No description available.

Inherited rickets of Corriedale sheep is a newly discovered skeletal disease of sheep with simple autosomal recessive inheritance. The clinical signs resemble rickets in other species and include decreased growth rate, thoracic lordosis and angular limb deformities. Radiographic features include physeal thickening, blurred metaphyseal trabeculae and thickened porous cortices. Computed tomography scanning of long bones reveals increased bone mineral content and cortical area, but decreased bone mineral density. Gross lesions include segmental thickening of physes, growth arrest lines, collapse of subchondral bone of the humeral head, thickened cortices and enthesophytes around distal limb joints. Microscopically there is persistence of hypertrophic chondrocytes at sites of endochondral ossification, inappropriate and excessive osteoclastic resorption, microfractures and wide, unmineralised osteoid seams lining trabeculae and filling secondary osteons. Affected sheep are persistently hypophosphataemic and hypocalcaemic. Normal serum 25-hydroxyvitamin D3 concentration accompanied by a two-fold elevation in 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) suggested a defect in endorgan responsiveness to vitamin D as a likely mechanism, but this was not supported by in vitro studies using cultured skin fibroblasts. These studies revealed normal vitamin D receptor function and the presence of 24- hydroxylase mRNA in cells from affected sheep, even without induction by 1,25(OH)2D3. Inappropriate overexpression of 25-hydroxyvitamin D3-24- hydroxylase, the enzyme that breaks down active vitamin D, is therefore considered the probable cause of inherited rickets in Corriedale sheep. Such a mechanism has not previously been described as a cause of inherited rickets in humans or other animal species. Treatment of affected sheep with high oral doses of vitamin D3 weekly for 3 months showed a trend towards increased bone mineral density, thus supporting an intact vitamin D receptor. Preliminary studies on immune function revealed reduced numbers of CD4+ and CD8+ lymphocytes and reduced interferon-? production by lymphocytes stimulated with parasite antigen. This new form of inherited rickets may be widespread in

No description available.

Chondrodysplasia of Texel sheep is a newly described recessively inherited disorder distinct from other chondrodysplasias described in sheep. Phenotypically normal at birth, affected lambs develop microscopic lesions as early as 9 days of age, and usually demonstrate gross deformities and markedly reduced rates of bone growth by 2 to 3 weeks. Individual bone growth rates are most severely affected in the proximal bones of the forelimbs. Chondrodysplastic lambs typically have short stature, angular limb deformities, a barrel-shaped chest and a wide-based stance. Gross lesions include tracheal narrowing and contortion, enlarged costochondral junctions, and erosion of articular cartilage in major limb joints. Microscopic lesions are confined to hyaline cartilage, and are characterised by degeneration of the interterritorial matrix and dense perichondrocytic rings consisting predominantly of type VI collagen. These lesions are identical in appearance to those in achondrogenesis 1b and diastrophic dysplasia, two diseases caused by defects of the diastrophic dysplasia sulphate transporter (DTDST) in human beings. An investigation to measure the uptake of radiolabelled sulphate by dermal fibroblasts in vitro did not provide evidence of a defect in the DTDST in chondrodysplastic Texel sheep. A linkage disequilibrium study of ovine chromosomes 1, 5, 6, 13 and 22 using microsatellite DNA markers was unable to identify evidence of a mutation causing this form of chondrodysplasia. Capillary electrophoresis of unsaturated chondroitin sulphate disaccharides demonstrated a relative reduction in the ratio of chondroitin 4-sulphate to chondroitin 6-sulphate in affected animals of all ages. This biochemical feature enables the potential determination of the phenotype of newborn lambs prior to the emergence of gross or microscopic lesions. The pathology of the disease, combined with the findings of the genetic, biochemical and in vitro studies, suggest that a mutation may be present in the CHST11 gene. This gene is a good candidate for future studies aimed at discovering the genetic defect in chondrodysplasia of Texel sheep and developing a test to identify heterozygous animals.

