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Rickets and osteomalacia are increasing in prevalence in people because of cultural practices, breast-feeding, decreased sun exposure, and increased sunscreen usage. Several hereditary forms of rickets owing to either renal phosphate wasting or defects in vitamin D metabolism are also reported in people. Rickets is well recognized in domestic animals, but published reports are not always supported by microscopic findings, and diagnoses based on clinical signs and radiology are unreliable. Most cases in domestic animals are caused by dietary deficiency of either vitamin D or phosphorus, but occasional inherited forms are reported in pigs, sheep, cats, and dogs. There is variation between species in susceptibility to dietary vitamin D and phosphorus deficiency and in the ability to manufacture vitamin D in their skin. A number of mouse models have been discovered or created to study human skeletal diseases and skeletal homeostasis. With the discovery that vitamin D is involved in not only calcium and phosphorus homeostasis but also in the immune system and cancer, there is great potential for new and existing animal models to generate valuable information about vitamin D and its many functions. This review presents an overview of vitamin D metabolism and rickets in domestic and laboratory animals and makes comparisons where appropriate with the disease in humans. Keywords bone, rickets, vitamin D, phosphorus, genetic diseasesRickets is a classic metabolic bone disease of humans and animals, first described in the first and second centuries. 158,165 With the discovery that vitamin D could prevent rickets, the prevalence of this disease in developed countries plummeted; however, it still occurs. In fact, the prevalence of rickets and vitamin D insufficiency is increasing in people of all ages in the developed world, due in part to decreased sunlight exposure and widespread sunscreen usage. 88 The disease is well recognized in animals, but published reports are uncommon and sometimes confusing.The pathogenesis of rickets involves impaired mineralization of physeal and epiphyseal cartilage during endochondral ossification and of newly formed osteoid. Most cases in domestic animals are caused by dietary deficiency of either vitamin D or phosphorus, but occasional inherited forms are reported. 109,200 Osteomalacia is caused by a failure of newly formed osteoid to mineralize, but it occurs in adults after closure of growth plates. 109In this article, we review vitamin D metabolism and rickets, with reference to the disease in domestic animals but presenting comparison with the disease in humans where appropriate. Biology of Vitamin D Activation of Vitamin DVitamin D is available from two sources: isomerization of 7-dehydrocholesterol (7-DHC) in the skin to vitamin D 3 following exposure to ultraviolet light or from ingestion of vitamin D 2 or D 3 in the diet. Only a few foods, including cod liver oil and fatty fish such as salmon and sardines, naturally contain high concentrations of vitamin D 3 .49 Vitamin D 2 i...

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Felis catus papillomavirus 2 (FcaPV-2) causes premalignant skin lesions in cats and has also been found in a proportion of cutaneous squamous cell carcinomas (SCCs) -a common and potentially fatal cancer of cats. Whilst this could suggest a role of the virus in cancer development, FcaPV-2 has also been detected in skin swabs of normal cats, making it difficult to discern whether the papillomavirus is causing the cancer or merely an 'innocent bystander'. To distinguish between these two possibilities, real-time PCR was used to determine the viral copy number and the transcriptional activity of FcaPV-2 infections present in 70 formalin-fixed paraffin-embedded skin lesions including 10 papillomavirus-induced premalignant lesions and 60 SCCs. FcaPV-2 gene expression was found in 21 of 60 (35 %) SCCs, all 10 premalignant lesions and none of 10 normal skin samples. The results showed two distinct subsets of SCCs. The majority of the SCCs had low copy numbers of FcaPV-2 DNA (mean of 17 copies per copy of reference gene DNA) and no FcaPV-2 gene expression, suggesting the virus was an incidental finding. In contrast, 20 SCCs had detectable FcaPV-2 E6/E7 gene expression and very high copy numbers of FcaPV-2 DNA, with a mean of 32 930 copies per copy of reference gene DNA. The relative quantity of E6/E7 gene expression and the viral copy number in this group were similar to those found in the papillomavirus-induced premalignant lesions, suggesting that FcaPV-2 may play a role in the development of a subset of feline cutaneous SCCs.

