Ryegrass staggers (RGS) is a nervous disease of sheep, cattle, horses and deer. The disease is common in NZ and Australia, and is reported from several other countries. The disease was of minor importance in Australasia but in the past 10 to 20 years outbreaks have become more frequent and more serious. RGS (sometimes called perennial ryegrass staggers) should not be confused with grass staggers (hypomagnesaemia) or annual ryegrass toxicity, a serious and usually fatal disease of sheep in Australia. Ryegrass staggers occurs in animals grazing pastures dominant in perennial ryegrass (Lolium perenne). Outbreaks occur mainly in summer and autumn under close grazing conditions.
Ryegrass staggers is very common and can be serious. Although the direct mortality rate from is low, the high morbidity rate may lead to significant mortality or misadventure and attack by predators. Affected stock are frequently drowned in dams, attacked by gulls and caught in hazards such as gullies, ditches and fences.
Losses from such sources may vary from 2% to 10% in serious ryegrass seasons. There is mounting evidence that sheep in seriously affected flocks have reduced growth rates and sheep may even have difficulty in mating.
Movement of animals is difficult and such procedures as rotational grazing and vital summer drenching of lambs may have to be totally abandoned until signs have subsided. Under such circumstances serious episodes of parasitism (e.g. haemonchosis) have occurred.
Farmers are often forced to use additional supplementary feed and labour to reduce the effects of a severe outbreak.
A symbiotic fungal endophyte (Neotyphodium lolii, previously Acremonium lolii) in perennial ryegrass which produces neurotoxins is responsible for this disease. A related endophyte, N. occultans, occurs in some cultivars of Italian ryegrass (L. multiflorum) but does not cause disease. N. lolii is likely to be present in hybrid ryegrasses.
The ryegrass / endophyte combination produces several toxins:
The endophyte is found in the leaf, sheath, stem, and seed of L. perenne. It completes its life cycle within the ryegrass and does not produce spores transmission is seedborne rather than from plant to plant. The endophyte does not survive storage in the seed for more than 2 - 3 years, although high temperature and humidity reduce its viability. The fungicide prochloraz, has also been used experimentally to produce low endophyte plants, although fungicides are generally less effective against endophytes.
Lolitrem B is found in highest concentration in the leaf sheath of the outer or oldest leaves and the seeds, particulary in the summer and early autumn. Thus grazing the lower parts of the plant will produce the greatest numbers of stock with ryegrass staggers. Toxins will survive in hay and silage.
The endophyte confers a wide range of benefits on the grass, not all of which can be attributed to the three main toxins.
Ryegrass may be examined for endophyte by the following method although the procedure is of limited value since 99% of ryegrass in the North Island and 70% in the South Island will contain some endophyte:
1. Discard the outer drying leaves.
2. Place the sheath (the part below the ligule) in a test tube.
3. Pour on Poppi stain (0.06g aniline blue dissolved in 50ml of lactic acid with 250ml of distilled water. Add 50ml glycerine and 50g phenol).
4. Boil 5 min or leave overnight.
5. Mount next day in lactophenol (phenol 20g; lactic acid 16.7ml; glycerine 40ml; water 20ml).
Lolitrem and ergovaline can be quantified using HPLC, but this is only suitable for reasearch rather than routine analysis. ELISA have also been developed.
The mechanism of neurotoxicity has not been established, however, paxilline (and most other fungal tremorgens, possiblly including lolitrem B) block high conductance calcium activated potassium (BK) channels which can regulate neurotransmitter release. This may be the mechanism for the effects on the gut and blood vessels but the mechanism of effects on skeletal muscle is less clear.
ryegrass staggers in a sheep Flash movie (5.3MB) or Quicktime movie (4.5MB)
Morbidity rates vary considerably between flocks and seasons. There is also a wide range of susceptibility to the disease.
On casual examination animals at rest show few obvious clinical signs. However, when disturbed and made to walk or run the clinical signs immediately become apparent. As forced movement continues, the signs increase in severity until a maximum response is reached which indicates the extent and severity of the disease present in the flock or herd.
Sheep develop signs within 7 14 days of being placed on toxic pastures. The mildest clinical signs are a slight trembling of the head and fasciculation of the skin muscles of the neck, shoulder and flank regions. As the neuromuscular disorder progresses, there is head nodding and jerky limb movements. Interference with postural reflexes follows; seen as swaying while standing and staggering during movement. As the condition worsens a stiff legged stilted gait may develop with short prancing steps, usually resulting in collapse to the ground. Sheep roll in lateral recumbency with head extended, arched back and rigid extended limbs held in a tetanic spasm of several minutes' duration.
