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 γ-aminobutyric acidA receptors and causes cell death in
cultured brain neurons. Hence, the clinical expression of the disorder is
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
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
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.
Last full review/revision August 2013 by Wayne Simpson, MSc (Microbiology), BHort Sc, DipHort