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Identify critical points for infection of live birds or contamination of poultry carcases with campylobacter & salmonella

Project Code: B03008

30/11/2002

Food Microbiology Collaborating Unit, Health Protection Agency, School of Clinical Veterinary Science,University of Bristol
Bull, S ;
Division of Farm Animal Science, Department of Clinical Veterinary Science, University of Bristol,
Allen, V; Corry, J;
Health Protection Agency
Jorgensen, F;
University of Bristol
Humphrey, T

A consortium of scientists from the Public Health Laboratory Service (now Health Protection Agency), the University of Bristol and the Silsoe Research Institute undertook this Food Standards Agency-funded project. It began 1/11/1999 and expired 31/12/2002. The research consortium worked closely with the UK poultry industry, particularly in England, and the cooperation of these companies and the help received from many staff members is gratefully acknowledged. Many thousands of samples were examined and a large body of data was produced. The following are key outputs from the project:

Salmonella spp. was occasionally isolated from the farm environment but was only very rarely found in chickens, even though many thousands of samples were tested.
Thinning, where a proportion of birds were removed at 33-35 days, appears to be a risk factor for the introduction of Campylobacter spp to the remaining birds in the flock.
A farm questionnaire, together with a survey of Campylobacter colonisation rates at slaughter, suggested that, rearing broilers alongside other farm animals, disposing broiler carcases by composting and evidence of rodents were risk factors for the introduction of Campylobacter spp.
The use of dedicated footwear in each house and the use of chlorine dioxide in drinking water appeared to protect against Campylobacter colonisation.
Campylobacter spp. was isolated from air in and around broiler houses but only after a flock was colonised. Isolation was also possible from the air in processing plants even during the processing of negative flocks.
When Campylobacter-negative flocks followed positive ones in the processing plant, carcases became contaminated although, in general, the prevalence was low, as were the numbers of these bacteria on the carcases.
In general, processing did not significantly affect the numbers of Campylobacter on carcases. Some reduction was seen, however, after the chilling process.
There were clear differences between farms in terms of their ability to produce Campylobacter-negative housed flocks and a cohort of farms with only low colonisation levels was identified.
Significant differences in chicken health (i.e. differences in flock performance measures such as hock- and pad burns and reject levels at slaughter) were identified between two farms. The farm, which achieved higher flock performance scores, was also significantly less likely to rear flocks which were colonised with campylobacters at slaughter. Further studies are needed to examine whether there could be a causal link between the two.
Although this study was not designed to determine the prevalence of Campylobacter-positive flocks in the UK, 50 of 97 randomly selected housed broiler flocks from one company examined between February and June 2002 were Campylobacter-positive.
Campylobacter were not always isolated from all the birds examined in a Campylobacter-positive flock and of 72 positive housed flocks, where 10-60 individual caeca were examined, Campylobacter was only isolated from ≤ 30 % of the caeca in 16 of the flocks.
While this project focused on housed broilers, routine monitoring of flocks between February and June 2002 indicated that 105 of 109 non-housed flocks were colonised with Campylobacter at slaughter.
There was no significant difference in the number of Campylobacter cells in caeca collected from housed and non-housed birds (log10 cfu per g caeca were 6.3 (SD = 1.8) and 6.5 (SD = 1.1) for housed and non-housed birds, respectively).

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