Many plants contain cyanogenic glycosides that act as deterrents to snails and insects. Within the plant the cyanide-containing compound is linked to a sugar and is harmless. When the plant is damaged (e.g. by chewing), hydrogen cyanide is released by hydrolysis.
In the body the cyanide blocks cellular respiration and in most situations results in sudden death. Affected animals may be seen to stagger for a short time before they collapse.
Perennial pastures that occasionally produce cyanogenic glucosides include birdsfoot trefoil, white clover, couch grass and greater lotus, but it is a very rare condition.
In WA an extremely unusual situation occurred where goats fed branches of Acacia saligna died from cyanide poisoning. This fodder tree is normally considered safe and not to contain cyanogenic glycosides.
However, the branches fed had been pruned because of gross malformations due to a heavy thrip and virus infection and these processes had induced the infected branches to produce cyanogenic glycosides. The normal (uncut) branches contained no cyanogenic glycosides.
Stagger syndromes:
There are a number of stagger syndromes involving different plants. In all cases, clinical signs are brought on or exacerbated by exercise. The conditions ‘perennial ryegrass staggers’, ‘phalaris staggers’, ‘paspalum staggers’ and ‘tagasaste staggers’ are specific to these species and are described under livestock disorders in the relevant species description.
Poisoning by ergot alkaloids (ergotism):
Ergot alkaloids are produced in the ergots of the fungus Claviceps purpurea, which can be found in the seed heads of some of the perennial grasses (couch, Paspalum dilatatum), or by the endophytic fungi Neotyphodium coenophialum in tall fescue and N. lolii in perennial ryegrass.
Ingestion of these alkaloids results in three prominent clinical syndromes – hyperthermia (pathologically high body temperatures), gangrenous ergotism (affecting peripheral parts of the body such as ears, tip of tail and hooves) and agalactia (substantially reduced or non-secretion of milk)/extended gestation/abortion. Generally, hyperthermia occurs in association with warmer temperatures and gangrenous ergotism with cooler temperatures.
Nitrate poisoning:
As a general rule, any plant containing greater than 1.5% potassium nitrate equivalent (DM) is considered at risk of causing nitrate poisoning, however the concentrations associated with clinical disease are frequently more than 5%.
Nitrate is converted in the rumen to nitrite, which when absorbed oxidises the iron in haemoglobin, rendering it ineffective in carrying oxygen around the body. This results in rapid and deep breathing, muscle weakness, coma and rapid death.
Nitrate poisoning appears similar to cyanide poisoning. Pregnant ruminants that survive a clinical episode of nitrate poisoning will often abort. Long-term intake of nitrate at levels just below those likely to cause clinical nitrate poisoning have been associated with, but not proven to cause, abortion, congenital abnormalities, reduced production and goitre.
Perennial pastures that have the potential to cause nitrate poisoning include lucerne, perennial ryegrass, kikuyu, small leaf bluebush and saltbush.
Specific plant associated conditions:
There are several conditions associated with specific pasture species: phalaris sudden death syndromes; kikuyu poisoning; ‘red gut’ (twisted intestine) in sheep grazing lucerne; and bloat in cattle grazing lucerne, strawberry clover and white clover. These conditions are discussed under livestock disorders in the relevant species descriptions.
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