Campylobacter

A range of tests are available many for testing food samples. Real time PCRs are available as kits but need to be used within a main laboratory. Real time PCR machines have been developed which can give test results within one hour and can detect low number of organisms. Polymerase chain reaction (PCR) - based assays have come into use, for example in Denmark, to screen poultry broilers, and a commercial PCR-based assay is available for meat samples. It should be noted that PCR-based assays detect both viable and non-viable organisms. Antigen-capture enzyme-linked immunosorbent assays (ELISAs) have been described in the literature.

Serology on paired titers may be helpful in some cases for human diagnosis.

Kits have been developed for the rapid identification of Campylobacter which have been grown in culture.

Yes.

BAX® System Real-Time PCR Assay for detection of C. jejuni, C. coli, and C. lari in poultry carcass rinses or processed products. The system is commercially available and has been validated by NordVal. It is performance tested and approved by AOAC.

See OIE Manual of Standards for Diagnostic Tests and Vaccines.

http://www.oie.int/eng/normes/mmanual/2008/pdf/2.09.03_CAMPYLO.pdf

Depends on the potential and whether there becomes a legal obligation to screen animals and birds before slaughter.

On farm kits which detect high colonization levels and allow scheduled slaughtering or the heat-processing/freezing of positive flocks.

GAP: Rapid identification tests are needed urgently.

May be required if a vaccine is developed.

• The development of kits to rapidly identify colonized flocks
• The development of kits which detect (high levels of) colonisation in birds
• The development of rapid diagnostics for campylobacteriosis in humans

GAP: Kits for rapid detection and quantification (also low levels) of Campylobacter in animals and on food products.

Under research only.

GAP: No effective vaccines available for livestock.

None.

No.

No.

Not applicable as no vaccines available.

If a cheap effective vaccine was developed there could be market in the poultry industry to reduce the levels of campylobacter in birds going for slaughter.

The issues are

• The short life of broilers
• Vaccination of an immunologically immature animal
• Vaccination in the presence of maternally-derived antibodies
• Appropriate presentation at the gut mucosal surface
• The absence of appropriate avain mucosal adjuvants
• Cheap, easy delivery as oral vaccine or in ovo

None forseen unless the vaccine is a derived from a genetically manipulated organism.

One vaccine under investigation is a GMO using a Salmonella as a vector of Campylobacter antigens.

Feasible,  a market exists especially for free-ranging birds.

No.

Develop a vaccine to prevent colonization of meat animals and birds in order to reduce levels of colonized animals going into abattoirs and the spread into the environment.

Antibiotic use not appropriate. Alternatives include bacteriophages and bacteriocins.

GAP: Further research and development of curative and preventive therapies (excl antibiotics).

Antimicrobial resistance in these bacteria is an emerging and increasing threat to human health.

GAP: Development of therapy for humans (excl antibiotics).

None

Not applicable.

None.

Bacteriophages or bacteriocins are reported to be effective if administered 3 days prior to slaughter. Field trials are urgently required in this area.

GAP: Field trials needed to investigate effects and consequences of bacteriophages or bacteriocins.

Diagnostics should be standardized, fast, cheap.

GAPS: Development of rapid tests for the detection of live Campylobacter (for genus and species identification) in different types of samples, even present in low numbers. Rapid methods for the quantification of live Campylobacter.

Long term.

Expensive.

None.

Not available at present but would require a rapid screening method which could identify animals carrying Campylobacter in the intestines.

Two approaches are under investigation

1. Subunit vaccines using microsphere presentation systems or similar adjuvants
2. Genetically engineered Salmonella vector expressing various Campylobacter antigens

Depending on when a candidate vaccine could be identified the timescale will be 5-10 years. Could be earlier if adjuvant problem solved.

GAP: Problem with finding a suitable adjuvant.

Expensive with the need to develop and undertake all the relevant tests to provide data to enable the product to be authorised.

To understand the biology of Campylobacter, and the host pathogen interactions at a molecular level and link this to differential virulence of Campylobacter in birds and animals would be useful but current knowledge is sufficient to generate a preliminary vaccine which could then be improved.

To investigate the immune mechanisms as immunity to Campylobacter appears to be strain-specific and complex, and the antigens conferring immunity are not well understood. This depends on the antigens under investigation. Most antigens have conserved as well as strain-specific and conformational as well as linear epitopes.