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During the summer of 2013 seven Italian Tyrolean Grey calves were born with abnormally short limbs. Detailed clinical and pathological examination revealed similarities to chondrodysplastic dwarfism. Pedigree analysis showed a common founder, assuming autosomal monogenic recessive transmission of the defective allele. A positional cloning approach combining genome wide association and homozygosity mapping identified a single 1.6 Mb genomic region on BTA 6 that was associated with the disease. Whole genome re-sequencing of an affected calf revealed a single candidate causal mutation in the Ellis van Creveld syndrome 2 (EVC2) gene. This gene is known to be associated with chondrodysplastic dwarfism in Japanese Brown cattle, and dwarfism, abnormal nails and teeth, and dysostosis in humans with Ellis-van Creveld syndrome. Sanger sequencing confirmed the presence of a 2 bp deletion in exon 19 (c.2993_2994ACdel) that led to a premature stop codon in the coding sequence of bovine EVC2, and was concordant with the recessive pattern of inheritance in affected and carrier animals. This loss of function mutation confirms the important role of EVC2 in bone development. Genetic testing can now be used to eliminate this form of chondrodysplastic dwarfism from Tyrolean Grey cattle.

Haemotropic mycoplasmas (haemoplasmas) are small epierythrocytic bacteria that have the potential to cause severe, life-threatening haemolytic anaemia. The aim of the current study was to evaluate feline haemoplasma prevalence using real-time polymerase chain reaction (PCR) from a convenience sample of New Zealand domestic cats, including blood film examination and a risk factor analysis. DNA was extracted from 200 blood samples submitted to a diagnostic laboratory for routine haematology over a 12-month period. Species-specific real-time PCR assays identified 62 cats that were positive for haemoplasma DNA, giving an overall prevalence of 31%. Twelve of the positive cats had dual infections. The prevalence of the three feline haemoplasmas was 25% for 'Candidatus Mycoplasma haemominutum', 7.5% for Mycoplasma haemofelis and 4.5% for 'Candidatus Mycoplasma turicensis' (CMt). All samples were positive for an internal control (feline 28S rDNA) by real-time PCR. Sensitivity and specificity of blood smear examination for haemoplasma infection in this study was 9.7% and 97.8%, respectively. Retroviral infection was tested using the Idexx Snap Feline Triple test on all samples. Twenty cats (10%) were feline immunodeficiency virus (FIV) positive and 11 cats (5.5%) were feline leukaemia virus (FeLV) positive. Statistical comparisons, using multivariate logistic regression, indicated that positive FIV status, male gender and non-pedigree breed were significantly (P <0.05) associated with haemoplasma infection, with odds ratios of 10.16, 5.04 and 3.03, respectively. The results of this study demonstrate the prevalence of the three main feline haemoplasma species in New Zealand for the first time, with prevalences correlating with previous overseas studies. This is the first report of CMt in New Zealand.

Osteosarcoma (OSA) is a malignant heterogeneous primary bone tumor responsible for up to 90% of all primary bone tumors in dogs. In this study, osteocalcin (OC) and osteonectin (ON) immunoreactivity was evaluated in 23 canine OSAs, 4 chondrosarcomas, 4 fibrosarcomas, 2 hemangiosarcomas, and 4 histiocytic sarcomas. The effects of three different decalcification agents (ethylenediaminetetraetic acid [EDTA], formic acid and hydrochloric acid [HCl]) on the immunoreactivity for OC and ON was also assessed. Immunoreactivity to OC was present in 19/23 (83%) cases of OSA and all cases of chondrosarcoma. In three OSAs the extracellular matrix showed immunoreactivity to OC. None of the fibrosarcomas, histiocytic sarcomas or hemangiosarcomas showed immunoreactivity to OC. The sensitivity and specificity for OC in canine OSA in this study was 83% and 71% respectively. For ON, 100% of both OSAs (23/23) and non-OSAs (14/14) showed cytoplasmic immunoreactivity to this antibody, giving a sensitivity of 100% but a complete lack of specificity. There were no significant differences in immunoreactivity for OC and ON between the different decalcification agents used. In conclusion, OC showed high sensitivity for identifying OSA but it failed to distinguish between OSA and chondrosarcoma, and the osteoid produced by neoplastic cells in most cases did not show immunoreactivity to OC. These factors may limit the practical utility of OC in the diagnosis of OSA in dogs when chondrosarcoma is a differential diagnosis. ON showed no specificity in detecting OSA and has little practical application for the diagnosis of OSA in dogs.