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 seen in 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 cattle and horses in Oregon. Outbreaks of ergot alkaloid toxicity in cattle on L rigidum have been reported in South Africa and should not be confused with annual ryegrass staggers.
In Australia, the responsible corynetoxins (members of the tunicaminyluracil group) are produced in seedhead galls induced by the nematode Anguina funesta and colonized by R toxicus. These bacteria-infected galls are present in infected annual ryegrass pastures from early spring onward, but they are most toxic when the plants senesce. Hence, animals show no sign of toxicity until late spring and summer. Spread of bacteria-infested nematodes to adjacent healthy annual ryegrass pastures is slow.
The corynetoxins are highly toxic glycolipids that inhibit specific glycosylation enzymes and therefore deplete or reduce activity of essential glycoproteins. Experimentally, the corynetoxins deplete fibronectins and cause failure of the hepatic reticuloendothelial system. Cardiovascular function and vascular integrity are consequently impaired, and peripheral circulation and oxygen distribution is compromised. Tunicamycin irreversibly downregulates the expression of specific γ-aminobutyric acidA receptors and causes cell death in cultured brain neurons. Hence, the clinical expression of the disorder is nervous.
Outbreaks occur 2–6 days after animals graze a pasture that contains annual ryegrass infected at a toxic level. Deaths occur within hours, or as long as 1 wk after onset of signs. Characteristic neurologic signs are similar to those of perennial ryegrass staggers (see Perennial Ryegrass Staggers). However, mortality from annual ryegrass toxicity is commonly 40%–50% and occasionally higher. The lesions include congestion, edema, hemorrhage of the brain and lungs, and degeneration of the liver and kidneys.
Diagnosis is based on the characteristic neurologic signs of tremors, incoordination, rigidity, and collapse when stressed, with animals often becoming apparently normal again when left undisturbed. When animals are severely affected, nervous spasms supervene, and convulsions could be precipitated by either forced exercise or high ambient temperatures. A thorough history and evaluation of the pastures will assist in differentiation of staggers caused by other grasses such as perennial ryegrass, phalaris, and the ergots of paspalum and other grasses. Polioencephalomalacia and enterotoxemia are other differential diagnoses.
Clinical signs identical to those of annual ryegrass toxicity have been described in Australia in animals grazing Agrostis avenacea (annual blown grass), Polypogon monspeliensis (annual beard grass), or Ehrharta longiflora (annual veldtgrass) infected with nematode galls containing R toxicus. These diseases have been called flood plain staggers, Stewart range syndrome, and veldtgrass staggers, respectively. Although the same bacterium is responsible for all the diseases, the Anguina nematode vectors of R toxicus for these three grasses are different species than the A funesta associated with annual ryegrass toxicity. Whereas the inflorescences of annual ryegrass infected with A funesta usually appear normal, nematode-infested inflorescences of these other grasses show distinctive signs.
A significant increase in survival of sheep experimentally poisoned with tunicamycin was observed after treatment with derivatives of β-cyclodextrin. The promising result with this toxin-binding agent offers hope for treatment of animals once they have become affected with annual ryegrass staggers. Losses from the disorder can be minimized by early recognition of signs and removal to safe grazing or by reducing grazing pressure. Gall identification is difficult in annual ryegrass pastures, and in south Australia the bacterium in emerging seedheads is detected and quantified by ELISA. Early detection of toxic fields enables farmers to mow the heads off grass or to allow grazing before the grass becomes too toxic. Grazing of hay aftermath from toxic pastures should be avoided. Burning annual ryegrass pastures in the fall destroys most of the galls colonized by bacteria and minimizes the risk of toxicity in the following season.