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When comparing thiamin deficiency signs among various species, it is seen that disorders affecting the central nervous system are the same in all species. This is explained by the fact that, in all mammals, the brain covers its energy requirement chiefly by the degradation of glucose and is, therefore, dependent on biochemical reactions in which thiamin plays a key role.
Numerous reports of thiamin deficiency in cats and, less frequently, dogs exist in the literature. In these, the dietary deficiency was attributed to destruction of thiamin by heat during cooking or processing (Loew et al., 1970; Read et al., 1977; Baggs et al., 1978; Hoffmann-La Roche, 1981) or by thiaminase-containing fish (Smith and Proutt, 1944; Jubb et al., 1956; Houston and Hulland, 1988).
The deficiency expresses itself clinically as anorexia (lack of appetite) and neurological disorders (especially of the postural mechanism), followed ultimately by weakness, heart failure and death. The induction of thiamin deficiency will determine clinical effects. An acute deficiency will produce severe neurological clinical signs and involve the brain, while chronic deficiency will involve changes in the peripheral nerves and myocardium. Because of its water-soluble nature and the body's limited capacity to store thiamin, clinical signs due to thiamin deficiency may be observed after a relatively short period of ingestion of a thiamin-deficient diet.
Diagnosis of thiamin deficiency in dogs and cats is made based on clinical signs and the dietary history of the animal. Diagnosis of thiamin deficiency initially depended upon recognition of the clinical signs in live animals, followed by confirmatory brain histopathology or clinical response to thiamin administration (Rammell and Hill, 1986). Moreover, sick animals react so promptly to treatment with thiamin (sometimes within hours) that early treatment with thiamin is used for confirming the diagnosis of deficiency.
Biochemical changes associated with thiamin deficiency include reduced blood, urine and tissue thiamin contents, dramatic elevation of blood pyruvate and lactate, and markedly reduced transketolase activity (Brunlich and Zintzen, 1976). Thiamin concentrations in blood and urine are decreased with a deficiency. Brin (1969) was able to show that blood (particularly the red cell) transketolase activity is a reliable index of the availability of coenzyme thiamin pyrophosphate (TPP), and thus correlated well with the degree of deficiency in animals. Transketolase is an excellent indicator in that it is useful in detecting a marginal thiamin deficiency. The best transketolase assay for assessing thiamin deficiency is based on the so-called TPP effect, which is the percentage increase in transketolase activity following addition of excess TPP to the sample. The in vitro measurement of erythrocyte transketolase stimulation by TPP (Noel et al., 1971; Read, 1979) has been used to diagnose thiamin deficiency in the dog and cat (Baggs et al., 1978; Deady et al., 1981a, b). However, a decrease in the concentration of TPP in the blood of rats has been shown to precede changes in transketolase activity (Warnock et al., 1978) and may be a superior test for both dogs and cats.
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Thiamin deficiency in dogs results from animals consuming diets where marginal thiamin concentrations have been destroyed in food processing or thiaminases are sufficiently high in the diet. A group of sled dogs that were fed a diet consisting of frozen, uncooked carp developed clinical signs of thiamin deficiency after a six-month period. The addition of oatmeal, a dry dog food, and 100 mg of thiamin daily to the affected dogs resulted in complete recovery within two months (Houston and Hulland, 1988). Thiamin deficiency was diagnosed in dogs fed fresh minced meat that contained sulfur dioxide as a preservative and less than 0.5 mg thiamin per kg (0.23 mg per lb) of diet (Studdert and Labuc, 1991).
Pathological changes due to thiamin deficiency predominantly involve the nervous system and heart. The pattern of pathological changes depends on the period of induction; acute deficiencies tend to involve the brain and produce severe neurological signs, whereas chronic deficiencies produce pathological changes in the heart and peripheral nerves (Read, 1979).
