VET CLINIC
In association with
Mark Andrews, BVM&S CertEP MRCVS, of
Equine Science Update
we are pleased to provide the latest Equine Veterinary Information
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GRASS SICKNESS
Equine grass sickness (EGS) is associated with damage to the autonomic nerve supply to the digestive tract, leading to gastrointestinal dysfunction. It is nearly always fatal. The disease is generally considered to be caused by a toxin, either ingested or produced within the digestive tract, but the actual cause is still unknown.
The first cases were reported in the east of Scotland about 100 years ago. Since then it has been found throughout the UK. It occurs most commonly in Scotland and north eastern England, and has been recognised across northern Europe. An apparently identical condition, "malo seco" (dry sickness), occurs in Argentina, Chile and the Falkland Isles. Grass sickness is seen only rarely, if ever, in Ireland, North America, or Australia.
Grass sickness tends to affect young adult horses (2-7 years of age). It can occur throughout the year, but is seen most often in spring or early summer (between April and July in the UK). As its name suggests, grass sickness occurs almost exclusively in grazing horses. It is rare for housed animals to be affected. Sometimes certain premises can be associated with repeated outbreaks of the disease. Cases often occur within weeks of being moved to new premises or pasture.
What are the signs of grass sickness?
The signs may vary but usually include difficulty or inability swallowing and abdominal pain. They can be divided into three groups: acute, sub-acute and chronic.
Acute form
In the acute form, the horse appears dull, and has difficulty eating and drinking. Saliva may drip from the lips. The horse may show frustration at being unable to drink by playing with its water, or pawing the ground. There may be muscle tremors at the shoulder and quarters. Sweating may be generalised or patchy. As the disease progresses the abdomen tends to become distended.
Signs of colic vary from mild to severe. The pulse rate is markedly elevated (100 beats/minute or more), and is often higher than would be expected for the degree of pain shown by the horse. There is reflux of watery brown-green stomach contents through the nose. This may happen spontaneously, or after the vet passes a stomach tube. Scanty faeces are passed, often covered with mucus. There may be drooping of the upper eyelids ("ptosis") which adds to the somnolent appearance.
The disease progresses quickly and the horse will die within 48 hours. In some cases it may even be found dead without any signs having been noticed.
Sub-acute form
The signs in the sub-acute form are essentially similar to the acute form, but they progress more slowly. The horse develops a "tucked -up" appearance, and has repeated bouts of low-grade colic associated with impaction of the large intestine. The pulse rate remains high. Most of these cases die or require euthanasia within 1 -2 weeks.
Chronic form
The signs develop insidiously. There is little sign of colic, but the horse passes fewer droppings, and has difficulty swallowing. Varying degrees of muscle tremor and patchy sweating are seen. The horse looks "tucked -up" and tends to stand with its feet close together. There is marked weight loss. The heart rate is moderately elevated ( 60 bpm). Often food material accumulates between the teeth and the cheeks.
How is grass sickness diagnosed?
Grass sickness is usually diagnosed on the basis of history and clinical presentation. However, it may be difficult to differentiate between acute grass sickness and colic due to conditions requiring surgical treatment - such as twists or displacements. An exploratory laparotomy (surgical exploration of the intestines under general anaesthetic) may be necessary. If so, a small tissue sample can be taken from the small intestine ("ileal biopsy"), which can be examined microscopically for characteristic signs of grass sickness.
Phenylephrine eyedrops have been used as a non-invasive aid to the diagnosis of grass sickness. When instilled into the eye they reverse the ptosis caused by grass sickness, but have little effect on ptosis due to other causes.
Post-mortem examination provides the definitive diagnosis. Typical degenerative signs are found in the nerve cells in the sympathetic ganglia.
What is the cause of grass sickness?
Despite much research, the cause of grass sickness remains uncertain. There is increasing evidence of the involvement of a neurotoxin produced by Clostridium botulinum type C growing within the digestive tract of affected horses (i.e. a "toxico-infection"). One study found botulinum neurotoxin type C in 74% of horses suffering from the acute form of grass sickness.
