Annual Ryegrass Toxicity
Also known as
Annual ryegrass staggers is a neurotoxic disease (often fatal) that occurs in livestock of any age that graze pastures in which annual ryegrass (Lolium rigidum) is present in the seed-head stage of growth. Sheep, cattle, horses, farmed deer, and llamas are susceptible.
Annual ryegrass toxicity is seen in western and southern Australia and in South Africa from November to March. Hay made from a certain fescue grass--Festuca rubra commutata --with seed-head galls infected by Rathayibacter toxicus (a gram-positive toxin-producing bacterium that parasitizes plants) 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.
Outbreaks of “staggers” occur 2–6 days after animals graze a pasture containing annual ryegrass infected at a toxic level. Death may occur within hours (affected animals are often found dead), or up to a week after onset of signs.
Characteristic neurologic signs are similar to those of perennial ryegrass staggers, but mortality from annual ryegrass toxicity is higher--commonly 40% to 50% of more of the affected animals die. At necropsy 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, but these animals often become apparently normal again when left undisturbed. When animals are severely affected, nervous spasms may occur, and convulsions could be precipitated by exercise or hot weather.
A thorough history and evaluation of the pastures can help a person differentiate between staggers caused by other grasses such as perennial ryegrass, phalaris (a family of grasses that include Reed canarygrass), and the ergots of paspalum (crowngrass) and other grasses.
Polioencephalomalacia and enterotoxemia are other differential diagnoses, since these diseases also cause signs of incoordination and staggering.
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, and death losses are not as high.
- High-stepping gait,
- Collapse when stressed,
- Convulsions in severe cases,
- Death within a few hours to a week
Annual ryegrass (Lolium rigidum) is the main host for the seed-gall nematode Anguina funesta. This nematode carries the toxin-producing bacterium, Rathayibacter toxicus, into ryegrass seed-heads. The toxins produced by these bacteria cause annual ryegrass toxicity in grazing animals when consumed in sufficient quantity.
The seed-head galls are created by the nematode Anguina funesta and colonized by R. toxicus. Nematodes are often called worms, but are actually tiny multicellular insects with smooth, unsegmented bodies.
Some live as parasites in digestive tracts of animals, some live in the soil and are part of a healthy soil profile, and some parasitize plants. The nematode species that feed on plants are so tiny that you need a microscope to see them.
The nematode Anguina funesta feeds on annual ryegrass by creating a gall (swelling or growth) in which it lives and feeds, but which can also become infected with bacteria). These bacteria-infected galls are present in infected annual ryegrass pastures from early spring on, but are most toxic when the plants mature and are no longer growing.
A yellow slime may be observed on infected ryegrass heads. Grazing animals usually show no sign of toxicity until late spring and summer.
Losses from the disorder can be minimized by early recognition of signs and removal of livestock to safe grazing or by reducing grazing pressure, though signs of disease may still appear intermittently in those animals for several weeks.
Gall identification is difficult in annual ryegrass pastures, and in southern Australia the bacterium in emerging seed-heads is detected and quantified by ELISA tests in a laboratory.
Early detection of toxic fields enables farmers to mow the heads off the grass or graze it before it 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 and minimizes the risk of toxicity the next growing season.
Controlling annual ryegrass removes the nematode’s breeding site, and without the nematode the bacteria are unable to enter the plant. Getting rid of annual ryegrass does not eliminate the nematode completely, and their numbers can quickly build up again if ryegrass comes back into that pasture.
In recent years, ryegrass stands have developed resistance to many commonly used herbicides. This can lead to increased nematode numbers, and increased populations of toxic bacteria, particularly where there has been a high intensity of cropping.
To manage herbicide resistance in annual ryegrass, many farmers are now adopting an integrated approach to ryegrass control, but using livestock to help control the ryegrass may expose these animals to toxic annual ryegrass.
Some farmers still try to spay the ryegrass, but to reduce the risk of toxicity it must be done early (even though it may damage the legume component of the pasture). By seed-set the galls are formed and rapidly developing toxicity.
Early spraying may fail to be effective, however, if rain occurs after spraying. This often results in regrowth of additional heads from the base of the plants.
To prevent having to re-spray, a person can graze sheep at a high stocking rate to remove this regrowth before it becomes toxic. Generally the regrowth tillers are not as infested with bacteria as the original heads.
Mechanically topping annual ryegrass pastures up to 10 days after the first heads emerge will reduce production of toxic bacterial galls. Any regrowth can be grazed with sheep to prevent toxicity developing.
The toxicity in the seed-heads increases rapidly as the seeds set and mature, so the grazing pressure must be sufficient to remove the heads before they become toxic. This method of control is risky, however, and requires careful management to ensure stock safety.
There is no effective treatment other than removing the animals from the offending pasture and hoping that they might recover.