In humans a candidate vaccine has been developed using an empirical approach. A vaccine  consisting of heat- and formalin-killed whole bacteria combined with LT as a mucosal adjuvant has been developed by the Navy Medical Research Institute (USA) and shown to provide 87% protection against intestinal colonization in a small number of volunteers challenged post vaccination with a pathogenic Campylobacter strain. Current studies have focussed on the use of flagellin or flagella-secreted protein FspA1 as candidate vaccines to be administered by the nasal route with attenuated LT R192G as an adjuvant. Vaccination of mice with FspA1 resulted in 64% protection against C jejuni challenge. The major outer membrane protein (MOMP) from C jejuni might be another promising candidate for a subunit vaccine, especially when made into proteoliposomes. An oral live multivalent vaccine expressing antigens from Campylobacter, Shigella and ETEC is also currently being developed as a travellers’ diarrhoea vaccine (see link below).

http://www.freepatentsonline.com/6790446.pdf

http://www.acebiosciences.com/index.php?option=com_content&view=article&id=55&Itemid=65

One problem for vaccination of humans is the risk of induction of GBS. Recently strains have been selected as vaccine candidates to avoid this risk.

In chickens the specificity of the immune response is not the same as in humans or other mammals. With the recent development of methods for delivering sunbunit vaccines Campylobacter antigens, selected on the basis of current knowledge and using post-genomic approaches can be tested as candidates in a challenge model.

GAP: More information needed on susceptibilities to currently available antibiotics.

Time to develop would depend on the product and the trials necessary to validate the test. Commercial production would then take further time.

Costly.

Campylobacter is a genus of Gram-negative, microaerobic, slender, curved, motile bacteria with a single polar flagellum at one or both ends. Members of the genus Campylobacter can colonise a variety of habitats. The most important species in terms of food-borne disease are considered to be the Campylobacter species, C. jejuni and C. coli and the closely related C.lari. These species are often referred to as “thermotolerant”, due to their growth optimum at 42 °C. This analysis will focus on these agents only.

In humans C. jejuni and C. coli are associated with campylobacteriosis which routinely presents as 3-5 days of prodromal fever followed by 3-7 days of acute diarrhoea, abdominal pain and fever. Diarrhoea can be watery or bloody. Most cases of campylobacteriosis are self limiting but about 10% of cases may require medical treatment including hospitalization. About 1% of cases have sequelae of infection which can include arthopathies, abortion, neuropathological symptoms (such as Guillain Barre Syndrome (GBS)) and irritable bowel syndrome.

Both C. jejuni and C.coli have highly diverse populations but there is no known association between human disease presentation and strain variation excepting that some strain types are more frequently associated with GBS than others which appears to be related to antigen mimicry. C. jejuni/coli rarely cause disease in other animals.

GAPS: Host- factors involved in clinical picture need to be clarified. In practice, no animal model is available to mimic human disease and test pathogenicity of strains. 

In the laboratory Campylobacter species are very intolerant of drying, heat, freezing, UV, disinfectants, extremes of pH, etc. However, in natural environments C. jejuni and C. coli  often survive for longer periods of time, depending on the surrounding conditions. Survival is supported by cold temperatures (4-10 ºC), darkness and a moist atmosphere. The conditions that poultry meat is stored at for retail are ideal for survival. Survival potential varies between strains and environmental stresses can affect host colonisation properties. Environmental stress can cause morphological changes from spiral to coccal. It may also render the organisms non-culturable but viable (VNC forms) though the importance of this to infection is as yet unknown. Coccal and VNC formation are independent events.

The mechanisms of survival are unclear but common mechanisms present in other Gram negative bacteria are not present in the genome of Campylobacter.

GAP: Markers of survival capacity required for informing risk assessments.

C. jejuni and C. coli can colonise the intestinal tract of most, if not all, mammals and birds. Also C. lari colonizes birds, including broilers and laying hens. In the laboratory C.jejuni and C. coli grow best at the body temperature of a bird (42 ºC), and seems to be well adapted to the avian gut. Poultry, especially chickens are colonised throughout their gastrointestinal tract and colonisation of the caecum can reach 10¹⁰ cfu per gram of caecal contents. These organisms can frequently be recovered from spleen and liver suggesting extraintestinal infection. Nevertheless this colonisation is asymptomatic and in experimentally challenged birds there are no obvious clinical signs or effect on production criteria.

