Annual ryegrass toxicity is an important neurological disease of sheep and sometimes cattle and horses which have grazed the annual ryegrass Lolium rigidum. It is not known to occur in NZ. It was first reported in South Australia and subsequently in Western Australia and South Africa. Other plants that have been associated with toxicity are Lolium temulentum (darnel), Festuca rubra commutata, Polypogon monspeliensis and Agrostis avenacea. A similar condition has been reported in pigs fed water damaged wheat.
The financial costs include those due to stock deaths, loss of grazing because of toxic paddocks, increased labour costs because of a need to check sheep daily and the costs of chemicals needed for ryegrass control. In addition there may be a decrease in the sale value of an affected farm and considerable stress is placed on the farmer because of the risk of spread of the disease.
Although it is not a mycotoxicosis per se, many of the clinical aspects of control and prevention pose similar problems to facial eczema and other common mycotoxicoses that occur in NZ.
Annual ryegrass toxicity is caused by corynetoxins that are produced by a plant pathogenic bacterium of the Clavibacter toxicus(Corynebacterium rathayi).
Following the germination of the ryegrass seeds in autumn, the seedheads which have been colonised by a plant nematode, Anguina funesta, break down and release larvae from the galls. Many of these nematodes have become infected with Clavibacter. Under certain conditions, the bacteria multiply causing the death of the nematodes in the seedhead gall and a bacterial gall is formed. The breakdown of these galls enables the cycle of infection to continue. When the proliferation of the bacteria in the galls is rapid the ryegrass seedheads have an appearance of being covered with a yellow slime.
It may take from 10 to 15 years from the introduction of infection into a ryegrass paddock before stock losses occur. The spread of the disease is probably associated with the transport of hay, contaminated seed, contaminated sheep and machinery, as well as by wind and water. The first cases of the disease usually appear when the ryegrass pastures begin to dry off and most losses occur in paddocks which have been cropped one year previously.
Corynetoxins are members of the tunicamycin group of antibiotics. The biological activity of tunicamycin and corynetoxins are essentially identical.
Toxicity is cumulative with an oral dose of 1 - 3 mg/kg resulting in death. Hay contaminated with tunicamycin is toxic.
There is usually a time lapse of at least a month between the introduction of sheep to toxic pasture and the signs of disease, although in some cases they may appear within 4 days.
Affected sheep appear normal unless disturbed, when some sheep will collapse and go into convulsions for a few minutes before getting up and staggering away with a stiff legged gait. As the disease progresses, nervous signs including trembling, opisthotonus, head nodding, fore and hind limb digital extension and convulsions may occur. In the final stages sheep are unable to rise and usually die in a terminal convulsion. These signs and losses may continue for up to 10 days after stock are removed from affected paddocks.
There is no treatment.
Sampling and testing of dry, mature ryegrass seedheads is a useful tool in ascertaining toxicity. Sheep grazing ryegrass dominant paddocks must be checked frequently for any signs of toxicity. In addition, all paddocks with dense stands of annual ryegrass should be regarded as potentially toxic and tested. Signs of bacterial infection include the yellow slime colour of seedheads and the distortion of some seedheads.
Alternative or "safe" paddocks need to be provided during danger periods. As there are no practical methods of controlling the bacteria, the best way to prevent its occurrence is to break the life cycle of the nematode, Anguina funesta. This can most easily be achieved by eradicating ryegrass from pasture and crop and destroying ryegrass plants each year before they flower.
Bourke C. A. and Carrigan, M. J. (1993). Experimental tunicamycin toxicity in cattle, sheep and pigs. Aust Vet J. 70: 5, 188 189.
Chapman, H.M. (1989). Annual Ryegrass Toxicity.Proceedings of the Sheep and Beef Cattle Society of the N.Z.V.A.19th Seminar.Palmerston North, New Zealand.268 276.
Creeper. J.H. Vale W and Walsh R. (1996). Annual ryegrass toxicosis in horses. Australian Veterinary Journal 74(6): 465 466.