Chondrodysplasia of Texel sheep is a newly described recessively inherited disorder distinct from other chondrodysplasias described in sheep. Phenotypically normal at birth, affected lambs develop microscopic lesions as early as 9 days of age, and usually demonstrate gross deformities and markedly reduced rates of bone growth by 2 to 3 weeks. Individual bone growth rates are most severely affected in the proximal bones of the forelimbs. Chondrodysplastic lambs typically have short stature, angular limb deformities, a barrel-shaped chest and a wide-based stance. Gross lesions include tracheal narrowing and contortion, enlarged costochondral junctions, and erosion of articular cartilage in major limb joints. Microscopic lesions are confined to hyaline cartilage, and are characterised by degeneration of the interterritorial matrix and dense perichondrocytic rings consisting predominantly of type VI collagen. These lesions are identical in appearance to those in achondrogenesis 1b and diastrophic dysplasia, two diseases caused by defects of the diastrophic dysplasia sulphate transporter (DTDST) in human beings. An investigation to measure the uptake of radiolabelled sulphate by dermal fibroblasts in vitro did not provide evidence of a defect in the DTDST in chondrodysplastic Texel sheep. A linkage disequilibrium study of ovine chromosomes 1, 5, 6, 13 and 22 using microsatellite DNA markers was unable to identify evidence of a mutation causing this form of chondrodysplasia. Capillary electrophoresis of unsaturated chondroitin sulphate disaccharides demonstrated a relative reduction in the ratio of chondroitin 4-sulphate to chondroitin 6-sulphate in affected animals of all ages. This biochemical feature enables the potential determination of the phenotype of newborn lambs prior to the emergence of gross or microscopic lesions. The pathology of the disease, combined with the findings of the genetic, biochemical and in vitro studies, suggest that a mutation may be present in the CHST11 gene. This gene is a good candidate for future studies aimed at discovering the genetic defect in chondrodysplasia of Texel sheep and developing a test to identify heterozygous animals.

Chondrodysplasia of Texel sheep is a newly described recessively inherited disorder distinct from other chondrodysplasias described in sheep. Phenotypically normal at birth, affected lambs develop microscopic lesions as early as 9 days of age, and usually demonstrate gross deformities and markedly reduced rates of bone growth by 2 to 3 weeks. Individual bone growth rates are most severely affected in the proximal bones of the forelimbs. Chondrodysplastic lambs typically have short stature, angular limb deformities, a barrel-shaped chest and a wide-based stance. Gross lesions include tracheal narrowing and contortion, enlarged costochondral junctions, and erosion of articular cartilage in major limb joints. Microscopic lesions are confined to hyaline cartilage, and are characterised by degeneration of the interterritorial matrix and dense perichondrocytic rings consisting predominantly of type VI collagen. These lesions are identical in appearance to those in achondrogenesis 1b and diastrophic dysplasia, two diseases caused by defects of the diastrophic dysplasia sulphate transporter (DTDST) in human beings. An investigation to measure the uptake of radiolabelled sulphate by dermal fibroblasts in vitro did not provide evidence of a defect in the DTDST in chondrodysplastic Texel sheep. A linkage disequilibrium study of ovine chromosomes 1, 5, 6, 13 and 22 using microsatellite DNA markers was unable to identify evidence of a mutation causing this form of chondrodysplasia. Capillary electrophoresis of unsaturated chondroitin sulphate disaccharides demonstrated a relative reduction in the ratio of chondroitin 4-sulphate to chondroitin 6-sulphate in affected animals of all ages. This biochemical feature enables the potential determination of the phenotype of newborn lambs prior to the emergence of gross or microscopic lesions. The pathology of the disease, combined with the findings of the genetic, biochemical and in vitro studies, suggest that a mutation may be present in the CHST11 gene. This gene is a good candidate for future studies aimed at discovering the genetic defect in chondrodysplasia of Texel sheep and developing a test to identify heterozygous animals.

