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CASE NOTES

Staggers Syndromes

Chris Bourke, Principal Research Scientist (Poisonous Plants)
Orange Agricultural Institute, Forest Rd Orange NSW

Posted Flock & Herd February 2011

Introduction

Many plant associated staggers syndromes can affect ruminants in Australia, many of these look similar, most have no associated gross pathological changes and few have pathognomonic microscopic changes. Some may hope that a barrage of biochemical tests will eventually point to a diagnosis, but alas they rarely do. Fortunately the easiest and most reliable ‘test’, for drastically reducing the differential diagnostic possibilities with staggers syndromes, is the eyeball test. The eyes and the optic lobe of the brain collectively form a very sophisticated piece of highly portable field equipment, which allows the veterinarian for no extra cost other than time, to piece together a precise clinical description of the presenting problem. Because affected animals cannot talk they do not give us incorrect, confusing or tangential messages, they simply display in the subtlety of their clinical signs the absolute reality of their pathological predicament. The challenge for the observer is to first see and then accurately interpret the severity, type, and duration of these signs.

The choice of clinical terminology, to describe staggers signs, varies between observers. My preference is not to use misleading and non-specific terms such as ‘ataxia’, ‘ataxic’, ‘paralysis’, ‘humped in the back’, ‘spastic’, ‘throwing a fit’, ‘tetanic spasms’, etc. I am also very cautious in my use of the terms ‘convulsions’ or ‘convulsing’, but alas many others are not. Genuine convulsions can only be present in an unconscious animal. A frightened animal for example that has fallen over and is struggling to get up again, is not ‘convulsing’. Likewise an animal which is able to remain standing may have a very bad case of tremors, but it is not experiencing convulsions. The most frequently encountered suite of locomotor signs is paresis, knuckling, falling, tremors, and convulsions.

Paresis develops early in a staggers problem. Paresis by definition is weakness and this may start in the hind legs but can progress to involve the forelegs as well. Paretic animals have reduced exercise tolerance and display increasing bouts of recumbency (usually sternal). Animals with limb paresis are not necessarily in-coordinated or ‘ataxic’, in fact they may be very coordinated within the constraints of their limb paresis. Paresis implies a disturbance to function in the antigravitational (typically extensor) muscle groups, it can form part of an entity called paralysis but most staggers affected animals are never ‘paralysed’.

Knuckling over in the fetlocks is an indicator of a proprioceptive deficit. This is a sensory problem and is only present in some staggers syndromes. Genuine knuckling will be present even when limb paresis is only mild to moderate, however when severe limb paresis is present animals may simply not bother to straighten the fetlock hence may display pseudo-knuckling. Animals with genuine knuckling are also inclined to experience in-coordination or ‘ataxia’ because of the imbalance they have between sensory inputs and motor outputs.

Falling over is not a chance event, rather it is highly characteristic of staggers syndromes that involve a disturbance to the maintenance of equilibrium. Falling classically reflects a cerebellum problem. It can occur without tremors or with just a very mild head tremor. Alternatively in some syndromes it occurs along with very obvious severe and persistent tremors. Falling is often more frequent when the animal is required to exercise a directional change or ‘turning’ movement.

Tremors involve a series of inappropriate waves of extension and flexion movements in groups of muscles. They are driven by a disturbance to any one of the three extensor-flexor coordination centres located at the level of the medulla oblongata, the thalamus, and the striatum. A muscle fasciculation is a tremor or twitch that is restricted to an individual muscle, it may result from muscle fatigue per se or it may indicate a CNS problem.

Convulsions are most commonly cerebral rather than spinal in origin. Intermittent and episodic convulsions typically result from a disturbance to the vascular supply to the brain, whereas terminal convulsions are more consistent with toxic or metabolic processes that interfere with normal neurotransmission. Genuine cerebral convulsions can be regarded as present if the animal is laterally recumbent, unconscious, has limb paddling movements, periods of extensor rigidity (tetanic spasms), periods of opisthotonos (neck arched backwards), twitches of the lips, face and ears, rotation of the eye balls, nystagmus, and apnoea with periods of cyanosis. In addition dilated pupils, salivation (mouth frothing), chewing (jaw champing), and urination and defaecation should also be observed.

