Annual ryegrass toxicosis is a severe, often fatal, neurologic disease of production animals due to ingestion of bacterial corynetoxins. Seed gall bacteria (Rathayibacter toxicus) attach to the outer cuticle of seed gall nematodes (Anguina spp) and are carried into developing seed heads of annual ryegrass (Lolium multiflorum) and several other grass species. Other affected grass species include blown grass (Lachnagrostis filiformis), annual beardgrass (Polypogon monspeliensis), and annual veldt grass (Ehrharta longiflora). Rathayibacter toxicus produces corynetoxins as a result of a complex interaction between the bacteria, the nematode, the host, and an associated bacteriophage (NCPPB3778). Two other Rathayibacter species, R iranicus and Rathayibacter sp EV, are suspected to produce corynetoxins, but have not yet been proven to do so.
Annual ryegrass toxicosis is endemic to agricultural areas of western and southern Australia; it also occurs in South Africa. The disorder has also been reported in geographically distant areas in association with annual ryegrass hay produced in Australia. A similar disease has been reported in the US and New Zealand in association with corynetoxin-like tunicaminyluracil glycolipids from nematode galls in Chewings fescue (Festuca rubra commutata).
Outbreaks usually occur 2–6 days after animals graze a pasture that contains annual ryegrass infected at a toxic level. Death can occur within hours or after a week or more. Characteristic neurologic signs are similar to those of perennial ryegrass toxicosis Perennial Ryegrass Toxicosis in Animals Perennial ryegrass toxicosis is due to secondary metabolites (mycotoxins) produced by Epichloë festucae, an endophyte which can infect perennial ryegrass (Lolium perenne). Clinical... read more . However, mortality from annual ryegrass toxicosis is commonly 40%–50% and occasionally higher. Postmortem lesions include congestion, edema, hemorrhage of the brain and lungs, and degenerative lesions of the liver and kidneys.
Diagnosis is based on the characteristic neurologic signs of tremors, incoordination, rigidity, and collapse when stressed, with animals often behaving apparently normally again when left undisturbed. In severely affected animals, convulsions can 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 annual ryegrass toxicosis from staggers syndromes associated with other forages including perennial ryegrass Perennial Ryegrass Toxicosis in Animals Perennial ryegrass toxicosis is due to secondary metabolites (mycotoxins) produced by Epichloë festucae, an endophyte which can infect perennial ryegrass (Lolium perenne). Clinical... read more , phalaris, paspalum 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 , and other grasses. Polioencephalomalacia Polioencephalomalacia in Ruminants Polioencephalomalacia is a common neurologic disease of ruminants. The main clinical signs reflect dysfunction of the cerebrum and include wandering, circling, cortical blindness, incoordination... read more and enterotoxemia are other differential diagnoses for the clinical signs.
Pathogenesis of Annual Ryegrass Toxicosis in Animals
Annual ryegrass toxicosis is due to corynetoxins, which are glycolipids belonging to the tunicamycin group of antimicrobials. These compounds inhibit N-linked glycosylation of a wide variety of glycoproteins, including enzymes, hormones, cell membrane and extracellular matrix structural components, and membrane receptors. Compromised vascular integrity in the brain causes hypoxic neuronal damage and focal necrosis. Corynetoxins can also cause hepatocellular necrosis, vacuolation, and fatty infiltration. Corynetoxins have proven lethal to all species exposed to them, including horses, donkeys, cattle, sheep, pigs, rats, mice, guinea pigs, and chickens. The oral lethal dose of corynetoxins in sheep administered as a slurry of toxic seed heads is 3.2–5.6 mg/kg. Toxicity is cumulative; lethal dose is the same whether administered as a single large dose or multiple smaller doses up to 2 months apart.
Clinical Signs of Annual Ryegrass Toxicosis in Animals
Ataxia, wide-based stance
Stumbling and falling
Tremors and convulsions
Clinical signs of annual ryegrass toxicosis are neurologic and appear suddenly after external stimulation—most commonly, being forced to move. Signs include staggering and stumbling, ataxia, wide-based stance, tremors, and convulsions. Animals may appear to recover, only to relapse with subsequent stimulation. Cattle may appear disoriented, wandering aimlessly in between convulsive episodes. Sheep can develop an exaggerated, high-stepping gait or a stiff-legged rocking-horse gait when forced to run. Sublethal toxicosis can cause poor wool growth, permanent testicular degeneration, fetal and dam death, and decreased body weight. Onset of clinical signs may be within a few days of exposure to toxic ryegrass pasture or hay, and clinical signs may continue weeks after exposure ceases. Most deaths occur within 24 hours of developing clinical signs.
Diagnosis of Annual Ryegrass Toxicosis in Animals
History of ingesting infected annual ryegrass
Laboratory confirmation (most commonly, immunoassay)
Diagnosis of annual ryegrass toxicosis is made via a combination of compatible clinical signs and a history of exposure to infected ryegrass or other susceptible forage. Bacterial seed galls can be identified grossly.
Postmortem lesions often include accumulation of perivascular eosinophilic material in the brain, particularly in the subarachnoid space of the cerebellum. Less common lesions include Purkinje cell necrosis, swelling of astrocyte processes, and focal degenerative changes.
Various analytical tests are available to confirm diagnosis; however, the most common are immunoassays. A semi-quantitative ELISA protocol has been used to detect and quantify R toxicus in pastures or hay. Another ELISA protocol is available to detect corynetoxins in forage or biological samples. Less common analyses include PCR assay (to identify R toxicus or the associated nematode) and analytical chemistry methods (eg, high-performance liquid chromatography and mass spectrometry) to detect and quantify corynetoxins.
Treatment of Annual Ryegrass Toxicosis in Animals
Removal of source
Minimization of stress and supportive care
No satisfactory medical treatment is available for annual ryegrass toxicosis. A cyclodextrin formulation showed promising results in one study; however, subsequent studies failed to reproduce the favorable results. Treatment is supportive, including removing source material to prevent reexposure and providing supportive care (eg, high-quality nutrition, water, shade, and protection from weather and predation). Anticonvulsants may be necessary to control seizures. Less severely affected animals may eventually recover.
Prevention of Annual Ryegrass Toxicosis in Animals
Inspection of forages for seed galls before feeding
Pasture management strategies
Bacterial seed galls can be identified grossly; forages should be inspected for seed galls before feeding. Useful strategies to prevent annual ryegrass toxicosis can include heavy stocking in winter and spring, strategic application of herbicides, cutting hay or silage before seed heads develop, and burning affected crop residues.
Annual ryegrass toxicosis is caused by bacterial neurotoxins (corynetoxins) in bacterial seed galls of annual ryegrass and other susceptible forages.
There is no effective treatment for annual ryegrass toxicosis; however, less severely affected animals may recover with supportive care.
Prevention includes strategies for controlling seed gall development in pastures as well as examining hay or silage for seed galls before feeding.