Encefalopatia hepática por Tephrosia cinerea em ovinos e tuberculose no sistema nervoso de bovinos

Abstract

This dissertation consists of two chapters. The first describes hepatic encephalopathy in poisoning by Tephrosia cinerea, plant that causes hepatic fibrosis periacinar in sheep in semi-arid region of Northeast with clinical signal of ascites. In a review of autopsy and histopathological slides in Animal Pathology Laboratory of the Federal University of Campina Grande, Patos Campus, it was found that in nine outbreaks, of which there were a total of 16 children, six sheep had description of drowsiness as a complaint and had brain changes that were characterized by white matter vacuolation and the junction between gray and white matter , and the presence of Alzheimer type II astrocytes, primarily nuclei of the base, cerebellar peduncle, colliculus, thalamus and cortex. All sheep showed varying degrees of hepatic fibrosis, which were best evidenced on tricômico staining of Masson. For investigation of vascular health in the brain of animals held periodic acid Schiff staining, in which no changes have been displayed. For finding astrocytic degeneration, immunohistochemistry was performed with anti-GFAP antibody, and four sheep showed low or absence of markup. While the antibody anti-S100 marked the cytoplasm of reactive astrocytes in 6 sheep. The experimental breeding resulted in two animals intoxicated with hepatic encephalopathy showing clinical signs, histopathological lesions and immunohistochemical findings similar to those reported in the natural poisoning. Concluding that some cases of severe liver failure, poisoning side T. cinerea, increased serum levels of ammonia causes astrocytic disorders that evolve into framework of hepatic encephalopathy in sheep, and include this disease as differential diagnosis of nervous system diseases of sheep. The second chapter is the description of six outbreaks of tuberculosis in the nervous system of cattle. The cases were necropsied on previously cited institution, where a total of 73 necropsies of cattle with tuberculosis, six showed lesions in the nervous system, and only three of these clinical neurological signs several, varying with the location and severity of the lesions. All six animals were of different breeds and were kept under a semi-extensive regimen, and most were older than 12 months. During the necropsy showed that five of the six cattle presented lesions in other organs besides the nervous system. In four animals to macroscopic lesions were characterized by thickening of the leptomeningeal in the brain’s basilar region, in an animal there was still the presence of granulomas in the wall of the ventricle and in another animal, there was the formation of a tubercle at the base of the cerebellum, causing cerebellar herniation and secondary hydrocephalus; in two animals the lesion extended the sacral spinal cord. Microscopically the changes consisted of granulomas, with necrotic center, rarely mineralized, enveloped by macrophages and multinucleated giant cells of the type Langehans, in cases without clinical signs the granulomas were compressed the adjacent neuropilo or they infiltrated it discreetly, while in cases with clinical disorders tissue adjacent to the granulomas showed malacia. When held the coloration of tricomic Masson, noticed that there was a shortage or there was no fibrous capsule delimiting the lesions in the nervous system, moreover, in this same coloration showed marked proliferation of vessel intimate tunic of the leptomeninges. In Von Kossa staining, showed the little intralesional mineralization in areas of whole neuropilo in one of the cattle. In all cattle were found numerous alcohol-resistant acid bacilli in Ziehl Neelsen staining and strong to moderate immunolabeling with anti- Mycobacterium tuberculosis. The macroscopic findings and vascular lesions in cases of bovine tuberculosis affecting the nervous system suggests that the bacteria spreading in the body through hematological ways, beginning from injuries in primary sites (such as the lungs). The location of the lesions in most cases suggests that the cycle of Willis encourages the installation of bacteria, because blood flow changes may happen in this structure.