Toxicity effects of toad (Rhinella jimi Stevaux, 2002) venom in chicken (Gallus gallus domesticus).

This study aimed to evaluate the pathological changes that occur after administering different doses of R. jimi (Stevaux, 2002) parotoid glands secretion to Gallus gallus domesticus chicks. Twenty-three animals were used in this study and were divided into 5 groups that received a toad venom dose of 0, 3.0 mg/kg, 6.0 mg/kg, 10.0 mg/kg, and 25.0 mg/kg. After 48 h, the necropsy and pathological examinations were performed. No clinical signs of toxicity were observed in any group. Macroscopically, hepatomegaly, areas of liver necrosis, splenomegaly, necrotic and hemorrhagic cardiac regions, hydropericardium, dark necrotic lesions of Meckel's diverticulum, and hemorrhages in the lungs and kidneys were detected. Histopathological changes included diffuse vacuolar degeneration of hepatocytes, severe sinusoidal congestion, focal areas of hemorrhage in the parenchyma, swollen cardiac fibers, necrotic myocardial fibers, moderate to acute diffuse alveolar hemorrhage, vacuolar degeneration of the renal tubular epithelium, necrosis of renal tubules, and extensive hemorrhagic areas below the brain and cerebellar meninges. In conclusion, pathological changes of the R. jimi toxins in chicks were noted in the heart, spleen, liver, Meckel's diverticulum, lungs, and kidneys. Most of the changes were similar to those observed in humans and animals exposed to toxins from other toad species.

Clinical and pathological effects of Calotropis procera exposure in sheep and rats.

This study aimed to describe the toxic effects resulting from the administration of Calotropis procera (Aiton) W. T. Aiton latex to rats and C. procera leaves to sheep. We studied male sheep that received C. procera leaves by gavage. Twenty male rats were separated into 5 groups and were subjected to an intra-peritoneal injection of fresh C. procera latex (without carrier solvent) at 1.0, 0.6, 0.3 or 0.1 ml of latex/kg of body weight, and control animals were injected with 0.9% NaCl. All rats were treated with the highest dose, but none of the rats from the other groups, died. The histological lesions were restricted to rats dosed with 1.0 ml of latex/kg body weight and included multi-focal coagulation necrosis of cardiac fibers and vacuolized hepatocytes. Subsequently, three groups of two sheep were treated with (1) a single dose of 30 g/kg, (2) a single dose of 60 g/kg or (3) 60 g/kg per day for 10 consecutive days. Exposure to the C. procera leaves was responsible for tachycardia and transitory cardiac arrhythmias in sheep from all groups. Gross pathological analysis of sheep dosed with 60 g/kg per day for 10 days revealed mild ascites, exudates on the trachea, pulmonary edema, mild hemorrhage in the liver, hydropericardium, flaccid heart, ulcers on the abomasum and kidneys presenting pale juxtamedullary cortex. The histological findings of the rat and sheep studies were similar and included multi-focal coagulation necrosis of cardiac fibers and vacuolized hepatocytes. In conclusion, our findings indicate that C. procera is a cardiotoxic and hepatotoxic plant.