Campylobacter jejuni or C coli  may be recovered from animals with diarrhoea but in the vast majority of cases this is more likely to reflect the washing out of commensal gut organisms due to other infections than to be causative of disease. Although most animals can be colonised proof of Koch postulates has not been successful in most animal hosts as there is generally high levels of naturally acquired immunity.

Yes. The mechanisms of pathogenicity to induce diarrhoea in humans are as yet unknown. A number of virulence properties have been described including mobility, adherence, invasion and cytolethal distending toxin (CDT) production. Strains vary in each of these properties but to date none have been able to account for the features of the disease. The major hindrance to understanding pathogenicity is the absence of a suitable animal model of disease.

GAPS: 

• Lack of animal model.
•  The only test of Koch’s postulates is experimental infections with purified organisms – this has been done with several volunteer studies for a limited number of organisms indicating a dose response relationship to colonization of humans but not to disease.
• Evidence of markers confirming pathogenicity (virulence) is lacking 

Arthropods may act as mechanical vectors.

C. jejuni and C. coli are common asymptomatic gut colonisers of all warm-blooded animals including livestock, domestic pets and wildlife. The fastidious growth requirements for these organisms means that amplification only occurs within a host. Organisms are shed in faeces and survive to become ubiquitous in the environment, including in surface waters. Consequently Campylobacter is recovered from multiple potential reservoirs and is transmitted to humans and other animals by multiple potential routes and vectors.

The prevalence of Campylobacter positive broiler flocks varies between countries. In Scandinavian countries prevalence is about 10% while in middle European countries e.g. the UK it is about 80% and in southern European countries it is about 100%. Prevalence also varies over season with summer peaks in most countries.

Cattle, sheep and pigs are frequently colonised with Campylobacter; with prevalence at slaughter of about 50%, 50% and 90% respectively.

There is some host-specificity in these Campylobacter species. C. jejuni is commonly found in ruminants and poultry; C. coli is commonly found in pigs and poultry; while C. lari is most often found in wild birds.

Transmission between hosts is via the faecal-oral route. Transmission from animals to humans is mainly through consumption and handling of contaminated animal food products or water but also via direct contact with colonised animals.

In broilers there is no detectable vertical transmission. The infective dose can be less than 10 cfu. Strains that are laboratory adapted are less infective. Transmission within a commercial broiler flock is very rapid and up to 100% of birds can become colonised within 5 days. Interestingly flocks are rarely infected until 2-3 weeks of age. This resistance to infection appears to be related to maternally-derived immunity although newly-hatched chicks can be colonised by challenges of less than 10 cfu.

There is some evidence for Campylobacter strain-associated differences in colonisation potential in broilers. Little is known about the transmission between other livestock.

GAPS:

• Differences in colonisation potential (in broilers) need to be clarified.
• Routes for transmission between other livestock than poultry have not been detailed 

Not applicable.

Campylobacter colonisation in poultry is asymptomatic and in experimentally challenged birds there are no obvious clinical signs or effect on production criteria regardless of age.

In young ostriches colonisation with C. jejuni can be associated with enteritis and occasional mortality but this is difficult to reproduce experimentally.

In ruminants (cattle and sheep) both C. jejuni and C. coli are recovered from about 50% of asymptomatic animals at slaughter. However, in pregnant ruminants infection can occasionally cause abortion with organisms recovered from the abortion products. The incidence of abortion is low and appears to be dependent on the timing of infection. Abortion tends to occur late in gestation. Abortion induces immunity which is long lasting.

Over 75% of pigs are asymptomatically Campylobacter positive at slaughter. Campylobacter-associated abortion in pigs has rarely been reported but abortion caused by a similar organism, Arcobacter, has been reported.

C. jejuni and occasionally C. coli have been associated with enteritis in dogs, cats and other animal species, but conclusive causative evidence is lacking.

The incubation period in ruminants and pigs is unknown. In experimentally challenged chicks and older (2-3 weeks) birds become maximally colonised 10¹⁰ cfu per g caecal contents within 3 days.

