1,077 research outputs found

    Vergelijkende erfelijke en pathogenische kenmerken van hypertrofische cardiomyopathie bij de kat en de mens

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    Hypertrophic cardiomyopathy (HCM) is characterized by a hypertrophic, non-dilated left ventricle. With a prevalence of approximately 0.2% in humans and 15% in cats, this is one of the most common heart diseases. The disorder is often inherited but may also be acquired during life. The clinical symptoms may differ. Genotypically affected individuals can exhibit (severe) symptoms of heart failure or die suddenly, but they can also stay asymptomatic during their entire life. More than 1400 gene polymorphisms have already been detected in thirteen genes that code for sarcomere proteins in the heart in humans. Some of them are, together with modifying genes and environmental factors, responsible for the development of HCM. To date, only three mutations have been identified in cats. Commercial tests are already available to diagnose them. These mutations are responsible for only a small fraction of the cases of HCM in cats. It is important to identify as many mutations as possible in order to develop a control strategy. There are a lot of common grounds between the human and feline forms of HCM. There are similarities in the mode of inheritance (autosomal), the clinical appearance and the histopathological changes. Still, there is not enough known about sarcomere proteins and their mutations to extrapolate information from humans to cats and vice versa

    Hemangiosarcoma of the third eyelid in a horse

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    A 12-year-old Belgian Warmblood mare was referred to the equine clinic of the Faculty of Veterinary Medicine (Ghent University) for a mass on the third eyelid of the right eye. The horse had been having a recurrent red-tinged ocular discharge for several months. After complete ophthalmologic examination, a large part of the third eyelid was surgically excised and submitted for histopathologic examination. The histopathologic examination revealed a proliferation of blood-filled vascular spaces lined by a single layer of flattened cells, which were identified as endothelial cells using immunohistochemistry. The tumor was identified as a cavernous low-grade hemangiosarcoma. No complications were reported six months after surgery

    Progress and problems in vaccination against necrotic enteritis in broiler chickens

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    Necrotic enteritis in broilers is caused by Clostridium perfringens type A strains that produce the NetB toxin. Necrotic enteritis is one of the gastrointestinal diseases in poultry that has gained worldwide importance during the last decade due to efforts to improve broiler performance. Prevention strategies include avoiding predisposing factors, such as coccidiosis, and in-feed supplementation with a variety of feed additives. However, vaccination with modified toxin or other secreted immunogenic proteins seems a logical preventive tool for protection against a toxin-producing bacterium. Formalin-inactivated crude supernatant has been used initially for vaccination. Several studies have been carried out recently to identify the most important immunogenic and protective proteins that can be used for vaccination. These include the NetB toxin, as well as a number of other proteins. There is evidence that immunization with single proteins is not protective against severe challenge and that combinations of different antigens are needed. Most published studies have used multiple dosage vaccination regimens that are not relevant for practical use in the broiler industry. Single vaccination regimens for 1-day-old chicks appear to be non-protective. This review describes the history of vaccination strategies against necrotic enteritis in broilers and gives an update on future vaccination strategies that are applicable in the field. These may include breeder hen vaccination, in ovo vaccination and live attenuated vectors to be used in feed or in drinking water

    Detection of arenavirus in a peripheral odontogenic fibromyxoma in a red tail boa (Boa constrictor constrictor) with inclusion body disease

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    A captive bred red tail boa (Boa constrictor constrictor) was presented with a large intraoral mass originating from the buccal gingiva, attached to the right dentary teeth row. Based on the clinical features and histological examination, the diagnosis of a peripheral odontogenic fibromyxoma was made. Sections of liver biopsies and circulating lymphocytes contained relatively few eosinophilic intracytoplasmic inclusion bodies, indistinguishable from those observed in inclusion body disease-affected snakes. Inclusion bodies were not observed in cells comprising the neoplastic mass. Using reverse transcription polymerase chain reaction (RT-PCR), arenavirus was detected in the neoplastic tissue. Two years after surgical removal of the mass, recurrence of the neoplastic lesion was observed. Numerous large inclusion body disease inclusions were abundantly present in the neoplastic cells of the recurrent fibromyxoma. Sections of liver biopsies and circulating lymphocytes contained relatively few intracytoplasmic inclusions. The RT-PCR revealed the presence of arenavirus in blood, a liver biopsy, and neoplastic tissue. The present case describes the co-occurrence of an arenavirus infection and an odontogenic fibromyxoma in a red tail boa
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