Experimental equine aflatoxicosis.
Abstract: Adult male Shetland ponies, two per dose level, were given aflatoxin daily at levels of 0.3, 0.15, or 0.075 mg/kg. Signs of toxicosis included inappetence, depression, tremors, and terminal prostration. Deaths occurred at 12 and 16 days (0.3 mg/kg), 25 and 32 days (0.15 mg/kg), and 36 and 39 days (0.075 mg/kg). Prothrombin time, sulfabromophthalein clearance time, total plasma bilirubin, and icteric index increased markedly before death. Elevations in plasma activity of aspartate amino transferase (AST) were observed 1 to 4 days after the start of aflatoxin administration in the high dose group; the AST activity increased significantly and was generally maintained at elevated levels in all groups. There were no elevations in blood urea nitrogen or plasma activity of creatine phosphokinase. At necropsy generalized icterus, hemorrhages, a brown to tan liver, dark reddish brown urine, and dark brown kidneys were consistently observed. Microscopic lesions included centrilobular fatty change, hepatic cell necrosis, and periportal fibrosis in all ponies. These lesions were more prominent in animals given 0.075 mg/kg and were accompanied by a mild bile duct proliferation. Bile stasis, irregularities in size and shape of hepatocytes, and binucleate hepatocytes were also present. A moderate toxic tubular nephrosis was present in some individuals. Ultrastructurally, both vascular endothelium and hepatocytes were severely damaged. There was consistent evidence of bile stasis and destruction of bile canaliculi. The clinical biochemical and pathological findings suggested that the liver was the target organ and that the renal changes were probably secondary.
Publication Date: 1982-09-30 PubMed ID: 7157368DOI: 10.1016/0041-008x(82)90381-7Google Scholar: Lookup
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- Journal Article
Summary
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This research explores the toxic effects of aflatoxin ingestion in Shetland ponies. In the study, various doses of aflatoxin were administered daily, and it was shown that the toxin caused a variety of harmful symptoms and ultimately, death. The research suggests that the liver was the primary organ affected, with kidney damage likely being a secondary effect.
Study Procedure
- Adult male Shetland ponies were selected for this research and they were divided into three groups, with each group receiving a different dose of aflatoxin daily: 0.3 mg/kg, 0.15 mg/kg, or 0.075 mg/kg.
- Signs of toxicosis were closely monitored in these subject animals. These toxins caused symptoms such as lack of appetite, depression, tremors, and final stage of weakness or exhaustion.
- Death occurred within timeframes which were directly related to the dosage level each group received.
Findings and Observations
- Several key metrics such as Prothrombin time, sulfabromophthalein clearance time, total plasma bilirubin, and icteric index significantly increased before death.
- There were increases in plasma activity of aspartate amino transferase (AST) within 1 to 4 days after the commencement of aflatoxin administration in the high dose group. This AST activity increase was significant and generally remained elevated in all groups.
- During necropsy, conditions such as generalized icterus, hemorrhages, a brown to tan liver, dark reddish brown urine, and dark brown kidneys were consistently observed across animal subjects.
Pathological Changes
- Microscopic examination of the affected animals revealed changes such as centrilobular fatty change, hepatic cell necrosis, and periportal fibrosis in all ponies.
- The researchers also observed a mild bile duct proliferation in animals given the lowest dose of aflatoxin (0.075 mg/kg).
- Additionally, it was discovered through ultrastructural study that both vascular endothelium and hepatocytes were severely damaged. It also confirmed signs of bile stasis and destruction of bile canaliculi.
Conclusion
- The study concluded that aflatoxin ingestion has severe impacts on Shetland ponies, resulting in several pathological changes, biochemical variances, and ultimately death.
- The primary target organ for aflatoxin damage appears to be the liver, with renal (kidney) changes likely as a secondary adverse effect.
Cite This Article
APA
Cysewski SJ, Pier AC, Baetz AL, Cheville NF.
(1982).
Experimental equine aflatoxicosis.
Toxicol Appl Pharmacol, 65(3), 354-365.
https://doi.org/10.1016/0041-008x(82)90381-7 Publication
Researcher Affiliations
MeSH Terms
- Aflatoxins / poisoning
- Alanine Transaminase / blood
- Animals
- Bile Ducts / drug effects
- Bilirubin / blood
- Horses / metabolism
- Liver Function Tests / veterinary
- Male
- Prothrombin Time / veterinary
- Time Factors
Citations
This article has been cited 1 times.- Feng Y, Li M, Zheng Y, Qu H, Li P, Dong B, Wang Y, Liu G, Jia B, Ma Q. Toxicokinetics of a Single Oral Dose of Aflatoxin B(1) in Plasma, Feces, and Urine of Male Donkeys. Toxins (Basel) 2025 Apr 20;17(4).
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