The standard clinical neurological examination performed on cooperative cats, dogs and horses does not work nearly as well in uncooperative ruminants. The best approach with these animals is to examine a group of affected animals at close quarters and to look for signs that are consistent across the affected group. Then try and refine your evaluation by subjecting selected individuals to a standard neurological examination, but be cautious in your interpretation of their responses. Normal sheep not infrequently give abnormal responses to neurological testing.

‘Staggers’ simply implies a dysfunction of the locomotor system but this may be nervous, muscular, or metabolic. In the process of piecing together a precise clinical description a practitioner can often confidently place the problem into one of these categories. By using the following clinical classification system the problem can then be short listed for its clinical group. Finally the most likely matching syndrome within that group can be determined.

Group 1. Limb paresis syndromes

Group 2. Limb paresis with knuckling syndromes

a) Simple

b) Complex

Group 3. Falling syndromes

Group 4. Falling with tremors syndromes

Group 5. Convulsive syndromes

a) those that start with intermittent and episodic convulsions

1. Tunicamycin-like group of syndromes

2. Thiaminase group of syndromes

b) those for which convulsions only occur terminally

Some forms of plant associated ‘staggers’ are peculiar to horses, these include ‘stringhalt’ caused by Hypochaeris radicata (flatweed, catsear, false dandelion) and the ‘walkabout’ disorders caused by the Star thistles (Centaurea solstitialis and C repens).

Staggers syndromes to be presented in more detail

a) Phalaris staggers
b) Perennial ryegrass staggers
c) Tribulus staggers
d) Stagger weed staggers
e) Flood plain staggers
f) Romulea staggers
g) Humpy back staggers

Phalaris staggers highlights

Only affects ruminants. It can occur on P aquatica, P minor, P arundinacea, or P canariensis. It can present as a chronic limb paresis syndrome, but more typically presents as an acute falling with tremors syndrome. Cattle are more affected in the cranial nerves and sheep more in the upper motor neurones. Cattle develop chewing and swallowing problems hence weight loss. Staggers is caused by indole alkaloids in the plant but the concurrent ingestion of surplus cobalt appears to allow the rumen microflora to incorporate these indoles into harmless cobalamin (vit B12-like) compounds. Horses will process indoles differently to ruminants hence they do not get staggers but they can give positive swabs for the indole bufotenine when they eat phalaris pasture or hay whilst in training for races.

Grasses are very poor accumulators of cobalt. Dietary cobalt is found in legumes and ingested pasture soil or dust. Basalt soils are cobalt rich but limestone soils are cobalt deficient. Outbreaks of staggers may occur within 10 days of grazing phalaris or not until several months after grazing has ceased. The indole alkaloid content of phalaris is highest in autumn and lowest in late winter — early spring, but the soil cobalt availability is highest in autumn and lowest in late winter — early spring, consequently outbreaks of staggers typically occur during the late winter — early spring period. Livestock on moderate to low cobalt soil types should be treated with rumen cobalt pellets. Use high quality 3 year slow release pellets and administer two per animal. Phalaris staggers can be confirmed by histopathological examination of brain sections.

Perennial ryegrass staggers highlights

Is known to occur on wild endophyte infected Lolium perenne pastures, and endophyte infected L perenne x L multiflorum hybrid pastures may also pose a risk. PRG staggers can affect all herbivores. It is a falling with tremors syndrome that develops within five or more days of the ingestion of toxic pasture, hay or grass seed. The causal toxin is Lolitrem B. Pastures can remain toxic for several weeks, typically in late summer — early autumn. In a mixed pasture the daily intake of lolitrem B will be much less than that found in the PRG sample that is sent to the laboratory to be tested. It is the average daily intake that dictates the risk not the lolitrem content of a PRG sample. Problems arise when lolitrem B ingestion levels of 1.8 — 2.0 mg per kg of dry matter per day are occurring.
In a typical mixed pasture situation the PRG sample tested would have to have a lolitrem B value of double this before a significant staggers risk would exist. Lolitrem B accumulates in the butt of the grass and in the seed head. Consequently avoid intensive grazing during the risk period and do not make hay or silage out of endophyte pastures that are setting seed. In NSW PRG staggers can occur as a small localised problem about every 3 years and as a more widespread and severe problem about every 15 years. In either case the risk period is only of several weeks duration. Affected flocks or herds are best handled by not being mustered or disturbed in any other way, just leave them alone during the period of risk and the impact of the staggers condition on their health and production will be minimized. PRG staggers is essentially a clinical diagnosis but brain histopathology can sometimes offer further reassurance of the diagnosis.

