Now researchers are asking whether a similar strategy can help to reduce the incidence of Campylobacter.

Professor Diane Newell from the Foodborne Zoonoses Consultancy told the recent British Poultry Council seminar Poultry Counts – Beating the Bugs in London, that the bacteria of both Salmonella and Campylobacter families effectively colonise the intestinal tract of chickens.

However, she said that they are not normal chicken gut flora but both can colonise to similar levels from doses as low as 10 cfu (colony forming units) with similar kinetics.

She added that both survive processing and contaminate poultry meat to cause human infection.

"What we did for Salmonella has succeeded and it is going down but Campylobacter is going up," Professor Newell said.

She added that to date the scientific approaches adopted have largely assumed that because the control of Salmonella in chicken has been successful then the same strategies should work for Campylobacter.

In the UK, by the time the birds come to slaughter, between 45 per cent and 90 per cent of the flocks have been colonised by Campylobacter although more accurate data is expected later this year.

Colonisation in flocks generally occurs between two to three weeks of age mainly in the mucous of the small intestine and caecum.

Professor Newell said that it is a huge level of colonisation – around 10⁹ cfu and it is a colonisation for the life of the bird.

"Once the broiler has become infected, it is going to stay at that level until slaughter," she said.

Faecal contamination of the carcass can occur during processing and although the organisms do not grow after the chicken has been slaughtered, they survive through to retail.

Because the organism survives processing, it can easily cross-contaminate other foods and a single drop of fluid can contain around 10⁶ cfu. It takes just 10³ cfu to be infectious to humans.

However, she said that it is not necessary to eradicate all the campylobacter to get a good reduction in risk. Quantitative risk assessment models show that a two log reduction of Campylobacter in carcasses could reduce the incidence of campylobacteriosis by up to 30 times.

Professor Newell showed that there are several ways to intervene to attempt to reduce the prevalence of Campylobacter.

Attempts can be made to prevent the flocks becoming colonised in the first place but this would mean identifying and eliminating the many sources of Campylobacter and there are concerns whether wholly effective interventions can be found.

While this was an effective method for Salmonella, as Campylobacter is all around the farm, it becomes far more difficult to control. It does not live in dry conditions and on bedding and feed but it is recoverable from many sites on the farm – soil, water, farmers, vehicles, wild birds, pets and other livestock.

Identifying on-farm sources requires strain tracking but Professor Newell said part of the problem is that unlike Salmonella, Campylobacter is unstable and the genome of the bacteria can change.

"Humans and equipment appear to be the main transmission vehicles into the house and the risk is probably related to the environmental load and is seasonal," Professor Newell said.

Another method to reduce the risk could be to reduce the number of colonised birds in each flock, but once the first bird is colonised, the spread is very rapid and uncontainable except by slaughter. One other method would be to introduce early slaughter to reduce the risk.

Professor Newell said that none of the actions taken against Salmonella appears to have affected Campylobacter prevalence in the flocks.

However, improved biosecurity can reduce flock prevalence by 50 per cent but the colonisation can be reduced further through interventions such as bacteriophages and vaccination. And finally, the risk can be reduced by decontamination of the carcasses following slaughter.

Professor Newell concluded that before further action can be taken, the present steps being undertaken by the Department of Environment Food and Rural Affairs in the UK to monitor and count incidence needs to be carried out.

"We know a lot – but still not enough – about the interaction between Campylobacter, its chicken host and their joint environment to develop appropriate and effective intervention strategies," Professor Newell concluded.