This talk is plagiarised from an AVJ article7 I co-authored with Adrian Philbey (principle author, who was then located at RVL, Wagga) and local Practitioner Mark Hawker. I have relisted Adrian’s references but not consulted them myself.
Stachys arvensis, commonly know as stagger weed, is an annual forb that has been associated with a locomotory disorder(‘stagger’ or ‘shivers’) in sheep, cattle and horses in Australia since 1895. Intoxication appears to be uncommon relative to the abundance of the plant on cultivated land. The syndrome has been reproduced in sheep in feeding trials with S arvensis, demonstrating that the seeds are the most toxic portion of the plant, the young sheep are more susceptible than adults and that lambs can become intoxicated by ingesting milk from ewes grazing the plant. S arvensis intoxication in sheep has been classified as a limb paresis with knuckling syndrome.
In the spring of two successive years on a wheat-sheep farm at Young, on the south western slopes of New South Wales, a large proportion of Merino sheep bred from a medium wool bloodline developed a locomotory disorder. The farmer reported clinical signs of 0.5% of 1000 mixed sex weaners aged 7 months in mid-November 1989, about 7 days after being introduced to a new paddock. The proportion of sheep affected progressively increased to almost 100% (at least 20% severely affected) by January 1990. During December 1989 and January 1990, 200 affected sheep died from misadventure. Most surviving affected sheep had recovered by February 1990. Fifty percent of 400 ewe hoggets, aged 15 months, grazing other pastures on the farm during this period, were also affected.
In mid-November 1990, 1000 mixed sex weaners, aged 7 months, were yarded to be examined for grass seed damage and to be jetted with cyromazine for the prevention of blowfly strike. About 850 were released into a 105 ha paddock that had been spray topped 10 days previously with glyphosate herbicide to control grass seed. The pasture in the paddock at the time of consisted of Trifolium subterraneum (subterranean clover), Hordeum leporinum (barley grass), Bromus sp (brome grass) and Aristida sp (silver grass) and was drying off as a result of the herbicide treatment. The owner first noticed clinical signs about 7 days after the sheep had entered the paddock.
At this stage I was consulted by the Vet Practitioner and his client and made a property visit on 11 December 1990. A typical staggers syndrome was observed and post-mortem findings also indicated grass seed infestation and sub-clinical parasitosis as complicating factors. In this mob of 850 merino weaners I was told that up to 150 had already died and I estimated another 150 to be showing symptoms of staggers. I then walked the paddock which this mob had grazed recently I eventually detected a sparse infestation of Stagger Weed.
Within a further 6 weeks approximately 90% of the sheep developed a locomotory disorder (40% severely) and 28% had died. The flock had been moved onto Pisum sativum (pea), Triticum aestivum (wheat) and Avena sativa (oat) stubbles that were free of S arvensis and supplemented with grain oats. Affect sheep slowly recovered, the last clinical cases being seen in late January 1991. Of the original 1000 weaners yarded in mid-November, 150 which had been observed to have grass seed damage, were drafted off and held in a paddock free of S arvensis. They did not become affected.
S arvensis had been introduced to the farm in 1986 and was well established in cropping paddocks. Samples collected from the farm in December 1990 were identified by the government botanist, Royal Botanic Gardens, Sydney as S arvensis.
Affected sheep displayed signs of a moderate to severe pelvic limb paresis, including a stilted gait, a slightly wide-based hind limb stance, frequent crouching or dropping of the hindquarters when in motion, a tendency to stumble and collapse when forced to exercise and progressive reluctance to move. They were often found recumbent in the paddock and deaths appeared to be a consequence of misadventure by drowning, dehydration, fly strike or crow pick. To prevent deaths, the farmer had to inspect the flock frequently and assist recumbent sheep that were unable to rise. Once assisted to stand, they were able to remain upright and return to grazing. Although the sheep were in good condition when introduced to S arvensis, they lost weight over several weeks and developed a ‘tucked up’ appearance. The seven clinically affected animal s examined had pelvic limb paresis and persistence of knuckling of the pelvic fetlock joints for 1 to 4 sec. One animal urinated frequently.
There were no gross lesions in the nervous systems of seven clinically affected sheep necropsied. One sheep, necropsied in late January 1991, had bilaterally symmetrical pallor of the semitendinosus muscles. No significant gross lesions were observed in any other tissues of the affected sheep. All sheep had grass seeds penetrating the skin and some had light to moderate burdens of gastrointestinal nematodes.
A mild degenerative myelopathy, characterised by symmetrical, Wallerian degeneration in the spinal cord was observed in sections from each of seven affected sheep distributed throughout the spinal cord white matter. There was mild, segmental fragmentation of myelin sheaths in the white matter of the spinal cord. In sections of the sciatic nerve from four sheep, myelin sheaths were mildly segmentally fragmented. The sheep with gross pallor of the semitendinosus muscles had a moderate bilaterally symmetrical degenerative myopathy.
A diagnosis of S arvensis intoxication in this flock was made on the basis of the clinical signs of a neurological locomotor disorder and the history of exposure to S arvensis. A degenerative myelopathy and peripheral neuropathy were detected histologically in affected sheep. Clinical signs reported previously in natural and experimental cases of S arvensis intoxication include staggers, shivers, frequent micturition, lagging behind the flock, reluctance to move, recumbency when forced to excerise and death. In this investigation affected sheep had pelvic limb paresis, indicated by dropping of the hindquarters, and a proprioceptive deficit, observed as knuckling of the hind fetlocks. Clinical signs were induced or exacerbated when sheep were excerised.
As with many plant poisonings, ever second farmer you show a toxic plant to says ‘Oh, I’ve got plenty of that on my place’. Stachys arvensis is an inconspicuous little weed — a hairy annual species with a minty odour and small pale pink flowers. It is ‘widespread through out Australia in cultivated land and pastures’.
The major predisposing factors in this case were:-
The only similar condition regularly diagnosed in this locality is Phalaris Staggers (an Autumn/Winter syndrome on Phalaris-dominant pastures). Perennial Ryegrass Staggers is seen in late Summer/early Autumn but is a totally different syndrome with excitability, forelimb hypermetria, episodic collapse with spasms and a high recovery rate.
1. Stanley E Shivers in horses. Agric Gaz NSW 1895; 6:32-35
2. Bailey FM. The weeds and suspected poisonous plants of Queensland. H Pole and Co, 1906:146
3. Henry M, Massey AE. Some neglected sheep diseases of New South Wales. Agric Gaz NSW 1911:22:109-117
4. Seddon HR, Hindmarsh WL, Carne HR. Further observations on Stachys arvensis. ‘Stagger Weed’ as a cause of staggers or shivers in sheep. J Proc Royal Soc NSW 1925;59:249-266
5. Seddon HR, Carne HR. An investigation into the shiver-producing principle of Stachys arvensis. NSW Dept Agric Sci Bull (Vet Res Rep No 4) 1929;33:104-106
6. Bourke, CA. The clinical differentiation of nervous and muscular locomotor disorders of sheep in Australia. Aust Vet J 1995;72:228-234
7. Philbey, AW. A neurological locomotor disorder in sheep grazing Stachys arvensis. Aust Vet J 2001 Jun;79(6):427-430
8. Auld BA and Medd RW. Weeds — an illustrated botanical guide to weeds of Australia.