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Perennial Ryegrass Staggers


Wayne Simpson

, MSc (Microbiology), BHort Sc, DipHort, Endophyte Mycology, Forage Improvement Section, AgResearch Limited

Last full review/revision Aug 2013 | Content last modified Jun 2016

This neurotoxic condition of grazing livestock of all ages occurs only in late spring, summer, and fall and only in pastures in which perennial ryegrass (Lolium perenne) or hybrid ryegrass are the major components. Sheep, cattle, horses, farmed deer, and llamas are susceptible. In New Zealand, a high incidence most years causes considerable loss and seriously disrupts management procedures and stock movement. Perennial ryegrass staggers occurs sporadically in parts of North and South America, Europe, and Australia.

The tremorgenic neurotoxins responsible are lolitrems, mainly lolitrem B. These indole diterpene alkaloids are produced in perennial and hybrid ryegrasses infected with the endophytic fungus Neotyphodium lolii. The amounts of fungal hyphae and lolitrem B in infected plants increase to toxic levels as the temperature rises in late spring and decrease again to safe levels in the cooler seasons. Mycelia of the fungus are present in all above-ground parts of infected plants but are especially concentrated in leaf sheaths, flower stalks, and seed. Infected plants exhibit no signs, and the fungus is spread only through infected seed. Viability of the endophyte gradually declines when infected seed is stored at ambient temperatures and moderate to high humidity, so that few seeds contain viable endophyte after 2 yr. Lolitrem B acts as a potent large conductance calcium-activated potassium (BK) channel inhibitor. It is thought that the incoordination observed when animals are exposed to lolitrem B is caused by interference with neuronal transmission in the cerebellum; no specific histologic lesion is recognized. N lolii also produces the ergopeptine alkaloid ergovaline, which is the alkaloid responsible for fescue toxicosis. Ergovaline raises the temperature of animals in the warmer months of the year, inducing heat stress. It also depresses prolactin levels, and reduced milk yield in cows has been recorded in New Zealand and Australia.

Signs develop gradually over a few days. Fine tremors of the head and nodding movements are the first signs noted in animals approached quietly and watched carefully. Noise, sudden exercise, or fright elicits more severe signs of head nodding with jerky movements and incoordination when first moved. Running movements are stiff and bounding with marked incoordination and often result in collapse in lateral recumbency with opisthotonos, nystagmus, and flailing of stiffly extended limbs. In less severe cases, the attack soon subsides, and the animal regains its feet within minutes. If the animal is again forced to run, the episode is repeated. Signs are most severe when the animal is heat stressed.

Within flocks and herds, individual susceptibility varies greatly, and this trait is heritable. In outbreaks, morbidity may reach 80%–90%, but mortality is low (0–5%). Deaths are usually accidental, often by drowning when drinking from ponds or streams, or due to the inability to forage for food and water.

The strict seasonal occurrence of characteristic tremors, incoordination, and collapse in several or many animals grazing predominantly perennial ryegrass pastures strongly implicates this disease. Reference to the botanical composition of the pastures will exclude annual ryegrass toxicity (see Annual Ryegrass Staggers Annual Ryegrass Staggers This often fatal neurotoxic disease occurs in livestock of any age that graze pastures in which annual ryegrass (Lolium rigidum) is present and in the seedhead stage of growth. It is... read more ) and paspalum staggers (see Paspalum Staggers in Animals Paspalum Staggers in Animals The incoordination known as paspalum staggers results from eating paspalum grasses (Paspalum spp) infested by Claviceps paspali and C clavispora. The life cycle of this... read more ), which have similar clinical signs and seasonality. Microscopic examination of the leaf sheaths of the ryegrass sward will reveal the extent of endophyte infection.

Because movement and handling of animals exacerbates signs, individual treatment is generally impractical. Recovery is spontaneous in 1–2 wk if animals are moved to nontoxic pastures or crops.

Because the endophyte and the lolitrems and ergovaline are not uniformly distributed within ryegrass plants, control by grazing management can help reduce or prevent the disease. Lolitrems and ergovaline are concentrated in the leaf sheath and inflorescences. If pastures are not overgrazed down into the leaf sheath zone or grazed when the plants are flowering, then animals should be relatively safe even when a high proportion of the ryegrass plants are infected with endophytes. Encouragement of growth of other grass species and legumes in established swards also reduces the intake of toxic grass.

Safe new pastures can be established using ryegrass seed with little or no endophyte infection. Alternatively, seed that has been stored at ambient temperatures for 18–24 mo probably contains few viable endophytes and would produce nontoxic pastures. However, the presence of endophyte in grasses makes the plants resistant to attack from many insects; thus, infected pastures are more persistent than endophyte-free pastures. Cultivars of ryegrass artificially infected with a strain of endophyte that does not produce lolitrem B or ergovaline are available in New Zealand. Signs of ryegrass staggers have not been seen in animals grazing these grasses. A strain of Neotyphodium that produces compounds known as epoxy janthitrems has been developed that offers an extended range of pasture insect resistance with the trade-off of sporadic occurrence of low-level staggers.

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