There is no mortality associated with Campylobacter infection in chicks or chickens. The organisms are frequently recovered from the gut, liver and spleen of dead birds but the infection is not causative.

In broilers shedding in faeces occurs detectably within 3 days of challenge. Colonisation is often chronic for the life of a conventional broiler (up to 7 weeks of age). Shedding can be erratic and is not a good indicator of colonisation. Colonisation can wane from 9 weeks after challenge which is thought to be associated with acquired immunity. However, some laying hens are still colonized in the caecum at slaughter (1.5 years old).

GAP: Quantitative data on shedding especially in free-range birds.

There is no known pathogenicity in broilers.

Pathogenicity in ruminants to cause abortion has not been investigated but similar mechanisms to those seen in Campylobacter fetus subsp fetus-associated abortion may prevail.

Campylobacter, are a major cause of food-borne bacterial enteritis in humans worldwide. In Europe there were over 200000 reported cases of campylobacteriosis in 2007. There is a significant underreporting of cases, hampering the possibility to calculate the total burden of the disease. The WHO estimates that 1% of the population contract campylobacteriosis each year. The incidence varies between countries depending on the quality of surveillance. The overall EU notification rate was 45.2 per 100,000 population in 2007. The incidence is higher in children (aged 0- 4) and in young adults (15- 24).

More information:

From EFSA:

• The Community Summary Report on Trends and Sources of Zoonoses and Zoonotic Agents in the European Union in 2007 is available at:http://www.efsa.europa.eu/en/scdocs/scdoc/223r.htm
• The Community Summary Report on Food Borne Outbreaks in the European Union 2007: http://www.efsa.europa.eu/en/scdocs/scdoc/271r.htm

From ECDC: http://www.ecdc.europa.eu/en/healthtopics/pages/climate_change_food_borne_diseases.aspx

The level of underreporting of campylobacteriosis is considered to be high for a number of reasons:

• (i) not all cases present to a general practioner,
• (ii) stool samples are rarely taken,
• (iii) detection of the causative agent is not optimal,
• (iv) not all confirmed cases are recorded.

It is estimated from community case control studies that the ratio of reported to unreported cases is 1:8- 1:10.

GAPS: 

• High level of underreporting of cases
• Differences between countries in reporting practices

The vast majority of human cases (about 99%) are sporadic rather than outbreaks. However, outbreaks, or clusters of disease caused by consumption of poultry meat and large water-borne outbreaks have been reported.

The Community Summary Report on Food Borne Outbreaks in the European Union 2007: http://www.efsa.europa.eu/en/scdocs/scdoc/271r.htm

Risk attribution studies have been undertaken using a variety of epidemiological methods. Epidemiological investigations, such as case-control and outbreak  studies suggest that 20-40% of cases are attributable to the mishandling and consumption of poultry meat. Scientific reports on risk factors for human infection indicate that the consumption of food (poultry meat, cross contaminated food products, raw milk and contaminated water) is the main source of infection, followed by direct contact with colonized animals.

Strain typing has been also extensively used to determine risk attribution. Strain typing has been undertaken by multiple phenotypic and genotypic methods. However, over the last few years multi-locus sequence typing (MLST) has become routinely adopted in some laboratories. These studies statistically indicate a degree of host specificity in Campylobacter populations and indicate that 50-80% of campylobacteriosis cases are attributable to campylobacters from the poultry reservoir. From this it can be speculated that a substantial proportion of disease is caused by “poultry campylobacters” transmitted via direct and indirect routes from poultry to humans i.e. poultry meat by contact with poultry faeces contaminated water or soil or other untreated foods. Such campylobacters may also colonise other animals including cattle, pigs and domestic pets.

Direct contact with colonised animals or material contaminated by their faeces may contribute to human campylobacteriosis.

The relative importance of various reservoirs may vary between countries. Travel is also a major risk factor but this is probably from consuming cross-contaminated foods.

GAP: Source attribution studies have only been performed in some countries. Difficult to get a clear picture, partly due to use of different methods (protocols) for strain characterization.

In humans, C. jejuni or C. coli diarrhea is usually self-limiting. C. jejuni and occasionally C. coli cause enteritis and as few as 500 organisms have been reported to cause illness. The disease varies from mild gastrointestinal distress that resolves within 24 hours to a fulminating or relapsing colitis. The most common symptoms of infection include diarrhoea, abdominal pain, fever, headache, nausea and vomiting. Symptoms usually start 2–5 days after infection, and last for 3–6 days. Relapses can occur in approximately 10-25% of cases.