This is followed by sudden muscular relaxation and apparent recovery. The animal then slowly regains its feet and walks away, often still showing tremors but with very little locomotory incoordination.
Rams may have greatly reduced sperm counts.
The signs seen in cattle are similar to those seen in sheep.
The clinical signs in horses are similar to other grazing animals. In severe cases, horses may develop a persistent unsteadiness. In one outbreak of ryegrass staggers in horses the following clinical signs were observed:
Seven horses out of a group of 45 (varying ages and breeds, both sexes) were acutely afflicted clinical signs included normal appetites, with hypermotile intestinal sounds, and mild to severe ataxia. All horses would stand with a sawhorse stance and stumble when forced to walk, often losing their balance. The most severely affected horse could hardly walk, and would easily lose its footing when the tail was pulled laterally, and would go recumbent when blindfolded. All horses slowly recovered following removal of the suspect hay, except for one filly that was recumbent for 2 days and was euthanised due to self inflicted trauma. The hay turned out to be 100% perennial ryegrass that had the seed heads intact and present. The hay contained extemely high levels of both lolitrem B and ergovaline.
Following an attack of ryegrass staggers, working horses may be unreliable for riding or driving for some time. Evaluation of the horse’s condition should be done before putting a horse back into work.
The predominant clinical signs of ryegrass staggers in young alpacas are head and neck tremors. Alpacas seem to be particularly sensitive, and should probably be kept off ryegrass over autumn.
There are no specific haematological or serum biochemical changes with ryegrass staggers. In the most severe cases there may be elevations in serum aspartate transaminase and creatine phosphokinase. No macroscopic changes are present in the nervous system.
In protracted cases histological lesions in the Purkinje cell axons have been reported. These are eosinophilic swellings (torpedoes). It has not been proven whether these changes are induced by the toxins directly or, as has been suggested, are the response to a number of factors, including repeated anoxic insults. Never the less, some diagnostic reports go as far as stating “The diagnosis of RGS was confirmed by the demonstration of spheroids in the inner granular layer of the cerebellum”.
Clinical signs and time of year.
Cattle and sheep other mycotoxins, lead poisoning, hypomagnesaemia (BSE?).
Horses neurological form of equine herpesvirus 1.
There is no known antidote for lolitrem B. Removing animals from the toxic pasture and providing other feed is the only practical treatment. Supportive care and feeding are necessary in severe cases.
The main preventative measure is to reseed paddocks with ryegrass cultivars containing "safe" endophyte varieties. The commonest is AgResearch's AR1 (in more than 50% of ryegrass seed sown in autumn 2004), which produces peramine to deter pests (but is not as good as wild endophyte) but no lolitrem or ergovaline. Several older varieties such as Endosafe and NEA2 produce both peramine and ergovaline, but not lolitrem. Seeds containing wild endophyte left in the ground can be a problem; a break crop such as brassicas may be necessary. A new endophyte, AR37, was released in 2006. This only produces small quantities of janthitrems, which deter Argentine stem weevil, Porina grubs, black beetle, mealy bug and root aphid more effectively than wild endophyte. This increases ryegrass's persistence and yields. Janthitrems can cause similar signs to lolitrem in animals, but only at high doses. There is also some indication that ryegrass with safe endophytes increases milk yield in cows.
There are several other options:
Sheep have been bred for resistance to lolitrem, but this strategy is less likely to be of general use.
Prognosis is usuallly good; cattle and sheep will respond within a few days of being given clean feed, but in severe cases in horses and deer ataxia may persist.
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Surveillance (1974) 1(1): 10Staggery sheep and cattle
Surveillance (1975) 2(5): 3Ryegrass staggers (sheep)
Surveillance (1976) 3(3): 8Ryegrass staggers
Surveillance (1982) 9(2): 2Good farm records reveal high cost of ryegrass staggers
Surveillance (1982) 9(3): 26 Ryegrass staggers in deer
Surveillance (1991) 18(4):33 Ryegrass staggers in wapiti deer
Surveillance (1994) 21(3):31 Ryegrass staggers in alpaca
Surveillance (1995) 22(2): 4Ryegrass staggers in horses, alpaca, elk and wapiti
Tor Agbidye, J.; Blythe, L. L.; Craig, A. M. Correlation of endophyte toxins (ergovaline and lolitrem B) with clinical disease: fescue foot and perennial ryegrass staggers. Veterinary and Human Toxicology 43 (3) : 140 146 2001