Read and Harrington (1981) induced clinical signs of thiamin deficiency in young beagles by feeding a diet containing 20 to 30 µg thiamin per kg (9.1 to 13.6 µg per lb) of diet. They reported three phases of disease: an initial phase where dogs appeared healthy but grew suboptimally, lasting 18 ± 8 days; an intermediate stage of variable duration (59 ± 37 days) of anorexia, loss of body weight and coprophagy; and either a short period of neurological illness or sudden death. The terminal period, which in most dogs was abrupt and short (8 ± 6 days), consisted of either a neurological syndrome or sudden, unexpected death. The neurological syndrome was characterized by anorexia, vomiting, central nervous system depression, paraparesis (partial paralysis of lower extremities), sensory ataxia, torticollis (twisting of neck), circling, tonic-clonic convulsions (relaxation alternating with spasms), profound muscular weakness and recumbency (Read and Harrington, 1981; NRC, 1985).
A prominent clinical sign of thiamin deficiency in dogs is anorexia. This progresses after a few days to ataxia with possible vomiting. These signs continue to tonic convulsions and can eventually lead to death of the animal. Dogs sometimes show cardiac hypertrophy (enlargement) with slowing of the heart rate and signs of congestive heart failure including labored breathing and edema. Read (1979) described the cardiac lesion as nonspecific multifocal myocardial necrosis, and suggested primary vascular damage may be involved. Brain lesions include symmetrical necrosis of the gray matter (Read et al., 1977), and histologically the reported peripheral neuropathy is characterized by diffuse bilateral myelin degeneration and axonal disintegration (Voegtlin and Lake, 1919; Street et al., 1941b; Read, 1979).
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Of all the domestic animals, the cat is most often reported to be clinically thiamin deficient (Illus. 1). This might well be expected as domesticated cats often consume fish, with the possibility of thiaminase being present in many cat foods (NRC, 1986). Cats appear to be more susceptible because of their high requirement for this vitamin in the diet and because of the tendency of pet owners to feed cats unconventional diets (Smith and Proutt, 1944; Loew et al., 1970). Most cases have been the result of feeding cats diets that contained a large proportion of raw fish (Smith and Proutt, 1944; Jarrett, 1970). Experimental studies with cats have produced signs of thiamin deficiency within 23 to 40 days of consuming diets composed solely of raw carp or raw salt-water herring (Smith and Proutt, 1944). The subcutaneous administration of thiamin to affected cats resulted in recovery in all cases. Thiamin deficiency in cats (also dogs) has been associated with feeding meat preserved with sulfur dioxide (Studdert and Labuc, 1991).
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For thiamin-deficient cats, anorexia and sometimes vomiting occur within two weeks of ingestion of a thiamin-deficient diet and are followed by the sudden development of neurological disorders, including abnormal posture (Illus. 1), ataxia and seizures, culminating in progressive weakness and death. Affected cats often show ventroflexion of the head when suspended by the rear legs or somersaulting when the cat leaps (Everett, 1944; Jubb et al., 1956). The impaired vestibulolocular reflexes observed include decreased nystagmus (eyeball movement) time and an impaired or slow pupillary light reflex. Affected kittens also have dilated pupils. Postural abnormalities are likely to develop and may include a spastic gait and curling up when lifted, or a head tilt. Seizures or abnormal behavior, dilated pupils, stupor or opisthotonos (spasms where head and heels bend backwards) may also be observed (Shell, 1995).
Electrocardiographic changes due to thiamin deficiency have been described (Toman et al., 1945). These included bradycardia, which developed as early as the second week. Tachycardia was less frequent and seen later. Disorders in heart rate regularity and impulse formation responded promptly to thiamin treatment. Cats affected with thiamin deficiency may exhibit spontaneous seizures, which may be accompanied by brief periods of tachycardia followed by severe bradycardia (Toman et al., 1945; NRC, 1986). A number of pathological changes of the central nervous system have been described. In acute cases, bilateral symmetrical hemorrhages of the brain in the periventricular gray matter have been recorded.
Depending on the severity of the case, deficiency signs in cats can be alleviated by the administration of thiamin; however, the hemorrhages that occur in the periventricular gray matter of the brain because of thiamin deficiency can permanently affect the animal. It has been found that cats who have recovered from experimentally induced thiamin deficiency have significantly greater difficulty in learning or remembering maze tasks (Ralston Purina, 1987).
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