The classic disease of polyneuritis in birds represents a late stage of thiamin deficiency resulting from a peripheral neuritis, perhaps caused by accumulation of intermediates of carbohydrate metabolism. Comparing thiamin deficiency signs in 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 animals, 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. In turkeys, thiamin deficiency also resulted in tissue alteration of amino acids, decreased concentration of epinephrine and ATP and increased serotonin in the brain of birds (Remus and Firman, 1989; 1990; 1991a, b). In addition to neurological disease conditions, the other main group of disorders involves cardiovascular damage.
Of all nutrients, a deficiency of thiamin has the most marked effect on appetite. Animals consuming a low-thiamin diet soon show severe anorexia, lose all interest in food and will not resume eating unless given thiamin. If the deficiency is severe, thiamin must be force fed or injected to induce animals to resume eating.
Poultry are more susceptible to neuromuscular effects of thiamin deficiency than most mammals. In chickens and turkeys, there is a loss of appetite, emaciation, impairment of digestion, a general weakness, opisthotonos or stargazing and frequent convulsions, with polyneuritis as an extreme clinical sign. Deficient birds can rapidly detect and discriminate against feeds that do not provide the vitamin and are high in carbohydrate content (Thornton and Shutze, 1960). Early signs are lethargy and head tremors. Chicks fed very low thiamin (0.4 mg per kg; 0.18 mg per lb) survived for only seven to 10 days, apparently only a few days after the supply of thiamin in the yolk sac was exhausted (Gries and Scott, 1972). Some chicks developed nervous disorders, apathy, and tremor as early as the third or fourth day of life. These signs increased in severity up to ataxia, inability to stand, and high-grade opisthotonos or twisting of the neck. Severity of the spasms increased when the chicks were frightened. Chicks that showed these high-grade nervous disorders died within a few hours. Cardiac abnormalities have also been reported in acutely thiamin-deficient chicks (Sturkie et al., 1954). A paralysis of the crop, manifested as delayed emptying, accompanies the general neuropathy of experimental thiamin deficiency in chicks (Naidoo, 1956). Deficiency in pigeons results in crop voiding (vomiting).
In mature chickens, polyneuritis (Illus. 1) is observed approximately three weeks after they are fed a thiamin-deficient diet (Scott et al., 1982). As the deficiency progresses, paralysis of the muscles occurs, beginning with the flexors of the toes and progressing upward, affecting the extensor muscles of the legs, wings and neck. The chicken sits on its flexed legs and draws back the head in a stargazing (opisthotonos) position. Retraction of the head is due to paralysis of the anterior neck muscles. At this stage, the chicken soon loses the ability to stand or sit upright and falls to the floor, where it may lie with the head still retracted.
