Natural Poisoning by Tephrosia cinerea in Sheep from Western Region of Rio Grande do Norte State, Northeastern Brazil

Abstract

Background: Tephrosia cinerea is a toxic plant responsible for liver fibrosis, which results in ascites and weight loss in sheep and probably goats. Although T. cinerea is widespread in Brazil, reports of poisoning are described in a few regions, named Eastern “Seridó” region of Rio Grande do Norte state, Central “Sertão” region of Ceará state, and “Sertão” of Paraíba state. Thus, this paper aimed to report the clinical-epidemiological, laboratorial, pathological and ultrasonographic findings of sheep spontaneously poisoned by T. cinerea in the Western region of Rio Grande do Norte state, Northeastern Brazil.

Cases: The evaluated cases occurred in sheep raised on properties located in the municipalities of Areia Branca and Tibau, Western region of Rio Grande do Norte state, Northeastern Brazil. In all visited farms, the pasture had a marked predominance of the T. cinerea. Clinical signs included progressive weight loss, dehydration, bilateral abdominal distension, and respiratory dyspnea probably due to diaphragmatic compression. Other less frequent clinical signs were hyporexia, pale mucosae, rough hair coat and polyuria. Hematology revealed leukocytosis by neutrophilia, while serum biochemical analysis revealed increased activities of GGT (mean 96.3 U/L, reference: 20-52 U/L) and ALT (mean 55.0 U/L, reference: 22-38 U/L) and reduced levels of total proteins (mean 5.3 g/dL, reference 6.0-7.9 g/dL), albumin (mean 2.0 g/dL, reference 2.4-3.0 g/dL), and globulins (mean 3.2 g/dL, reference 3.5-7.0 g/dL). Abdominal ultrasonography was performed in one sheep, revealing a large amount of anechoic peritoneal effusion without floating echogenic debris or spots, and distention of hepatic vessels and portal veins. On the other hand, the ultrasonographic examination did not reveal changes in gallbladder, in right kidney and in the size of the liver. Gross pathological findings included severe ascites, moderate hydrothorax and hydropericardium, and liver showing irregular nodular surface, whitish areas and hardened consistency. The ascetic fluid was clear and is volume ranged from 8 to 13.5 liters. Microscopic evaluation of liver revealed hepatocyte necrosis, diffuse deposition of collagen fibers, and ductular proliferation.

Discussion: Definitive diagnosis of poisoning by T. cinerea was made by the association of epidemiological, clinical, laboratory and pathological findings. It is known that the plant is part of the botanical composition of the diet of sheep all year long, but the poisoning becomes important mainly during the dry season. Affected sheep showed a typical ascitic condition due to diffuse liver fibrosis. Main ultrasonographic findings corresponded to hyperechoic diffuse diseases patterns, such as lipidoses and toxic liver diseases. The alterations observed in the biochemical panel are consistent with hepatic damage caused by the plant. The hematological findings are suggestive of immune system interference of poisoned sheep, but it is not possible to infer if it were the direct action of some component(s) of the plant or if it would be secondary to the severe nutritional deficiency induced by the poisoning. The toxic principle of T. cinerea remains undetermined, but it is already known that it is not pyrrolizidine alkaloids. The probable pathophysiological mechanism of ascites is the increased blood pressure on the portal vein walls due to the greater resistance of the liver parenchyma, but there should also be some contribution of hypoalbuminemia, which reduces plasmatic colloid osmotic pressure.