Polioencefalomalacia em ruminantes

Abstract

In the first portion of this thesis, epidemiology, clinical signs and distribution of lesions in the brain of thirty one cases of polioencephalomalacia (PEM) in cattle from the Southern (13 cases) and Midwestern (18 cases) Brazil were studied. Morbidity (0.04%-6.66 %), mortality (0.04%-6.66 %), and lethality (50%-100%) rates were similar in both regions studied. Cases occurred mainly in cattle raised at pasture; in the Southern the disease affected mainly young cattle while mainly older cattle were affected in the Midwest. Clinical signs more frequently observed included blindness, incoordination, circling, opisthotonus, recumbence and paddling movements. Clinical course varied from 12 hours to 8 days. In 11 cases no gross changes were observed in the brain. Main gross findings in the brain of remaining cases included congestion with swelling and flattening of gyri, softening and yellow discoloration of cerebral cortex, hemorrhagic foci in the brain stem, cerebellum and telencephalon, and cerebellar herniation. The main histopathological changes were in the cortex of occipital, parietal and frontal telencephalic lobes; however less prominent and less frequently found lesions occurred in the hippocampus, basal nuclei, thalamus, midbrain, and cerebellum. The type of microscopic cortical lesions was consistent in all cases and included segmentar laminar neuronal necrosis, spongiosis, swollen of vascular endothelial nuclei, Alzheimer type II astrocytes and infiltration of gitter cells. In 20% of the cases there was mild lymphohistiocytic cellular infiltrate and in 13% of the cases there was mild infiltrate by neutrophils and eosinophils. Additionally, mild to moderate necro-hemorrhagic lesions were observed in 49% of the cases in the basal nuclei, in 39% of the cases in brain stem and in 26% of the cases in the thalamus. In the cortical laminae of the occipital, parietal and frontal telencephalic lobes, most frequently affected cortical layers both by neuronal necrosis and edema were external and internal granular layers. Both gyri and sulci were equally affected. In the second portion of the thesis, one experimental model for the study of the etiology, pathology, and pathogenesis of polioencephalomalacia in ruminants was established. The condition was induced in five sheep by oral administration of amprolium at daily doses of 500 and 1,000 mg per Kg of live body weight respectively for 28-59 days and for 13-39 days. Clinical course varied from 3 to 7 days. Clinical signs included depression, incoordination, midriasis, grinding of the teeth, blindness, and laying down with opisthotonus and paddling movements. Drooling and a sawhorse stance were observed in one sheep and myoclonus in another one. Main gross lesions were restricted to the central nervous system and included swelling of the brain with flattening of telencephalic gyri, and hemorrhages in the parietal and occipital lobes of the telencephalon. Histologically, there was segmental laminar neuronal necrosis (red neurons) associated with edema, swelling of endothelial cells, hemorrhages and infiltration by foamy macrophages (gitter cells). These changes were more marked in the frontal, parietal and occipital telecephalic lobes and there was sharp demarcation between the lesions and the adjacent normal neuropile. Additionally, similar, but less marked lesions were seen in the mesencephalon, thalamus and hippocampus. Considering the consistent reproducible aspects of polioencephalomalacia in sheep using amprolium, this may be an useful model for the study of the disease.