Natural and experimental poisoning of goats with the pyrrolizidine alkaloid-producing plant Crotalaria retusa L.

Crotalaria retusa L. (rattleweed), estimated to contain about 4.96% monocrotaline (MCT) in the seed, was associated with a natural poisoning outbreak in goats. The poisoning was experimentally reproduced by the administration of C. retusa seeds containing approximately 4.49% of MCT. Thus, 1 of 3 goats given a single dose of 5 g/kg bodyweight (bw) of seeds (248 mg MCT/kg bw) and 2 goats given a single dose of 347 mg MCT/kg bw showed acute clinical signs and were euthanized 10-11 days after dosing. Clinical signs and gross and histologic lesions were characteristic of acute centrilobular liver necrosis.

Pulmonary and hepatic lesions caused by the dehydropyrrolizidine alkaloid-producing plants Crotalaria juncea and Crotalaria retusa in donkeys.

The effects and susceptibility of donkeys to Crotalaria juncea and Crotalaria retusa poisoning were determined at high and low doses. Seeds of C. juncea containing 0.074% of dehydropyrrolizidine alkaloids (DHPAs) (isohemijunceines 0.05%, trichodesmine 0.016%, and junceine 0.008%) were administered to three donkeys at 0.3, 0.6 and 1 g/kg body weight (g/kg) daily for 365 days. No clinical signs were observed and, on liver and lung biopsies, the only lesion was a mild liver megalocytosis in the donkeys ingesting 0.6 and 1 g/kg/day. Two other donkeys that received daily doses of 3 and 5 g seed/kg showed initial respiratory signs 70 and 40 days after the start of the administration, respectively. The donkeys were euthanized following severe respiratory signs and the main lung lesions were proliferation of Clara cells and interstitial fibrosis. Three donkeys ingested seeds of C. retusa containing 5.99% of monocrotaline at daily doses of 0.025, 0.05 and 0.1 g/kg for 365 days. No clinical signs were observed and, on liver and lung biopsies, the only lesion was moderate liver megalocytosis in each of the three donkeys. One donkey that received a single dose of 5 g/kg of C. retusa seeds and another that received 1 g/kg daily for 7 days both showed severe clinical signs and died with diffuse centrilobular liver necrosis. No lung lesions were observed. Another donkey that received a single dose of 2.5 g/kg of C. retusa seeds showed no clinical signs. The hepatic and pneumotoxic effects observed are consistent with an etiology involving DHPAs. Furthermore, the occurrence of lung or liver lesions correlates with the type of DHPAs contained in the seeds. Similarly as has been reported for horses, the data herein suggest that in donkeys some DHPAs are metabolized in the liver causing liver disease, whereas others are metabolized in the lung by Clara cells causing lung disease.

Comparative potential therapeutic effect of sesame oil and peanut oil against acute monocrotaline (Crotalaria) poisoning in a rat model.

BACKGROUND: Many Crotalaria plant species contain hepatotoxic pyrrolizidine alkaloids (such as monocrotaline) that can cause acute and chronic poisoning in cattle and other animals. HYPOTHESIS: Peanut oil, atropine sulfate, and antidiarrheal agents are used to treat acute monocrotaline poisoning. The effect of sesame on acute monocrotaline poisoning has never been investigated. ANIMALS: Fifty male Sprague-Dawley rats were used for toxicity studies. METHODS: Experiment 1: Group I, control. Groups II-IV were given monocrotaline (205.2 mg/kg) and euthanized 6, 12, and 24 hours later. Experiment 2: Group I, control. Group II monocrotaline alone (205.2 mg/kg). Groups III-VI were given monocrotaline (205.2 mg/kg) and 1 hour later, Groups III and IV were given sesame oil (1 and 2 mL/kg) and Groups V and VI were given peanut oil (1 and 2 mL/kg). RESULTS: Monocrotaline significantly decreased (P < .05) serum amylase activity, but, over time, increased (P < .05) pancreatic and lung injury. AST and ALT activity and liver injury peaked at 24 hours. Sesame oil and peanut oil (P < .05) inhibited the changes in all tested parameters in acute monocrotaline poisoning. Although peanut oil inhibited acute monocrotaline poisoning, it induced steatosis, but sesame oil did not. CONCLUSION AND CLINICAL IMPORTANCE: We hypothesize that early pancreatic and lung injury and late liver injury contribute to acute monocrotaline poisoning and that sesame oil is more efficacious than peanut oil against acute monocrotaline poisoning in rats. However, additional studies are needed to confirm that these oils have the same effects in cattle and other animals.

Poisoning of sheep by seeds of Crotalaria retusa: acquired resistance by continuous administration of low doses.

Seeds of Crotalaria retusa containing 6.84% (dry weight) of monocrotaline (MCT) were administered experimentally to sheep. Three sheep that received 136.8mg MCT/kg bw daily for 70 days had no clinical signs. Five out of six sheep ingesting single doses of 205.2 and 273.6mg MCT/kg bw died with acute (three sheep) or chronic intoxication (two sheep). Acute intoxicated sheep had periacinar liver necrosis and chronic intoxicated sheep liver fibrosis and megalocytosis. Another three sheep had no clinical signs after the ingestion of 20 daily doses of 136.8mg MCT/kg, followed by seven doses of 273.6mg MCT/kg, and one single dose of 342mg MCT/kg. These experiments demonstrated that sheep are susceptible to acute intoxication by MCT being intoxicated by a single oral dose of approximately 205.2mg/kg. In contrast, they develop strong resistance to MCT after the daily ingestion of non lethal doses (136.8mg/kg). It is suggested that chronic poisoning does not occur by the repeated ingestion of non acutely toxic doses, but probably by the ingestion of single toxic doses. It is also suggested that sheep do not become intoxicated with the ingestion of C. retusa in the vegetative non-seeding stage.