Bacterial chondronecrosis with osteomyelitis ('femoral head necrosis') of broiler chickens: a review
- PMID: 19184815
- DOI: 10.1080/03079450050118386
Bacterial chondronecrosis with osteomyelitis ('femoral head necrosis') of broiler chickens: a review
Abstract
Bacterial chondronecrosis with osteomyelitis (BCO) in chickens was first reported in 1972 and is now recognized as an important cause of lameness in broiler chickens. Recent systematic studies of causes of lameness in birds reared in Northern Ireland have shown that it was the most common cause of lameness, being present in 17.3% of lame birds. Furthermore, it was also detected in birds presented as ''found dead''. Overall losses in male birds due to BCO were estimated to be 0.75% of all birds placed, which, in addition to welfare concerns, represents considerable economic loss. The disease has been seen in birds ranging from 14 to 70 days of age, but most cases occurred around 35 days old. It is most commonly caused by Staphylococcus aureus, but Escherichia coli, coagulase-negative staphylococci and Enterococcus spp. are sometimes involved, as are, rarely, other bacteria. The lesions are most commonly found associated with the growth plates of long bones, particularly the proximal growth plate of the femur and tibiotarsus, but other bones may also be affected. Since lesions were visible to the naked eye in only 40 to 67% of cases, histological examination is recommended where no lesions are visible macroscopically. As the lesion may be present in only one growth plate, and because histological examination is often not carried out, BCO is almost certainly underdiagnosed. The exact pathogenesis of the condition is unknown, but it is thought that adherence of blood-borne bacteria to exposed cartilage at the tips of metaphyseal blood vessels is fundamental. Under controlled experimental conditions, infection of birds with the immunosuppressive viruses chicken anaemia virus and infectious bursal disease virus increased the incidence of the disease, while restricting feed intake reduced the incidence of disease. S. aureus strains identical to, or closely related to, isolates recovered from naturally occurring cases of the disease (as determined by pulsed-field gel electrophoresis) have been recovered from fluff-debris in hatcheries, and also from the environment of breeding flocks, indicating that infection in the breeding farm and in the hatchery could be an important source of infection. It has also been shown that humans can carry poultry strains of S. aureus on their hands. There is a higher incidence of BCO in birds hatched from floor eggs. Thus, hygiene and management practice on breeder farms and in the hatchery may influence the occurrence of the disease. Bacteraemia is a prerequisite for BCO. Indeed, in some flocks suffering losses due to BCO, there are also losses due to staphylococcal septicaemia. Thus, appropriate treatment of affected flocks should reduce losses due to septicaemia. It should also reduce the occurrence of bacteraemia and the development of further cases of BCO. However, birds in which BCO has already developed, are unlikely to respond to treatment. Control of BCO by vaccination seems unlikely in the short term. Simple bacterins have not been effective and much basic research is needed to identify the important virulence factors. Furthermore, more than one type of bacterium is capable of causing the disease. Bacterial interference has been used successfully in humans and turkeys to prevent staphylococcal diseases, and warrants investigation for the prevention of BCO in chickens. This may have an advantage in that the interfering bacterium may also exclude some of the other bacteria that can cause BCO. The recent development of a disease model in which S. aureus is given by a natural route allows the potential for further investigation of the role of predisposing factors, and intervention strategies, including vaccination and bacterial interference, for the prevention of BCO.
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