Where toxicants interrupt good health
To understand how toxicants cause damage to livestock, look at the biochemistry of the toxicant and where it affects the animal. For example: with sorghums, a cyanogenic glycoside, dhurrin, is formed. Enzymatic action releases free cyanide from dhurrin. Inhibition of cytochrome oxidase causes acute cyanide toxicosis. This results in rapid ATP deprivation and a cascade of symptoms ending in death.
In contrast, tall fescue toxicosis is caused by the endophyte ergot alkaloid ergovaline, which leads to hyperthermia and various heat stress-related symptoms. In fescue toxicosis, blood flow to peripheral tissues is reduced. The animal is unable to dissipate heat normally, causing body temperature to rise. The vasoconstriction effects of the ergot alkaloids contribute to this symptom.
Each toxicant affects different animal biochemical pathways leading to different symptoms and severity of impact. Understanding the biochemistry involved can lead to more appropriate management and preventative measures.
- Goitrogenic glycosides
- Grass tetany
- Mineral toxicities
- Poisonous plants
- Prussic acid (HCN)