Cynoglossum officinale (hound’s-tongue)–a cause of pyrrolizidine alkaloid poisoning in horses.

This research presents evidence that ten horse deaths were caused by consuming grass hay with hound’s-tongue, a plant that causes pyrrolizidine alkaloid poisoning, which results in weight loss, photosensitization, and liver damage.

Study of Pyrrolizidine Alkaloid Poisoning in Horses

• The core concern of this research paper is an investigation into the deaths of ten horses that were suspected to have been caused by the ingestion of hound’s-tongue, a plant also known by its scientific name Cynoglossum officinale. This plant is known to contain toxic pyrrolizidine alkaloids, which are destructive to the liver of horses, and can result in symptoms such as weight loss, icterus (jaundice-like symptoms), photosensitivity, and hepatic encephalopathy (brain disorder due to liver damage).
• The study design involved a retrospective analysis of affected horses that exhibited significant health issues and tracing back their feed to establish a common denominator. This revealed that the horses had been fed on dried grass hay that contained hound’s-tongue.

Histologic Findings and Evidence of Toxicity

• Using histologic examination, which is the microscopic study of tissue, the liver of three of the affected horses was analyzed post-mortem. The examination revealed liver damage that is characteristically associated with pyrrolizidine alkaloid poisoning. The main findings were megalocytosis (a condition involving abnormally large cells), biliary hyperplasia (an increase in the number of bile duct cells), and fibrosis (thickening and scarring of connective tissue).
• Upon analysis of the hound’s-tongue plant itself, it was found to contain a significant quantity of toxic pyrrolizidine alkaloids, in the range of 0.6% to 2.1% on a dry matter basis. To definitively determine the effect of the alkaloids from hound-tongue on horses, the researchers fed one pony with it for a period of 20 days. This resulted in liver fibrosis and biliary hyperplasia, thereby conclusively establishing the toxicity potential of the plant.