AVIAN THIAMIN DEFICIENCY

Abstract

A correlation of the histopathology and clinical behavior of thiamin deficient pigeons has been undertaken. Opisthotonus in acutely deficient pigeons was frequently attended by no degenerating nerve fibers or neurons in either the central or peripheral nervous systems. When the deficiency was complicated by starvation, it developed more slowly, opisthotonus appeared later, and many degenerating nerve fibers were usually present. In both instances the opisthotonus disappeared in a very short time after thiamin was injected intramuscularly. A more chronic deficiency, characterized by leg weakness (opisthotonus being absent) appeared when the ration was partially deficient in thiamin, or occasionally when the caloric intake was grossly inadequate. In birds of this type degenerating nerve fibers were always found in the peripheral nerves. The number of such fibers in the sciatic nerves corresponded closely with the degree of paralysis, and during repair which occurred when thiamin (irrespective of other factors) was added to the ration, nerve fibers regenerated (increased in number) at a rate which paralleled the clinical improvement closely. The large and long nerve fibers, many of which could be traced directly into the dorsal ganglia, degenerated first, and if the deficiency were prolonged, smaller nerve fibers became affected as well. In many of these pigeons with marked leg weakness, cell bodies in the dorsal ganglia exhibited lysis of chromatin and eccentricity of their nuclei. This was observed nowhere else in the nervous system. During repair and until after the paralysis had been recovered from completely, these phenomena (chromatolysis) persisted. In chronically thiamin deficient pigeons large and long degenerating nerve fibers were found in two regions of the spinal cord at all levels. One group of these in the ventral funiculus was thought to arise in the reticular region of the medulla oblongata, and the other which was situated in the posterior part of the lateral funiculus could be followed to the lateral surface of the medulla oblongata, and from there by way of the inferior cerebellar peduncles into the medullary portion of the cerebellum. In the central as well as the peripheral nervous system the long and large nerve fibers degenerated first. Medium and small sized fibers were affected later and the degeneration became quite generalized. In many of the chronically deficient pigeons with leg weakness, incidental postmortem findings compatible with cardiac failure were encountered. In the hearts from many of these pigeons, microscopic examination revealed many areas of focal necrosis, some of which had become infiltrated with polymorphonuclear leucocytes. In a peripheral neuron of a thiamin deficient pigeon the first consistent morphological alteration appeared in the axis cylinder. No doubt a period of functional impairment of the neuron (such as produced opisthotonus) preceded this. The axis cylinder followed by the myelin sheath degenerated at a point most distal to its trophic cell body. This process of disintegration proceeded toward the trophic cell body for a variable distance, depending upon the severity and duration of the deficiency. The cell body (in a dorsal ganglion) appeared to shrink first and later exhibited chromatolysis. When thiamin was administered the axis cylinder (and myelin sheath) regenerated, and when this was complete, the cell body returned to normal. It has been concluded that the opisthotonus of thiamin deficiency is a manifestation of decerebration due to a functional impairment of the neurons which have an inhibitory influence upon the lower brain stem centers. Leg weakness (when produced by the same deficiency) is due to degeneration of peripheral nerve fibers within the sciatic nerve. Heart failure may be attended by no visible histological changes, but in many instances necrosis of myocardial fibers occurs.