completely within 4 years of infection and animals again become susceptible to Campylobacter infection.
Sheep and goats also develop an active immunity following abortion by producing antibodies, mainly of the IgM and IgG types.
Most Campylobacter organisms are pathogens of the reproductive and gastrointestinal tracts. C. fetus subsp venerealis infection in cows is principally characterized by temporary infertility and prolonged oestrous cycle. The cows become infected during breeding. Although fertilization and implantation are normal, C. fetus subsp venerealis, which has a marked tropism for chorionic epithelium, soon kills the embryo and induces endometritis. Neither death of the embryo nor endometritis are manifested by clinical signs. Endometritis may prevent conception at succeeding oestrous periods, but most cattle conceive before resolution of the disease. Recovered cows are usually resistant to re-infection. C. fetus subsp venerealis, on occasions may also cause observable abortions usually between 4 and 7 months of pregnancy.
|Drug||Dosage, administration and withdrawal times||Life stages||Adverse affects||Drug resistance||Type|
|Erythromycin||Dose = 4-25 mg/kg daily, i.m, orally; withdrawal = 7-14 days. Always seek veterinary advice before administering treatment.||All Stages/All Stages/Lamb||No||Drug|
|fluoroquinolone||Dose rate (guide only, 3-20 mg/kg) and withdrawal times should be adjusted for the individual animal; i.m., s.c. or orally, every 6, 12 or 24 h. Always seek veterinary advice before administering treatment.||All Stages/All Stages/All Stages/All Stages||Neurotoxicity, vomiting, diarrhoea, convulsions||No||Drug|
|streptomycin||dose = 7.5-12.5 mg/kg every 12 h, i.m., s.c. Withdrawal time regulated by each country. Always seek veterinary advice before administering treatment.||All Stages/All Stages/All Stages/All Stages||Ototoxicity, nephrotoxicity||No||Drug|
|tetracycline||Dose = 5-20 mg/kg every 8, 12 or 24 h, i.m., i.v. or orally. Withdrawal time = 1-22 days. Always seek veterinary advice before administering treatment.||All Stages/All Stages/All Stages/All Stages||Yes||Drug|
|Vibriovax bivalent vaccine||Bivalent vaccine (C. veneralis, C. intermedius). 2 ml (2 doses, 4-5 weeks apart) + annual booster. Always seek veterinary advice before administering treatment.||Bull/Cow/Heifer||No||Vaccine|
Erythromycin and tetracycline are effective against C. jejuni, although resistance to both anti microbials have been reported. Parenteral administration of streptomycin or topical administration of an aqueous solution of penicillin and streptomycin into the prepuce is used for treating bulls with venereal Campylobacter infection. Penicillin is the most effective treatment for aborting ewes and goats. Aborting animals should be isolated from apparently healthy animals.
An outbreak of C. jejuni in a flock of lambs with severe diarrhoea and high mortality was brought under control with daily injection of 4 mg/kg erythromycin followed by a single intramuscular injection of long-acting oxytetracycline (Stansfield et al., 1986).
Most resistant strains of Campylobacter come from developed countries due to indiscriminate use of antimicrobial agents, usually as growth promoters, in animals destined for human consumption. Significant increases in the prevalence of fluoroquinolone-resistant Campylobacter in poultry and infections in humans have been recorded in many countries following the introduction of fluoroquinolones for use in poultry production. In the UK, both Houses of Parliament have been critical of imprudent use of antibiotics in animals (see House of Lords Select Committee Report: http://www.parliament.the-stationery-office.co.uk/pa/ld199798/ldselect/ldsctech/081vii/st0701.htm). In the USA, meat inspections were increased following emergence of resistant strains.
The use of antimicrobials in livestock is controversial and may lead to the emergence of resistant organisms that could be transmitted to humans through the food supply. Anderson et al. (2001) investigated the potential public health risk from C. jejuni and fluoroquinolone (FQ)-resistant C. jejuni. They estimated that approximately 16,000 individuals in the USA may be infected by C. jejuni derived from both ground beef and fresh beef sources. Furthermore, the probability of adverse consequences arising from both C. jejuni and FQ-resistant C. jejuni was predicted. The results from quantitative risk assessment model were lower when compared to similar public health outcomes for beef products estimated by the Centers for Disease Control (CDC) and the US Department of Agriculture's Economic Research Service (USDA-ERS). However, incorporation of uncertainty and variability in estimates from this model and the CDC and USDA-ERS suggest that the disparity among the estimates is small.
|Vaccine||Dosage, Administration and Withdrawal Times||Life Stages||Adverse Affects|
|Vibriovax bivalent vaccine||Bivalent vaccine (C. veneralis, C. intermedius). 2 ml (2 doses, 4-5 weeks apart) + annual booster. Always seek veterinary advice before administering treatment.|
Control measures include careful following of hygienic measures such as disinfection protocols, cleaning in the veterinary surgeries and kennels and hand washing. Vigorous control of breeding programmes based on sound husbandry practices reduces the risk of introducing Campylobacter into the herd. Careful selection of replacement cows and bulls can also prevent introduction of Campylobacter to the herd. Only bulls that were tested negative for Campylobacter and cows from herds with known history should be allowed to enter the herd. Campylobacter can be eliminated from infected females by resting the herd for one breeding season and replacing the bulls. Administration of bactericins before breeding can prevent the disease in endemic herds. Artificial insemination is a very effective way of controlling and eradicating the disease in cattle, sheep and goats.
Immunological treatment is not available for gastrointestinal diseases caused by campylobacters. Annual vaccination can prevent Campylobacter infections of the reproductive tract.
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(OIE Reference Experts and Laboratories, accessed 30 May 2013)
Dr Jaap Wagenaar
Animal Sciences Group (ASG)
Division of Infectious Diseases
Central Veterinary Institute
P.O. Box 65
8200 AB Lelystad
Tel: +31-320 23 81 57 Fax: +31-320 23 89 61
Date of report: 30/05/2013
© CAB International 2013. Distributed under license by African Union – Interafrican Bureau for Animal Resources.
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.