Rise in Mortality in Free-range Layer Flock17 April 2012
UK - Backyard flock health problems with a multifactorial aetiology often involved with Marek’s disease were observed in the latest AHVLA Scanning Surveillance Report dated January 2012.
A rise in mortality was investigated in a 64-week-old free-range layer flock. Postmortem examination revealed generalised carcase septicaemia with enlarged livers and spleens from which profuse growths of Erysipelothrix rhusiopathiae were isolated. In addition, cloacal pecking damage was evident, presumed to be the portal of entry for infection. Further enquiries revealed that an outdoor group of fattening pigs was located adjacent to the affected flock, separated by a wire fence, and sheep were also present on the farm, but remote from the hens.
Broilers & Broiler Breeders
Elevated broiler chick mortality was investigated in a number of flocks with the submission of 1- to 8- day-old birds. Consistent necropsy findings included septicaemia with hepatic and splenic enlargement in combination with yolk sac infection, pericarditis and occasionally septic arthritis. In the majority of these cases profuse growths of E. coli were obtained on culture of a range of affected tissues. However, in two concurrent submissions of 3-day-old chicks from the same unit, Pseudomonas aeruginosa septicaemia was diagnosed. A review of hatchery hygiene was to be undertaken. In a separate flock of 24,000 broilers, 4-day-old chicks were submitted to investigate increased chick losses and poor growth rates. Starve-out was diagnosed following postmortem examination where chick upper gastrointestinal tracts were found to be empty or containing only litter and yolk sac reserves were exhausted.
Increased mortality associated with neurological signs (torticollis) in 8-day-old chicks was attributed to Enterococcus hirae septicaemia. Necropsy findings included swollen spleens and focal areas of reddening of the midbrain on direct visual examination of sagittal brain sections. Histopathological examination revealed lesions of encephalomalacia in the midbrain, but not in the cerebellum, consistent with E. hirae associated encephalomalacia. The diagnosis was confirmed by bacteriological culture of spleens yielding heavy growths of Enterococcus species with biochemical features consistent with E. hirae, subsequently confirmed by molecular methods. This is a self-limiting condition which typically occurs in chicks between 3 and 8 days of age, often associated with transient mortality and neurological signs. However, neurological signs may not always be discernable, as demonstrated by an investigation of increased mortality in 6-day-old broiler breeder chicks. E. hirae was isolated from spleen cultures and pulmonary congestion was the main necropsy feature.
Clinical and/or production problems affecting broiler flocks in the east, north east and midland regions of England were investigated, resulting in the detection of different Infectious Bronchitis virus (IBV) variant strains by molecular methods. IBV 4/91 (793/B) was detected from one 24-day-old broiler flock showing signs of scour and wet litter. Investigation of a range of problems in 24- to 32-day-old broiler flocks, including diarrhoea, wet litter, reduced feed intake and growth rates, lameness, mortality and airsacculitis resulted in the detection of European QX-like IBV strains. An increased number of 50-dayold broiler carcase condemnations at processing were also associated with European QX-like IBV infection.
Necrotic enteritis was diagnosed in a flock of 24-day-old broilers. At necropsy, liver lobe discolouration and large areas of mucosal necrosis of the mid small intestine and sloughed debris were seen. Wet smear examination of intestinal scrapings revealed numerous coccidial oocysts. Histopathological examination of mid gut revealed widespread, acute mucosal necrosis and coccidial forms consistent with Eimeria maxima. Mucosal damage induced by coccidial infection is considered a predisposing factor in the development of necrotic enteritis which is associated with Clostridium perfringens.
Cardiohepatic syndrome was diagnosed in a 24-day-old turkey from a 300-bird flock. Necropsy findings included marked dilation and enlargement of the heart with a shrunken and firm liver. Typically in commercial flocks, incidence peaks at two weeks of age and disappears at three weeks. Rapid early growth and environmental conditions are thought to be predisposing factors.
Backyard flock health problems with a multifactorial aetiology were commonly diagnosed, often involving Marek’s disease and other infections. Clinical presentations varied from ill-thrift, mortality (with up to 50 per cent losses over eight weeks reported in one flock of 45 birds), to signs indicative of the classical form of Marek’s, including progressive wing paresis. At necropsy, peripheral nerve enlargement was seen in such birds with histopathological findings of pleomorphic lymphocytic nerve infiltrations confirming the diagnosis. In one flock of 35 chickens, six birds had died. Necropsy of one casualty revealed multifocal, white infiltrative lesions of the liver and spleen, which were also enlarged, and diffuse thickening of the small intestine. Marek’s disease was confirmed following histopathology with concurrent coccidiosis and splenitis associated with Listeria monocytogenes infection. Listeriosis is uncommon in poultry, but disease is often associated with other risk factors including immunosuppression and concurrent infections. Both conditions were considered to be secondary to the debility and immunosuppression associated with Marek’s disease. In some other backyard flocks infections including coccidiosis, Brachyspira intermedia, endoparasitism and red mite (Dermanyssus gallinae) were diagnosed concurrently with Marek’s disease.
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