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Last week many interesting meetings took place at the EMA in London. At the Committee for Medicinal Products for Veterinary Use (CVMP) meeting, the re-examination of the appeal to the opinion for veterinary medicinal products containing zinc oxide
to be administered orally to food producing species was discussed. The
Committee adopted by consensus a final opinion recommending the refusal
of granting of new marketing authorisations and the withdrawal of the
existing authorisations for veterinary medicinal products containing
FECAVA has opened nominations for the new Didier-Carlotti award which recognises outstanding service in the fields of inter-professional communication and/or continuing education for companion animal veterinarians in Europe.
As global understanding and concern for animal welfare continues to change, so must the veterinary community evolve to embrace these changes and reflect societal expectations. Animal Welfare is a core mandate of the veterinary community generally and of veterinarians individually. Veterinarians must be engaged, knowledgeable, and prepared to use their skills and expertise in Animal Welfare to assist and support animal caregivers, industry, policy makers and the public to ensure best practices are in place that promote good animal welfare.
Following the recent recall of four dried cat food products due to low thiamine levels, BSAVA wanted to provide a brief update on thiamine deficiency.
Thiamine (vitamin B1) deficiency occurs most commonly in anorexic cats or cats that are fed an all fish diet containing thiaminase. However, it but has also been associated with excessive cereal in the diet, uncooked soy products, heating foods to excessive temperatures and the use of sulphur dioxide as a preservative. Thiamine deficiency can also occur in dogs.
Thiamine plays an essential role as a cofactor for enzymes in carbohydrate metabolism, it forms a compound with ATP to form thiamine diphosphate/thiamine pyrophosphate. It does not affect blood glucose. Thiamine deficiency leads to energy depletion and neuronal necrosis resulting in polioencephalomalacia, particularly of the oculomotor and vestibular nuclei, the caudal colliculus and the lateral geniculate body.