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Thiamine deficiency in dogs and

Clinical deficiency occurs sporadi- to thiamine injection, but can be con- the food is‘complete and balanced’. Such cally in dogs and cats in New Zealand and firmed by blood testing. The MQM Ani- a claim is ideally substantiated by AAF- usually manifests as ai1 acute neurological mal Health Laboratory network offers a CO feeding trials or by meeting AAFCO syndrome, leading to death ifuntreated. The thiamine assay (requiring 2 ml EDTA established levels for or dog deficiency usually results from thefeeding of blood) and a blood thiamine concentra- foods. However, under New Zealand commercial or homemadefoods with an inad- tion of 50-80 nmol/ 1 is regarded as mar- food regulations, the basis for the claim equate thiamine content. ginal. The histopathological brain lesions does not have to be specified on the label. are characteristic. These consist of bilat- The incidence of the disease in the dog erally symmetrical foci of haemorrhagic Most cases of thiamine deficiency diag- and cat populations in New Zealand is necrosis in periventricular grey matter nosed at MQM Health Laborato- unknown, but is not common. The MAF involving consistently, and most severe- ries have involved dogs fed exclusively Quality Management (MQM) Batchelar ly, the caudal colliculi, but often also on a single brand of untested commercial Animal Health Laboratory, which re- other brain stem nuclei(3’.A few dogs dog roll. A few cases have been seen in ceives submissions from veterinary prac- have focal myocardial degenerati~n‘~). fed exclusively on fresh minced meat, titioners throughout the lower half of the which may have contained sulphite pre- North Island, diagnoses a few cases each do not synthesise thiamine or servatives. The disease has also occasion- year, mainly in dogs. store significant amounts in the body ally affected farm dogs onunsupplement- and therefore depend upon a regular ed diets of cooked mutton or beef. with thiamine deficiency dis- dietary intake to maintain good health‘?). ease usually present with acute neuro- The AAFCO (Association of American Pet owners can follow an easy rule-of- logical signs, which are preceded by an- Feed Control Officials) minimum re- thumb to ensure that their animal’s in- orexia. These signs typically become pro- quired concentrations of thiamine in dog take of thiamine and other is gressively more severe over several days and cat foods are 1.0 and 5.0 mg/ kg DM, sufficient. At least 70% of the dog’s or and often, particularly in dogs, end in Meat, fish, cereal grains, cat’s food should be comprised of a com- death. In dogs the signs commonly de- dairy products and yeast extracts are sig- mercial coinplete and balanced food, and velop in the following chronological or- nificant sources of thiaminec4).However, up to 30% of the diet may consist of der: anorexia, emesis, lethargy, CNS de- thiamine is heat labile and cooking or untested commercial foods or homemade pression, paraparesis, , spasticity, processing can result in losses(6).Some foods. However, if owners give their pets tonic-clonic convulsions and death‘’). fish species contain a thiaminase, which mainly untested commercial food, they Occasionally dogs die suddenly without may significantly reduce the thiamine are less likely to encounter nutritional neurological signs and this is believed to content of the food(’). Cats in particular disorders if they feed a mixture of brands be caused by acute cardiac failure(”. In should not be fed tinned fish exclusively and types of food (dry, rolls, canned). cats the convulsions are characterised by unless it is labelled as being AAFCO kyphosis (ventroflexion of the head), tested. Sulphites, which are commonly hyperaesthesia and dilated unresponsive added as preservatives to fresh pet pupils(2’. Parenteral thiamine injection minced meat, also destroy thiamine@). References early in the course of the disease usually (I ) Read DH, Harrington DD. Experimentally results in rapid complete recovery. Manufactured pet foods cannot be as- induced thiamine deficiency in Beagle dogs: sumed to contain an adequate thiamine Diagnosis is often based on the response concentration unless the label states that Coiitinued next page

16 Surveillance 24(3) 1997 Thiamine deficiency in dogs and cats Continued from page 16

Clinical observations. American Journal of Veterinary Research 42,984-91, 1981. Oliver JE, Greene CE. Diseases of the brain. In: Ettinger SJ (ed). Textbook of Veterinary Internal Medicine: Diseases of the Dog and Cat (2nd edition). Pp 460-.532.WB Saunders, Philadelphia, 1983. Jubb KVF, Huxtable CR. The nervous sys- tem. In: Jubb KVF, Kennedy PC, Palmer N (eds). Pathology of Domestic Animals (4th edition). Pp 267-439. Academic Press, San Diego, 1993. McDowell LR. in animal . Academic Press, San Diego, 1989. Association of American Feed Control Offi- cials: Official Publication AAFCO Inc, At- lanta, 1993. Read DH, Jolly RD, Alley MR. Polioencephalomalacia of dogs with thiamine deficiency. 14, 103, 1977. Jubb KV, Saunders LZ, Coates HV. Thia- mine deficiency encephalopathy in cats. Jour- nal of Comparative Pathology 66, 217-27, 1956. Studdert VP, LabucRH. Thiaminedeficiency in cats and dogs associated with feeding meat preserved with sulphur dioxide. Australian Veterinary Journal 68, 54-7, 199 1.

Patrick Stuplrs MAF Quality Management Batchelar Animal Health Laboratory Email: [email protected]

Surveillance 24(3) 1997 17