Causes of morbidity and mortality were investigated for 108 green turtles (Chelonia mydas) stranded in south-east Queensland between 1990 and 1996. This study was undertaken as part of a broader carcass salvage program for south Queensland, and within the context of a population study of C. mydas in the Moreton Bay feeding ground. Accurate pathological characterisation of disease in C. mydas was achieved by detailed necropsy and histological examination. Varied inflammatory responses and degenerative changes were observed in stranded C. mydas. Supportive disciplines of microbiology, parasitology, and clinical chemistry were used to elucidate aetiology and pathogenesis of selected conditions. Heavy metal and pesticide levels were assessed in a sub-sample of turtles. Direct anthropogenic causes (including trauma, foreign body ingestion and drowning) accounted for 34% of mortalities of C. mydas in this study. The majority of the trauma cases were turtles with skull fractures resulting from blunt impacts. The remainder had boat propeller injuries, or miscellaneous trauma. Almost half of the turtles with lethal boat propeller damage had evidence of pre-existing disease which may well have predisposed them to boat strike, emphasising the importance of full necropsy examination, even when the cause of death appears obvious. Fishing line was the only ingested foreign body consistently implicated in the production of fatal intestinal obstruction. Marine turtle fibropapillomatosis, a panzootic viral disease which is considered to involve some indirect anthropogenic factors, accounted for 7% of mortalities. The findings in this study were consistent with much of the previously described pathology of this condition. Naturally-occurring diseases (for which human influences are unknown) accounted for the remaining 59% of strandings. Coccidiosis, caused by Caryospora cheloniae, was recorded for the first time in wild C. mydas. It occurred both as an epizootic (in 1991) and as sporadic cases. A variety of manifestations, including disseminated and enteric forms, were recognised. Infection with a Cryptosporidium-like protozoan appeared to occur concurrently with coccidiosis in one turtle in this study. Attempts to establish experimental coccidial infections in hatchling C. mydas were unsuccessful. Infections with cardiovascular (spirorchid) flukes were almost universal in stranded C. mydas in this study. They ranged from mild, incidental findings (such as occasional fluke vii egg granulomas evident microscopically in otherwise normal tissues) to a variety of severe changes, including thrombosis, which were likely to have produced morbidity. The present study clarified the range of cardiovascular lesions associated with spirorchidiasis, including the sequence of thrombus resolution and exteriorisation from vessels. In some cases spirorchid vasculitis was associated with fatal disseminated bacterial infections. Other sporadic, naturally-occurring diseases included mycotic pneumonia, bacterial meningoencephalitis and a miscellany of gastrointestinal conditions, including chronic intestinal tympany and obstipation, for which the underlying cause could not always be determined. Evidence indicated that gastrointestinal motility in C. mydas was prone to both direct and indirect disturbance and that tympany and obstipation could be final common outcomes of a range of insults. Eighteen abnormally buoyant turtles were examined during this study. The cause could usually be ascribed to an underlying disease, including (in decreasing order of frequency) trapped internal gas, usually intestinal; neurological disease such as traumatic brain injuries; and pulmonary disease. In two cases, no underlying cause was detected. Trace metal (arsenic, cadmium, mercury, selenium and zinc) concentrations were determined in the livers and kidneys of 50 turtles of mixed species (mostly C. mydas). These results were considered to provide baseline data for sea turtles in SE Qld. This study offered the largest dataset available for some metals in C. mydas, and provided evidence of high background levels of cadmium as a normal feature for the species. Some unusual age–related trends in metal accumulation were detected. Concentrations of cadmium, zinc and selenium in the kidney decreased with increasing age, whereas zinc concentrations in the liver tended to increase. Determining the impact of disease on wildlife populations is an increasingly necessary task, which will require multidisciplinary teams. Necropsy surveys like the present study are an essential component of the growing field of conservation medicine. In addition to providing data relevant to management, such as the relative proportions of anthropogenic and naturally-occurring mortalities, necropsy surveys can identify a range of endemic pathogens, and help to collect prevalence data for determining disease impacts at the population level.