The pathology of organomercurial poisoning in swine
The pathological and clinical features of disease in young pigs resulting from the oral ingestion of organornercurial compounds has been characterized and related to tissue levels of mercury. In three experiments, the toxic effects of methylmercuric dicyandiamide (MMD), ethylmercuric chloride (EMC) and phenylmercuric chloride (PMC) have been studied. The experimental period lasted 60-90 days and the dosage range studied was 0.19-4. 56 mg. Hg/kg. daily. In general, daily dosage levels ranging from 2.28 to 4.56 mg. Hg/kg. were toxic regardless of organic form. Lower daily dosages, 0.38 and 0.76 mg. Hg/kg. were toxic only when administered in the form of alkyl compounds (MMD and EMC). The primary toxic effects of these mercurial compounds was manifested pathologically by degenerative changes in the susceptible cells of target organs. Alkyl mercurials caused enteric, renal and CNS disease, while aryl mercurials caused renal and enteric disease. The analysis of levels of mercury in tissues of animals receiving the organomercurials indicates that there is a direct association between tissue level and evidence of injury. The disease produced by MMD is largely one of the central nervous system and is related primarily to neuronal necrosis. Cortical neurons are most susceptible to injury and those in subcortical nuclei, in spinal gray matter, and in sensory ganglia are injured at higher doses. In the chronic form of toxicosis, there occurs, in addition to neuronal necrosis, secondary gliosis, capillary endothelial proliferation and degenerative arteriopathy in leptomeningeal blood vessels supplying injured cerebral cortex. The character of the vascular lesions in chronic MMD toxicosis is compatible with the ones of regional hypertension. Chronic poisoning with EMC was manifested by disease of the CNS entirely similar to that described previously for MMD. The subacute form of the disease seen in animals receiving higher doses of EMC had, in addition, lesions in the large intestine characterized by edema of the mesocolon associated with degenerative arteriopathy in serosal vessels and pseudomembranous colitis and typhlitis. Analytic findings indicated that, in EMC poisoning, most tissues contained relatively high levels of mercury. The disease occurring in PMC intoxication results from injury to the kidney and large intestine. The primary lesions are pseudomembranous colitis and typhlitis and nephrosis characterized by degeneration, necrosis, and regeneration in the epithelium of the proximal tubules. The pathology of this disease is similar to that described for mercuric chloride poisoning and reflects the ease with which phenylmercuric chloride is metabolized to release free mercuric ions.
Doctor of Philosophy (Ph.D.)