Perennial ryegrass toxicosis is due to secondary metabolites (mycotoxins) produced by Epichloë festucae, an endophyte which can infect perennial ryegrass (Lolium perenne). Clinical signs of perennial ryegrass toxicosis can include muscle tremors and fasciculations, ataxia, a stiff or spastic gait, weakness, recumbency, heat stress, dehydration, collapse, and death. Treatment relies on removing affected forage and minimizing stress to animals.
Endophyte-infected perennial ryegrass (Lolium perenne) can contain a wide variety of alkaloids produced by the fungus, some of which are toxic to mammalian herbivores. Alkaloid profiles vary depending on the ryegrass cultivar, the endophyte strain, the environmental conditions during plant growth, and the time of year. Tremorgenic indole diterpenes, primarily lolitrem B and epoxy-janthitrems, are responsible for the neurologic syndrome known as ryegrass staggers. The syndrome has been reported in horses, cattle, and sheep. Most outbreaks have occurred in Australia and New Zealand, with sporadic cases occurring in Europe and the Americas. Ergopeptine alkaloids, primarily ergovaline, can cause vasoconstriction, thermoregulatory dysfunction, heat stress, agalactia, dystocia, and prolonged parturition. Type and severity of clinical signs vary depending on alkaloid profile, animal species affected, and environmental conditions, and can range from slight production decreases to catastrophic losses.
Pathogenesis of Perennial Ryegrass Toxicosis in Animals
Perennial ryegrass toxicosis is due to lolitrem B and other indole diterpenes. These inhibit large-conductance calcium-activated potassium channels (BK channels), which are responsible for cellular hyperpolarization and cessation of an action potential. Inhibition of these channels leads to prolonged cellular depolarization and sustained impulse transmission at the motor endplate.
Ergovaline and other ergopeptine alkaloids are structurally similar to biogenic amines, facilitating nonspecific interaction with dopaminergic, serotonergic, and adrenergic receptors throughout the body. Ergopeptine alkaloids can act as agonists, antagonists, and partial agonists, depending on receptor location and subtype. Physiologic effects include vasoconstriction and suppressed prolactin release.
Clinical Signs of Perennial Ryegrass Toxicosis in Animals
Muscle tremors and fasciculations
Stiff or spastic gait
Collapse and recumbency
Heat stress and dehydration
Clinical signs of perennial ryegrass toxicosis usually develop within 2 or 3 days of exposure to toxic amounts of alkaloids. Animals can develop a variety of clinical signs, alone or in combination. Possible neurologic abnormalities include head tremors and muscle fasciculations; stiff, spastic, or hypermetric gait; ataxia and incoordination; collapse; opisthotonos, nystagmus, and extensor rigidity. Signs are precipitated or exacerbated by exercise, loud noises, or when animals are otherwise startled or frightened. Animals may recover and appear completely normal between episodes.
Other possible clinical signs are similar to those that occur with fescue or ergot toxicosis, and include decreased feed intake, poor body condition, a rough, unkempt coat that fails to shed appropriately, decreased milk production, lameness, and heat stress. In temperate geographic areas, mild heat stress can cause decreased production, because animals spend less time grazing and more time seeking shade and water. In hotter, drier climates, severe heat stress can cause panting, drooling, dehydration, collapse, and death due to heat stroke or misadventure. Massive death losses have occurred in Australia due to dam crowding (ie, heat-stressed animals seeking relief wade into water sources and drown).
Diagnosis of Perennial Ryegrass Toxicosis in Animals
Compatible clinical signs
History of ingesting perennial ryegrass
Alkaloid quantitation of perennial ryegrass
A complete dietary history, including composition of pasture, hay, and other forages, can confirm or rule out the presence of perennial ryegrass. Other possible causes of the clinical signs, including annual ryegrass, dallisgrass, tall fescue, and ergotized grasses or grains should also be considered as differential diagnoses or compounding factors if present in the diet.
Chemical analysis of perennial ryegrass, often using high-performance liquid chromatography, can determine concentrations of any toxic alkaloids present. Detection of toxic alkaloids at or above tolerance levels can confirm a suspected diagnosis.
Treatment of Perennial Ryegrass Toxicosis in Animals
Removal of affected forage
Minimization of stress
Heat-stress mitigation measures
Removing affected forage and minimizing stress to the patients are key to facilitating recovery from perennial ryegrass toxicosis. Shade structures, fans, and sprinklers can provide animals relief from high ambient temperatures. Proximity to ample clean, fresh water is important to prevent dehydration. Protective measures such as providing water in troughs can allow animals access to water but prevent them from drowning. Domperidone has been used to facilitate prolactin release from the pituitary ( See also page Fescue Poisoning in Animals) and can be useful for individual animals. Treatment is generally not logistically or financially practical in a herd situation. Consideration must also be given as to whether the stress of handling animals may offset any potential benefits of treatment.
Mildly affected animals generally recover from neurologic abnormalities within several days after cessation of exposure. More severely affected animals can take longer to recover, as can those with heat stress, loss of condition, decreased production, and other clinical signs.
Prevention of Perennial Ryegrass Toxicosis in Animals
Adherence to good grazing management practices
Mixed pasture use (rather than monoculture)
Use of novel endophytes or endophyte-free perennial ryegrass strains
Lolitrems and ergopeptines are concentrated in the leaf sheath and inflorescences. Preventing overgrazing and cutting hay or baleage before the plants flower can minimize alkaloid concentrations in forage even when the endophyte is present. Encouraging growth of other grass species and legumes in established perennial ryegrass swards also decreases the intake of toxic grass.
Safe new pastures can be established using endophyte-free perennial ryegrass seed (seed that has been stored at ambient temperatures for 18–24 months probably contains few viable endophytes and would produce nontoxic pastures). However, alkaloids produced by the endophytes confer upon the plant resistance to insect attack, giving endophyte-infected strains a competitive advantage over endophyte-free strains.
Several cultivars of perennial ryegrass available are infected with strains of endophyte that do not produce lolitrem B or ergovaline. Some of these strains produce higher concentrations of epoxy-janthitrems, which can produce staggers when ingested in high concentrations; however, these are considered much less toxic than lolitrem B. These strains may offer the best compromise, providing a high level of insect resistance to the plants while minimizing detrimental effects to production animals.
Key Points
Perennial ryegrass toxicosis is due to alkaloids (mycotoxins) produced by the perennial ryegrass endophyte.
There is no practical medical treatment for perennial ryegrass toxicosis in most cases; however, less severely affected animals may recover with supportive care including mitigation of heat stress.
Prevention includes grazing management strategies, encouraging growth of other grasses and legumes in ryegrass pastures, and use of perennial ryegrass strains infected with novel endophytes.
For More Information
Also see pet health content regarding ryegrass poisoning.
