Ryegrass is found in pastures throughout the world. Without careful management, it can be toxic to horses and other livestock.
Annual Ryegrass Staggers
This often deadly toxic disease affects the nervous system. It is seen in livestock of any age that graze pastures in which annual ryegrass (Lolium rigidum) is in the seedhead stage of growth (western and southern Australia and in South Africa from November to March). Hay of Festuca rubra commutata (Chewing's fescue) with Rathayibacter toxicus-infected seedhead galls has caused a similar disease in horses in Oregon.
In Australia, the responsible toxins are caused by a microscopic worm that carries a bacteria into seedhead galls of annual ryegrass. These bacteria-infected galls are present from early spring onward, but they are most toxic when the plants mature. Hence, animals show no signs until late spring and summer. Spread of worms to nearby healthy annual ryegrass pastures is slow.
Outbreaks occur 2 to 6 days after animals graze a pasture that contains infected annual ryegrass. Deaths can occur within hours, or up to 1 week after signs begin. Tissue changes include congestion, fluid buildup, ruptured blood vessels of the brain and lungs, and degeneration of the liver and kidneys.
Diagnosis is based on the characteristic nervous system signs of tremors, lack of coordination, rigidity, and collapse when stressed, with animals often becoming apparently normal again when left undisturbed. Nervous spasms can begin unexpectedly, and convulsions can be caused suddenly by either forced exercise or very hot weather. A thorough history and evaluation of the pastures will help differentiate staggers caused by other grasses.
Signs identical to those of annual ryegrass toxicity have recently been described in Australia in animals grazing annual blown grass (Agrostis avenacea), annual beard grass (Polypogon monspeliensis), or annual veldtgrass (Ehrharta longiflora) infected with worm galls. These diseases have been called flood plain staggers, Stewart range syndrome, and veldtgrass staggers, respectively.
Perennial Ryegrass Staggers
This toxic condition affects the nervous system of grazing livestock and horses of all ages only in late spring, summer, and fall and only in pastures in which perennial ryegrass (Lolium perenne) or hybrid ryegrass are the major components. This includes parts of North and South America, Europe, and Australia.
The toxins are produced in perennial and hybrid ryegrasses infected with the fungus Neotyphodium lolii. The amounts in infected plants increase to toxic levels as the temperature rises in late spring and decrease again to safe levels in cooler weather.
The toxin affects the nervous system, causing lack of coordination. It also raises the temperature of animals in the warmer months of the year, causing heat stress. Signs develop gradually over a few days, beginning with fine tremors of the head and nodding movements. Noise, sudden exercise, or fright causes more severe head nodding with jerky movements and lack of coordination. Running movements are stiff and uncoordinated, often resulting in collapse with muscle spasms causing backward arching of the head, neck, and spine, involuntary rhythmic movement of the eyes, and flailing of stiffly extended limbs. In less severe cases, the attack soon subsides and within minutes the animal regains its feet. If the animal is again forced to run, the episode is repeated. The death rate is low (0 to 5%). Deaths are usually accidental, often by drowning when drinking from ponds or streams, or because the animals are unable to forage for food and water.
Because movement and handling of animals worsens signs, individual treatment is generally impractical. The condition resolves on its own in 1 to 2 weeks if animals are moved to nontoxic pastures or crops.
Last full review/revision July 2011 by Barry R. Blakley, DVM, PhD; Cheryl L. Waldner, DVM, PhD; Rob Bildfell, DVM, MSc, DACVP; William D. Black, MSc, DVM, PhD; Herman J. Boermans, DVM, MSc, PhD; Cecil F. Brownie, DVM, PhD, DABVT, DABT, DABFE, DABFM, FACFEI; Raymond Cahill-Morasco, MS, DVM; Keith A. Clark, DVM, PhD; Gregory F. Grauer, DVM, MS, DACVIM; Sharon M. Gwaltney-Brant, DVM, PhD, DABVT, DABT; Larry G. Hansen, PhD; Safdar A. Khan, DVM, MS, PhD, DABVT; Garrick C. M. Latch, MASc, PhD; Gavin L. Meerdink, DVM, DABVT; Lisa A. Murphy, VMD; Frederick W. Oehme, DVM, PhD; Gary D. Osweiler, DVM, MS, PhD; Mary M. Schell, DVM; David G. Schmitz, DVM, MS, DACVIM (LA); Norman R. Schneider, DVM, MSc, DABVT