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Author: search.filters.author.Hunt, HayleyHas files: Yes

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    Investigations of a novel retinal disease in Wiltshire sheep : a thesis presented in partial fulfilment of the requirements for the degree of Master of Veterinary Studies in Veterinary Pathology at Massey University, Palmerston North, New Zealand
    (Massey University, 2014) Hunt, Hayley
    In 2011 and 2012, nine cases of adult-onset blindness were identified in a single flock of Wiltshire sheep. Affected sheep typically developed detectable night blindness at 2 to 3 years of age, which progressed to complete blindness by 4 to 5 years of age. Opthalmoscopically, the disease was characterised by progressive tapetal hyperreflectivity and attenuation of retinal blood vessels, indicative of retinal thinning and atrophy. Retinal histology revealed a selective loss of rod photoreceptors in the early stages of the disease, with preservation of cone photoreceptors. Secondary loss of cone photoreceptors was seen later in the course of the disease. Retinal degeneration was not accompanied by any other ocular or central nervous system abnormalities. Progressive retinal degeneration targeting rod photoreceptors has not been previously reported in sheep, but this disease has several similarities to inherited retinal dystrophies in other species, particularly progressive retinal atrophy in dogs and retinitis pigmentosa in humans. The disease in sheep is thought to be inherited in either an autosomal dominant or autosomal recessive manner, although additional cases identified recently provide further support for an autosomal dominant mode of inheritance. Initial investigations into the molecular basis of the disease, using a comparative candidate gene approach, did not identify any exonic single nucleotide polymorphisms (SNPs) in the rhodopsin gene of affected sheep that would alter the amino acid sequence. Homozygosity mapping of affected sheep revealed an identical-by-descent region on chromosome 5, but none of the genes within or surrounding this segment were considered to be plausible candidate genes except for GPR98, which is associated with retinitis pigmentosa and sensorineural hearing loss in humans. Investigations into the inheritance and molecular basis of this novel retinal degeneration in Wiltshire sheep are continuing, as this disease may prove to be a useful model for retinal dystrophies in other species, including retinitis pigmentosa in humans.
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    Epidemiological, pathological and metabolomic characterisation of an acquired myopathy of dogs in New Zealand : a thesis presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Veterinary Science at Massey University, Manawatū, New Zealand
    (Massey University, 2018) Hunt, Hayley
    ‘Go Slow’ myopathy (GSM) is an idiopathic myopathy in dogs in New Zealand, characterised by an acute onset of trembling, weakness and collapse, followed by a prolonged period of exercise intolerance. In the first part of this thesis, the epidemiology of the disease was investigated using a telephone survey to obtain information regarding the diet, exercise, and health of affected dogs. Eighty-six confirmed cases were included in this study, and ingestion of wild pig in the week prior to the onset of clinical signs was a consistent finding (76/86 dogs; 88%; 95% confidence interval = 82 – 95%). Cases occurred most commonly in the upper North Island, particularly in Northland. The aim of the second part of this thesis was to characterise the pathology of GSM in the same 86 dogs included in the epidemiological study, using serum biochemistry (78 dogs), histology (20 dogs), and electron microscopy (4 dogs). Acutely, affected dogs had increased serum creatine kinase and aspartate aminotransferase activities, corresponding with the histological finding of skeletal muscle degeneration in the absence of inflammation. Ultrastructural changes in skeletal muscle included mitochondrial hypertrophy, intramitochondrial inclusions and increased sarcoplasmic glycogen. Similar lesions were observed in the skeletal muscle of wild pigs from areas where GSM occurred in dogs. Affected dogs also had increased serum alanine aminotransferase activities due to accumulation of lipid and glycogen in hepatocytes. Overall, the microscopic findings were consistent with a toxic myopathy. To further investigate the pathogenesis of the disease, liver samples were collected from 15 affected dogs and 24 clinically normal dogs for untargeted metabolic profiling using liquid chromatography-mass spectrometry. Comparison of spectra between affected and normal dogs revealed a widespread decrease in phospholipids, and increases in selected dicarboxylic acids and N-acetylated branch chain amino acids in affected dogs. No causative compounds were identified although several candidate mass spectrometric features were identified for future investigation. Taken together, the results of these studies suggest that ‘Go Slow’ myopathy is a toxic mitochondrial myopathy in dogs that is associated with the ingestion of wild pork. The findings reported aid in the prevention, diagnosis, and management of cases, with the primary suggestion being that owners avoid feeding wild pork in areas where the myopathy occurs. Further work is required to elucidate the cause of this disease.