The pathologies in proximal femora of broilers with lameness attributed to disorders of the proximal femur, including so-called 'femoral head necrosis', are described. Samples were collected from a variety of flocks, farms and production systems. Ten 'normal' broilers were also examined. Birds were identified by a characteristic lameness whereby they used a wing for support during locomotion and hip flexion (i.e. whilst sitting down). The appearance of the proximal femora at post mortem was used to place 67 proximal femora in three categories: (a) gross disintegration of the epiphysis, physis and/or metaphysis (43 samples); (b) epiphysiolysis-separation of the cartilaginous epiphysis from the underlying femoral metaphysis (growth plate) (17 samples) and (c) apparently normal (seven samples). Samples from each category were collected for mycoplasmology, virology and bacteriology. All the samples were negative for Mycoplasma, and there was no correlation between pathology and the presence or absence of viruses, but bacteria were cultured from about half the proximal femora and most of these femora showed histological evidence of bacterial infection. Although bacterial culture was negative, evidence of bacterial infections was seen in tissue sections from a further 15 proximal femora. Serial sections were required to find the foci on bacterial lesions. 'Femoral head necrosis' was not considered appropriate to describe the pathologies seen and the term proximal femoral degeneration (PFD) was adopted. Histological examination showed that PFD was most frequently due to a bacterial chondritis and osteomyelitis, with frequent involvement of surrounding tissues. Non-lame controls all had non-bacterial pathologies in the proximal femur which were also seen in many of the lame birds and may have provided a foci for the establishment of bacterial infections. The non-bacterial pathologies when severe were considered the cause of non-infectious PFD which would cause lameness in some cases. Epiphysiolysis was either a post or peri-mortem artefact, traumatic in origin, or could be attributed to underlying growth plate (physeal) pathology which in some cases was due to bacterial infection.

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SUMMARYThe efficacy of Lixiscope examination in detecting tibial dyschondroplasia (TD) is assessed utilising a thorough post-mortem examination with good histological backup. Forty-seven per cent more broilers had TD at post-mortem examination than when examined solely by Lixiscope. TD lesions detected by Lixiscope examination had a mean score greater than 3. The additional lesions detected at post-mortem examination usually had a score of 1. This indicates that the Lixiscope examination failed to detect small lesions. The prevalence of dyschondroplastic lesions in the proximal tarsometatarsi indicates that this site may be of value to score in addition to the proximal tibiotarsus and use in selection. Disruption of the proliferative zone within some dyschondroplastic growth plates indicated that in a proportion of broilers there is a link between TD and rickets. The Lixiscope is an effective tool for detecting large TD lesions, but fails to detect smaller lesions. To minimize the susceptibility of genetic lines of broilers to TD it may be necessary to use progeny testing.

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1. Large White male turkeys from a heavy commercial male-line were fed 16 diets containing 4 concentrations of calcium (6, 10, 14 and 18 g/kg) and available phosphorus (3, 5, 7 and 9 g/kg) in a 4 x 4 factorial experiment. There were three replicates (pens) of each treatment and the skeletal health, morphology and mineral status of 4 turkeys from each pen were assessed at 7, 10 and 13 weeks of age. 2. The prevalence of tibial dyschondroplasia increased after 7 weeks of age and was present in 50 and 71% of turkeys respectively at 10 and 13 weeks. The lesion was localised in the caudal aspect of the proximal tibiae. Dietary calcium and available phosphorus did not affect the prevalence of the lesion except in turkeys on the diet containing 6 g calcium/kg, where body weight and the incidence of tibial dyschondroplasia were low. 3. Histological investigation showed no evidence of rachitic changes. 4. Low dietary calcium was associated with lower tibial plateau angles at 10 and 13 weeks of age. Tibial torsion and the angle of rotation were not affected by dietary treatments or age. Tibial torsion and the angle of rotation were not affected by dietary treatments or age. 5. Increasing dietary calcium increased tibial radiodensity, cortical density and the widths of the cortex and proximal tibiotarsus. Radiodensities increased to 10 weeks and were significantly lower at 13 weeks of age. 6. Bone ash, calcium and phosphorus declined with age, particularly between 10 and 13 weeks, whereas bone calcium: phosphorus ratios were not affected by dietary treatment or age. 7. Dietary calcium was positively associated with blood calcium and calcium ion concentrations and was without effect on blood phosphorus. Available phosphorus was associated positively with increased blood phosphorus and lower calcium ion concentrations but had no effect on total calcium. Alkaline phosphatase activity was low at high concentrations of dietary calcium with low available phosphorus and there was higher activity on diets containing low calcium and high available phosphorus.