Complications are uncommon; however, reactive arthritis, haemolytic uremic syndrome and septicaemia can occur. Rare complications include meningitis, recurrent colitis, acute cholecystitis, massive lower gastrointestinal hemorrhage, mesenteric adenitis, appendicitis.  Cases of C. jejuni-associated abortion have been reported. Immunosuppressed individuals are at a high risk for severe or recurrent infections or for septicemia.

Deaths are rare in C. jejuni infections and are seen mainly in patients with cancer or other underlying conditions (eg AIDS, chronic liver disease). The estimated case/fatality ratio for C. jejuni infections is one in 1,000. The incidence of  Guillain-Barré syndrome (GBS) per 100000 population is 0.6- 1.9; up to 5% of these patients may die and 30% or more may have residual weakness or other neurologic defects. C. jejuni infection precedes onset in 20-50% of all GBS cases.

Person-to-person transmission is unusual, but can occur if personal hygiene is poor and has been reported in nurseries and old persons homes. C. jejuni is found in the faeces and can be shed for as long as 2 to 7 weeks in untreated infections. Although humans rarely become chronic carriers, some people have excreted C. jejuni for a year or more.

There is no disease issue with chickens or the majority of livestock. Abortion in ruminants is infrequent and generates immunity against further infection.

Control measures in conventional broilers currently only involve enhanced biosecurity.  Some extreme biosecurity measures may impact on welfare. Vaccination, bacteriophages and bacteriocins have all been suggested as control measures at the farm level and research is ongoing.

GAPS: Research required on vaccination, bacteriocins and bacteriophages as control measures. Further, more information on the effect of biosecurity measures under different climatic conditions is required. 

Unlikely.

No.

The organisms are ubiquitous in animals and the environment worldwide. The disease affects humans worldwide.

Campylobacter is endemic in the developing world, and infection is usually limited to children, suggesting that a high level of exposure in early life leads to the development of protective immunity.

Sero-epidemiological studies in Europe suggest that exposure is also common in the developed countries when a person is being exposed at least once per year.

Clear seasonal patterns of infection are seen in some countries, especially in northern countries but less so in temperate and warmer geographical areas. The seasonal peak in humans usually preceeds the seasonal peak in prevalence of positive chicken flocks. Other livestock also have seasonal peaks though not necessarily at the same time. Thus the main driver of seasonality of Campylobacter remains elusive.

GAP: Understanding of the basis of seasonality in humans and chickens is required.

Outbreaks in humans are rare (less than 1% of all reported cases). In a large sentinel surveillance study in the UK, at the most 5% of cases were estimated to be associated with household outbreaks. Poultry-meat associated outbreaks can occur but tend to be due to multiple strains. However in one study at least 27% of human isolates implicated broilers as the source, and several clusters of disease were genetically and temporally matched with broiler isolates suggesting the potentials for outbreaks.

Outbreaks have been mainly attributed to contaminated water or milk as point sources. Waterborne outbreaks tend to include large numbers of cases, last a short time and are usually related to failure in chlorination (or breakdowns at water plants)

Colonisation in a broiler house is also considered as an outbreak. The rate of spread in these conditions is very rapid (about 3-5 days).

GAP: Disagreement/ different opinion about the occurrence (and size of) of outbreaks in household and/or due to poultry meat. Could be due to differences in study design, different interpretation of data, and lack of harmonisation of typing methods 

Spread to adjacent broiler houses is very rapid and common. Such spread occurs largely via human traffic (farmers etc) but might also occur through flies and fomites. 

Situation with transboundary spread is not relevant, but theoretically possible by international trade of colonized live animals.

Studies indicate relationship between prevalence of flock positivity and temperature and/or rainfall.

Most campylobacteriosis cases in humans are sporadic, peaking in the summer months. However, clear seasonal patterns of infection are identified in northern countries, but not in temperate and warmer geographical areas.

Heavy rainfalls may cause problems for water purification systems and lead to water-borne outbreaks.

The geographical variation in the timing of the seasonal peak suggests that climate may be a contributing factor to Campylobacter transmission.

