Bacterial and viral agents associated with tenosynovitis in broiler breeders in Western Australia

Abstract

SUMMARYThe pathology and infectious agents associated with several outbreaks of clinical tenosynovitis in poultry were investigated. Staphylococcus aureus were recovered from tendon tissue of from 51.9% to 97.8% of affected chickens in different outbreaks of the disease. 5. aureus were also present in the liver and heart blood and were considered to contribute to the high mortality observed following occurrence of clinical tenosynovitis in individual chickens. Bacteria otherthan S. aureus were also recovered but in a much lower proportion of chickens than was S. aureus. Adenoviruses and reoviruses were also recovered from tendon tissue of chickens with a concurrent bacterial infection. Although the pathology observed in clinically affected chickens was suggestive of a bacterial aetiology it is hypothesised that the tenosynovitis outbreaks investigated were due to an early viral infection which normally remained subclinical and that secondary infection with bacteria, particularly S. aureus, was responsible for the development of clinical signs.

Pathogenicity of four strains of staphylococci isolated from chickens with clinical tenosynovitis

“…Histological lesions in tendons, intertarsal joints and bones were seen where bacteria were isolated; no lesions were observed where the tissues were negative on culture. The lesions in tendon sheaths and tendons and in the intertarsal joints were indistinguishable from natural cases of tenosynovitis reported previously (Kibenge et al, 1982a), the tendon sheaths were thickened by hyperplastic synoviocytes and heterophilic infiltration, and there was bacterial embolism in the metaphysis and necrosis of articular cartilage of the long bones examined.…”

“…In naturally occurring tenosynovitis it has been suggested that early reovirus-induced tendon damage contributes to the colonisation of S. aureus in tendon tissue (MacKenzie and Bains, 1977;MacDonald et al, 1978;Kibenge et al, 1982a). The pathogenesis of the disease experimentally produced with S. aureus would suggest that S. aureus alone does not result in primary colonisation of tendon tissue, and supports the secondary nature of S. aureus infection following primary reovirusinduced tendon damage.…”

“…and at 48 hour intervals to quantify the number of bacteria in the blood. Chickens that died during the experiment, and all chickens still surviving 8 days p.i., were necropsied; swabs of tendon fluid, bone marrow, liver and heart blood were cultured and tissues were collected and processed for histopathological examination as previously described (Kibenge et al, 1982a).…”

“…The isolation rate of reoviruses from lesions has been low and the isolation rate of S. aureus relatively high, and the predominantly heterophilic inflammatory response observed in tendon lesions was more suggestive of a bacterial rather than viral aetiology (Kibenge et al, 1982a).…”

“…They were isolated from cases of tenosynovitis (Kibenge et al, 1982a) and phage typed as previously described (Kibenge et al, 1982b) using the basic avian phage set of Shimizu (1979). The two strains of the principal phage types were S. aureus strain 1781, phage pattern CH42/CH43/CH17/CH64A+, and S. aureus strain 1036 phage pattern CH64A+.…”