The major causes of leg weakness/lameness were investigated in two male commercial broiler flocks. The numbers of dead and lame birds culled from the flocks each day were recorded by the flock managers. Forty-four lame birds and 22 sound birds were examined postmortem during a period of six weeks and the proximal and distal end of each femur, tibiotarsus and tarsometatarsus were examined histologically. Attempts were made to isolate bacteria and viruses from the proximal end of each femur. Blood samples were examined for antibodies to chicken anaemia virus (CAV), infectious bursal disease virus (IBDV) and Mycoplasma species. Bacterial chondronecrosis with osteomyelitis was identified in the proximal end of the femur of eight of the 44 lame birds, and in the proximal end of the tibiotarsus of a further bird (20.4 per cent). Gram-positive bacteria were present in all the lesions. Staphylococcus aureus was recovered from 62.5 per cent of the lesions confirmed by histology. Bacterial chondronecrosis associated with S aureus has thus been identified as an important cause of leg weakness in these commercial broilers. Lesions suggestive of the condition were visible macroscopically in only 11.1 per cent of the cases subsequently diagnosed by histology and bone histology is therefore required before a diagnosis can be excluded. Angular limb deformities (13.6 per cent) and spondylolisthesis (11.4 per cent) were the most common macroscopic lesions identified as causes of lameness. The overall incidence of tibial dyschondroplasia was similar in both the lame and sound broilers, but severe lesions were found only in lame birds (4.5 per cent).

No abstract

No abstract

Amplification of avian paramyxovirus serotype 1 (APMV-1)-specific nucleic acid fragments, followed by restriction endonuclease analysis (REA) using BglI, was carried out to type strains according to their virulence. Primer sequences were used to amplify a 202 base pair fragment, encompassing the fusion protein cleavage site, in a one-step reverse transcriptase-polymerase chain reaction (RT-PCR) test for detection of a range of field cases and reference strains of APMV-1. Subsequent REA of the amplified fragments enabled differentiation of low virulent lentogenic field and vaccine strains from more virulent mesogenic and velogenic field strains of APMV-1, including pigeon PMV-1. In the present paper, we report the development and application of a one-step RT-PCR test coupled with REA as a fast, specific method for both the detection and typing of APMV-1 from field samples.

Abstract. Thousands of harbor seals (Phoca vitulina) died in European seas during 1988. Respiratory distress and oculonasal discharge were common clinical signs. We necropsied 76 affected seals. The main necropsy finding was severe pneumonia. Microscopic lung changes were characterized by proliferation of type I1 pneumocytes, filling of alveolar lumina with serofibrinous exudate, leukocytes, and macrophages, and necrosis of bronchial and bronchiolar epithelium. Intracytoplasmic and intranuclear acidophilic inclusion bodies characteristic of morbillivirus infection were seen in bronchial and bronchiolar epithelial cells. Microscopic lesions of non-suppurative demyelinating encephalitis were seen in the brain. There was degeneration and necrosis of neurons, focal gliosis, perivascular cuffing, and patchy demyelination. Many neurons and astrocytes contained intracytoplasmic and intranuclear inclusions. Using an immunoperoxidase technique, we detected morbillivirus antigen in many tissues including lung, brain, spleen, and urinary bladder. The origin of the seal morbillivirus is unknown.A major disease epizootic killed thousands of harbor seals (Phoca vitulina) in European seas during 1988.The first signs were abortion and death in seals along the western coast of Denmark in April 1988. By late June the disease had spread to the coasts of The Netherlands and southern Norway. The most consistent pathologic finding in affected animals was acute pneumonia. A herpesvirus and a picornavirus were initially implicated as primary causes of the disease.*' Subsequently, it was shown that the epizootic was unrelated to these viruses, but serologic examination of convalescent seals indicated rising antibody titers to canine distemper or a closely related morbillivirus.22 In August 1988 seals in the Irish Sea became affected. We found lesions similar to canine distemper in many of these animals." The purpose of this report is to document histopathologic and immunocytochemical changes in affected seals. Materials and MethodsMeasles antiserum from a human with subacute sclerosing panencephalitis was used as primary antibody. Biotinylated goat anti-human immunoglobulin-G (IgG) (Bethesda Research Laboratories, Inc., Gaithersburg, MD) was used as second layer antibody. The other reagents used in this technique were part of a commercially available SAB kit (Histostain-SPO Kit, Zymed Laboratories, Inc., South San Francisco, CA). Reagents included in this kit were normal goat serum and streptavidin-peroxidase conjugate. All steps, unless indicated otherwise, were done at room temperature in a dark humidified chamber. Fresh Tris-saline buffer, pH 7.6, was used for each washing step.Sections were cut at 5 Fm and placed on clean glass slides coated with 3-aminopropyltriethoxysilane as a section adhesive, deparaffinized in xylene, and placed in alcohol. Endogenous peroxidase was inhibited by transferring sections to a freshly prepared solution of 0.5% hydrogen peroxide in methanol for 30 min. After washing in tap water, sections were placed...