Several hypotheses have been tested to explain how Campylobacter are introduced into broiler flocks. There is no evidence that vertical transmission to broilers is important. The majority of flock infections result from horizontal transmission from the environment. Campylobacter can be easily spread from bird, or other animal, to bird through a number of routes including common water sources or through contact with infected faeces. Molecular epidemiology has demonstrated the presence of strain types in the poultry farm environment (ie in puddles or cattle) before the flock becomes positive with the identical type.

Other livestock including cattle, sheep and pigs rapidly become Campylobacter positive after birth by acquiring infection from their dams. They also have maternally-derived immunity which appears to protect from disease. 

Arthropods may act as mechanical vectors for humans and livestock.

For conventionally-reared broilers major risk factors include poor biosecurity, age of birds, season, multiple species farming, multiple age birds in the flock and free-ranging at any stage, In some studies (possibly country related) flies, ‘thinning’ and source of drinking water are risk factors.

In humans, volunteer studies have shown that protective immunity to Campylobacter enteritis occurs after primary infection but is short lived and strain specific. However, the epidemiology of disease in the developing world and in occupationally-exposured individuals clearly indicates that repeated exposure results in cross-reactive immune protection.  The human humoral immune response includes the rapid induction of anti-Campylobacter IgG, IgM, and IgA antibodies in serum, as well as secretory IgA from the intestinal mucosa, directed against a number of surface antigens including flagellin and the major outer membrane protein. Proinflammatory cytokines are also induced and there is an inflammatory response to infection in the intestinal mucosa. The self-limiting nature and rapid resolution of the disease in most humans suggests that this immune response is extremely effective. It has been suggested that the immune response contributes to the disease mechanism and that diarrhoea is an immunopathological event in humans.

In chickens similar humoral and cellular immune responses occur though an inflammatory response is not seen. These responses have been well characterised. Nevertheless the colonisation is persistent suggesting that this immunity is poorly effective at eliminating the infection.

There is little known about the immune responses to colonisation in other livestock.

GAP: More research is required in this field.

There are no serological assays in routine use for the detection of colonisation of C. jejuni/C. coli in livestock. However antigen-capture enzyme-linked immunosorbent assays (ELISAs) have been described in the literature for all host species. A standardised assay has recently been described in humans for use in sero-epidemiological studies.

Sanitation and management can help prevent colonization in intensively reared poultry. The main factor is biosecurity. This needs to include house-dedicated clothing or proper use of disinfection dips. Particular focus on visitors and catchers. Species-specific farms. No domestic pets on the farm. High housing standards with concrete surrounds. Exclusion of rodents and other wild animals and wild birds and insect populations should be controlled. Chlorination of drinking water may help prevent water-borne transmission. All-in/all-out management, with decontamination of housing between flocks should be applied.

GAP: Problems with implementing all biosecurity measurements and make the farmer fully aware of the need for the strict actions.

Good hygiene and disinfection should be used to prevent spreading Campylobacter from one house to another by farmers or on fomites during an outbreak.

Two ISO (International Organization for Standardization) procedures for detection and enumeration of Campylobacter exist: a horizontal method for detection and enumeration of Campylobacter in food and animal feeding stuffs (ISO 10272 Part 1 and Part 2: 2006), and a procedure for the detection and enumeration of Campylobacter from water (ISO 17995). However, neither of these standard methods may be optimal for the isolation of campylobacters from live animals. An appendix to ISO 10272 on this topic is currently being developed.

In mammals and birds, detection of intestinal colonisation is based on the isolation of the organism from faeces, rectal swabs and/or caecal contents. Agar media containing selective antibiotics are required to isolate these bacteria from faecal/intestinal samples. Alternatively, their high motility can be exploited using filtration techniques for isolation. Enrichment techniques to detect intestinal colonisation are not routinely used. Preliminary confirmation of isolates can be made by light microscopy. Under phase-contrast microscopy the organisms have a characteristic rapid corkscrew-like motility. Phenotypic identification is based on reactions under different growth conditions. Biochemical and molecular tests can be used to confirm various Campylobacter species. Polymerase chain reaction assays also can be used for the direct detection of C. jejuni and C. coli.

There are no effective vaccines available for the prevention of enteric Campylobacter colonization in birds or mammals. However, vaccination using Salmonella as a vector for Campylobacter antigens or subunit vaccines with appropriate mucosal adjuvants are under active research.

