There is a recent trend to feed pet dogs and cats in Britain and other developed countries on raw meat and animal by‐products using either commercial preparations or home recipes. This shift from heat‐treated processed food has been driven by perceived health benefits to pets and a suspicion of industrially produced pet food. The diets of wild‐living related species have been used as a rationale for raw feeding, but differences in biology and lifestyle impose limitations on such comparisons. Formal evidence does exist for claims by raw‐feeding proponents of an altered intestinal microbiome and (subjectively) improved stool quality. However, there is currently neither robust evidence nor identified plausible mechanisms for many of the wide range of other claimed benefits. There are documented risks associated with raw feeding, principally malnutrition (inexpert formulation and testing of diets) and infection affecting pets and/or household members. Surveys in Europe and North America have consistently found Salmonella species in a proportion of samples, typically of fresh‐frozen commercial diets. Another emerging issue concerns the risk of introducing antimicrobial‐resistant bacteria. Raw pet food commonly exceeds hygiene thresholds for counts of Enterobacteriaceae. These bacteria often encode resistance to critically important antibiotics such as extended‐spectrum cephalosporins, and raw‐fed pets create an elevated risk of shedding such resistant bacteria. Other infectious organisms that may be of concern include Listeria, shiga toxigenic E scherichia coli , parasites such as Toxoplasma gondii and exotic agents such as the zoonotic livestock pathogen Brucella suis, recently identified in European Union and UK raw pet meat imported from Argentina.
During 2007-2009 a UK-wide, 3-year stratified randomized survey of UK chicken broiler flocks was conducted to estimate the prevalence of Campylobacter-infected batches of birds at slaughter. Thirty-seven abattoirs, processing 88·3% of the total UK slaughter throughput, were recruited at the beginning of the survey. Of the 1174 slaughter batches sampled, 79·2% were found to be colonized with Campylobacter, the majority of isolates being C. jejuni. Previous partial depopulation of the flock [odds ratio (OR) 5·21], slaughter in the summer months (categorized as June, July and August; OR 14·27) or autumn months (categorized as September, October and November; OR 1·70) increasing bird age (40-41 days, OR 3·18; 42-45 days, OR 3·56; ⩾46 days, OR 13·43) and higher recent mortality level in the flock (1·00-1·49% mortality, OR 1·57; ⩾1·49% mortality, OR 2·74) were all identified as significant risk factors for Campylobacter colonization of the birds at slaughter. Time in transit to the slaughterhouse of more than 2·5 h was identified as a protective factor (OR 0·52).
SUMMARYAs part of further investigations into three linked haemorrhagic fever with renal syndrome (HFRS) cases in Wales and England, 21 rats from a breeding colony in Cherwell, and three rats from a household in Cheltenham were screened for hantavirus. Hantavirus RNA was detected in either the lungs and/or kidney of 17/21 (81%) of the Cherwell rats tested, higher than previously detected by blood testing alone (7/21, 33%), and in the kidneys of all three Cheltenham rats. The partial L gene sequences obtained from 10 of the Cherwell rats and the three Cheltenham rats were identical to each other and the previously reported UK Cherwell strain. Seoul hantavirus (SEOV) RNA was detected in the heart, kidney, lung, salivary gland and spleen (but not in the liver) of an individual rat from the Cherwell colony suspected of being the source of SEOV. Serum from 20/20 of the Cherwell rats and two associated HFRS cases had high levels of SEOV-specific antibodies (by virus neutralisation). The high prevalence of SEOV in both sites and the moderately severe disease in the pet rat owners suggest that SEOV in pet rats poses a greater public health risk than previously considered.
A baseline survey on the prevalence of Campylobacter spp. in broiler flocks and Campylobacter spp. on broiler carcases in the UK was performed in 2008 in accordance with Commission Decision 2007/516/EC. Pooled caecal contents from each randomly selected slaughter batch, and neck and breast skin from a single carcase were examined for Campylobacter spp. The prevalence of Campylobacter in the caeca of broiler batches was 75·8% (303/400) compared to 87·3% (349/400) on broiler carcases. Overall, 27·3% of the carcases were found to be highly contaminated with Campylobacter (≥1000 c.f.u./g). Slaughter in the summer months (June, July, August) [odds ratio (OR) 3·50], previous partial depopulation of the flock (OR 3·37), and an increased mortality at 14 days (≥1·25% to <1·75%) (OR 2·54) were identified as significant risk factors for the most heavily Campylobacter-contaminated carcases. Four poultry companies and farm location were also found to be significantly associated with highly contaminated carcases.
Background: Mycoplasma agalactiae is the main cause of contagious agalactia, a serious disease of sheep and goats, which has major clinical and economic impacts. Previous studies of M. agalactiae have shown it to be unusually homogeneous and there are currently no available epidemiological techniques which enable a high degree of strain differentiation.
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