Tribulus staggers highlights

Two similar but different locomotor disorders occur in sheep grazing Tribulus dominant pastures in central and northern NSW. Grazing T. terrestris (caltrops, cathead) can result in a limb paresis syndrome with a distinctly asymmetric presentation, and grazing T. micrococcus (yellow vine) can result in a limb paresis with knuckling syndrome which is bilaterally symmetrical. Many months of grazing are required before a problem will start to develop. Sheep affected by T. terrestris may not develop signs until after they have ceased grazing this plant but regardless they will never recover, often displaying signs for many months before they finally die of misadventure. Sheep affected by T. micrococcus can fully recover within several weeks of ceasing to graze this plant. The prevalence of these disorders is significantly higher in british breed crossbred sheep than it is in pure merinos. Neither condition has so far been reported in either cattle or horses. Tribulus staggers is essentially a clinical diagnosis but brain and spinal cord histopathology can sometimes offer further reassurance, provided the pathologist is familiar with the mild associated changes that occur.

Stagger weed (Stachys arvensis) staggers highlights

Stachys arvensis is a weed of cultivation paddocks. The toxicity risk that it poses will be enhanced by prior application of a knock down herbicide. Stachys staggers affects all herbivores, especially juveniles and suckling infants. Seeding growth stage plants are the most toxic and this coincides with the period late Nov to late Jan. When Stachys dominates a pasture it can cause staggers in a very large number of animals. Toxicity starts after about 7 days. Any deaths are the result of misadventure. Recovery occurs within several weeks of cessation of plant ingestion. The condition is a limb paresis with knuckling syndrome. Histopathological examination of spinal cord sections can demonstrate changes that are consistent with this disorder.

Floodplain staggers (and similar tunicamicin-like syndromes) highlights

This is a convulsive syndrome that affects all herbivores. The occurrence of seizures is initially episodic but eventually terminal. The toxin causes a blood vessel wall impairment that results in a failure to supply cerebral cortical neurones. The condition is not unlike polioencephalomalacia, however the histological changes of PE are not present in brain sections. Animals must ingest toxin for about 4 days before any clinical signs can develop. Outbreaks only occur when the causal bacterium, its nematode vector, and large amounts of the host grass, are all actively growing in a pasture. In NSW this only seems to happen in years where flood waters from south-west Queensland arrive in north west NSW in the period late autumn to late winter.

Affected pastures become toxic as soon as the infected grass starts to mature in late spring and early summer. The diagnosis of this condition is heavily based on the correct interpretation of the clinical signs. Histopathology of a range of tissues (including brain) will reveal a variety of non specific changes, and confirmation that PE is not involved. An absolute diagnosis requires the discovery of yellow-orange slimy or crusty bacterial galls on some grass seed heads and the demonstration of tunicamycin-like toxins in these infected seed heads.

Romulea staggers

Romulea rosea (Onion grass, Guildford grass etc) is an autumn-winter-spring growing perennial corm. It can either cause reproduction problems (possibly requiring a Helminthosporium fungal cofactor) or a staggers syndrome. The latter is a limb paresis with knuckling syndrome which is probably reversible, with deaths being due to misadventure. Histopathology on spinal nerve roots and peripheral nerves should reveal myelin degeneration and axonal swelling (with spheroids). Brain and spinal cord sections from more advanced cases have perivascular cuffs (lymphocytes) and some macrophages that contain golden-brown pigments.

Humpyback staggers

This is a rather poorly defined syndrome of uncertain aetiology. It tends to be over-diagnosed in northern NSW by Queensland graduates who confuse it with other locomotor disorders that occur in northern NSW. It may or may not be associated with the ingestion of Malvastrum spicatum (Mulberry mallow) or of a Sida spp (also a Malvaceae) or of Solanum esuriale (Quena, wild tomato). All attempts at reproducing it by feeding the latter plant have failed. Some Solanum spp can cause CNS staggers syndromes but none anywhere has ever caused a myopathy. Humpyback is a clinical myopathy much like that caused by Malva parviflora (Marsh mallow) and in fact it cannot be differentiated from it. The presentation is that of a limb paresis syndrome. Some have erroneously assumed it to be a neurotoxic disorder but the limited CNS changes reported (mild Wallerian degeneration in the spinal cord) were also demonstrated in clinically normal animals from the same flock.

 

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