Deficiency diseases-thiamine deficiency (hypothiaminosis), Biology

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Thiamine deficiency (hypothiaminosis)


Thiamine deficiency is characterized by signs of nervous system. The primary  thiamine deficiency is not common in animals. However, secondary deficiency has been reported in different species of farm animals.


Aetiology:
Ruminants synthesize thiamine in rumen, whereas in monogastric animals, thiamine is microbially synthesized in alimentary tract. Primary thiamine deficiency of dietary origin  is  rare as most plants, especially the seeds and milk contain appreciable quantity of thiamine. An incidence of primary thiamine deficiency due to deprivation of feed during transport has been reported in literature.Secondary thiamine deficiency occurs due to destruction of the vitamin by the enzyme thiaminase. Cooking also destroys thiamine. Ingestion of excessive quantity of bracken fern and horsetail causes thiamine deficiency because of the high concentration of enzyme thiaminase. The coccidiostat amprolium is thiamine antagonist and its prolonged use can induce the deficiency of the vitamin.

Clinical findings: Bracken fern poisoning, a principal cause of secondary thiamine deficiency in horses, is clinically manifested by incoordination, falling and bradycardia. Horsetail poisoning is also characterized by similar signs. Initially there is swaying from side to side followed by pronounced incoordination, crossing of forelegs, arching of back, muscle tremors, and clonic convulsions followed by opisthotonous at the terminal stage. Hemiplagia of vocal cords is also found in horses.Experimentally induced hypothiaminosis in pigs was characterized by inappetance, emaciation, and leg weakness and falling. Lambs show signs of anorexia somnolence, and loss of condition followed by titanic convulsions.


Diagnosis: Signs of paralysis and reduced blood thiamine levels from normal range of 8-10 µg/dl to 2.5-3 µg/dl increased pyruvic acid concentration from normal values of 2-3 µg/dl to 6-8 µg/dl are indicative of thiamine deficiency in horses. Cases of encephalomyelitis caused due to other factors than thiamine deficiency fail to respond to thiamine treatment.


Treatment and Prevention:
Parenteral administration of thiamine @ 5 mg/kg body weight at 3 hourly intervals induces rapid therapeutic response. Daily oral doses of thiamine for 10 days, and correction of dietary abnormalities are effective therapeutic and preventive measures. Diet of monogastric animals should be supplemented with yeast, cereals and grains.


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