GAP: Today there are no effective vaccines available for livestock (incl poultry).

Human cases are usually not treated with antibiotics unless patient is bacteraemic or disease develops into life threatening condition. Use of antibiotics enhances development of resistance.

Appropriate cleaning and ventilation, safe handling of litter and manure, elimination of standing water around houses, appropriate use of house dedicated clothing or boot dips. Prevention of the entrance of animals (including wild birds and insects) into poultry houses.

Not appropriate.

No preharvest tools available at present.

GAP: Today there are no effective vaccines available for livestock (incl poultry).

Surveillance is implemented in many countries and a harmonised EU baseline survey of broiler flocks and broiler carcasses was carried out in 2008. Many national surveys have been conducted on poultry flocks, as well as cattle, sheep and pigs at slaughter.

Difficult to control Campylobacter colonization in animals and birds using biosecurity alone. Nevertheless, decreasing prevalence are seen in some countries where biosecurity is implemented as part of a national action plan

Preliminary cost-benefit analysis has been undertaken in the Netherlands by the CARMA project

 http://www.card.iastate.edu/food_safety/papers/Havelaar.CARMApaper.pdf 

Only bovine genital Campylobacteriosis is a reportable disease.

No.

http://www.oie.int/index.php?id=169&L=0&htmfile=chapitre_1.11.4.htm

http://www.oie.int/fileadmin/Home/eng/Health_standards/tahm/2.04.05_BGC.pdf

http://www.oie.int/fileadmin/Home/eng/Health_standards/tahm/2.09.03_CAMPYLO.pdf

There is a significant economic impact through loss of working time as a result of infection with campylobacter.

Data available from the Netherlands CARMA project: http://www.card.iastate.edu/food_safety/papers/Havelaar.CARMApaper.pdf

Data available from the Netherlands CARMA project: http://www.card.iastate.edu/food_safety/papers/Havelaar.CARMApaper.pdf

GAP: Country specific costs.

No direct impact.

Costs of biosecurity and hygiene practices in abattoirs.

GAP: Country specific costs.

Limited indirect impact.

Nil as it is not considered of major importance in trade regulation. The OIE Terrestrial Animal Health code only refers to bovine genital campylobacteriosis. There are no trade standards for other infections.

Nil at the moment. Targets and performance objectives may be developed in the future in EU.

Nil.

• Persistence of the pathogens in animals
• Persistence of the pathogen in the environment.
• The need for strict biosecurity which is difficult to sustain
• Difficulties of putting in place effective health education campaigns for consumers to prevent household cross-contamination
• Multiple strains and molecular epidemiology poorly understood
• Lack of effective vaccines or other on-farm measures.
• EU legislation restricting use of post harvest chemical treatments

• Effective vaccines or other effective on farm measures
• Experimentally it has been shown that application of bacteriocins during the three days prior to processing reduces 5 to 6 logs of C. jejuni per gram faeces and is likely to similarly reduce the levels on the processed broiler carcasses.
• Also the use of bacteriophages may reduce the number shed by colonized birds.
• Incentives for farmers to comply with biosecurity measures (e.g. higher price for compliance with biosecurity guidelines).

Campylobacter remains the main food poisoning agent in developed countries and has a major impact in the developing countries.

Bacteriophage research may be important. Phages are naturally occurring agents that target and destroy bacteria with a high degree of efficiency, and do so selectively and specifically, without affecting beneficial bacteria or body cells. There is the possibility with new technologies to develop bacteriophages which may be effective in reducing the levels of Campylobacter in the intestines but also on food. In vivo trials have been carried out. Results showed that a quantitative reduction of the faecal Campylobacter load in chickens was possible.

Nonetheless, regulatory and technical issues (production of large amounts) need to be solved.

Expert group members are included where permission has been given

Eva Olsson Engvall - National Veterinary Institute Sweden (SVA) - [Leader]

Lieven De Zutter, University of Gent, Belgium
Diane Newell, Foodborne Zoonoses Consultancy, UK
Thomas Alter, Free University Berlin, Germany
Giacomo Migliorati, ISTITUTO GIUSEPPE CAPORALE, Italy

Project Management Board

17th September 2010

1st October 2010.