Is there any treatment for grass sickness?
Horses with acute or sub-acute grass sickness do not respond to treatment and should be euthanased on humane grounds as soon as the diagnosis is made.
Treatment may be successful for some horses with the chronic form of the disease. Long-term supportive care will be required, maybe lasting for weeks. The horse is fed by stomach tube several times a day. Drugs (eg cisapride) can be used to encourage intestinal motility. Only those horses which have at least some ability to swallow and some appetite are likely to respond successfully to treatment.
If the horse survives, it is likely to be capable of returning to work. It may show residual signs such as excessive sweating, and silky hair, and may be prone to episodes of choke and colonic impactions.
How can grass sickness be prevented?
As yet there is no certain way of preventing grass sickness. A knowledge of the risk factors associated with the disease allows some recommendations to be made.
For example, it is more common in horses which are turned out to grass and are not receiving any supplementary feeding. This has lead to the recommendation that horses should receive some supplementary food when turned out. It is also more common following a period of rain after a cool, dry spell - special care should be taken under such circumstances. Where a case has occurred, in-contact horses should be moved to another paddock, brought in to the stable for at least a couple of hours a day, and fed hay and concentrates .
If neurotoxins produced by Clostridium botulinum type C are confirmed as the cause of grass sickness, it may be possible to develop a vaccine to give protection against the disease.
For further information on Grass Sickness please visit the Grass Sickness Fund Website on
www.grasssickness.org.uk
Barnaby
Barnaby was a 10 year old part-bred gelding; his summer holiday was almost over when he was struck down. This is his story:
It was a saturday morning nearly at the end of July (1987). I was doing my usual weekly wander around the field, checking the hedges and fencing, etc. Barnaby and his pal Toby appeared peaceful and content as they grazed but the longer I spent in their presence I knew Barnaby was not quite himself. There were no evident signs of anything at all but the horse "just wasn't right"; I still cannot explain it to this day but I knew something was wrong. As I continued with my jobs I noticed that some of the droppings were rather loose for horses that had spent over 5 weeks out in their summer pasture; this seemed odd in itself but as there nothing I could pinpoint, no other signs, all I could do at that stage was keep a close eye.
A couple of hours later Barnaby was laid out in the field, something that I had never seen him do in 5 years of ownership but it was the first warm, sunny day after quite a few days of the typical English summer (cool and dullish). I went over to him, he readily got up and took a carrot off me; he was bright and fussy, his coat shining in the sunshine, but I still was not happy, something was nagging inside me, so I moved both horses to the paddock right by the house; that way I could keep a closer watch.
About teatime Barnaby got down again, so I brought him in and gave him a thorough check over but still nothing untoward was evident, he looked a picture of health. I decided to give him a bran mash with a few tasty morsals in it which he happily ate. I checked him regularly throughout the night but by early morning, although Barnaby had eaten a little hay and drunk some water, he had not passed anything. I called the vet immediately. At this stage Barnaby was still bright-eyed, his membranes were the right colour and his coat sleek and glossy; he was affectionate and talkative but I felt sick inside, something was wrong, but worse - something was telling me my horse had contracted grass sickness though I don't know why as it was a disease I had only read about and he was not exhibiting any of the typical early warning signs. I began watching Toby like a hawk as well, but he was his usual cheeky little self; there were no alarm bells inside me as far as he was concerned.
The vet diagnosed an impaction, a little of which he was able to remove and gave Barnaby a dose of liquid paraffin. That at least explained the loose dropping in the field; in the early stages fluids can still pass the impacted matter making faeces from matter in the digestive tract beyond the impaction more watery. The vet returned a few hours later and we were encouraged as there were gut noises and a little more of the impacted material could be removed. He was confident that by morning all would be well although Barnaby would feel pretty uncomfortable once everything "started moving again" (he might become colicky) so he left me a couple of painkilling injections.
I checked Barnaby on the hour through the night and although the poor horse lay flat out making the odd groaning noises, he did not appear to be in distress, he was not at all sweaty, there were no muscle tremors and encouraging gurgling noises emanated from his stomach but as the night worn on the dreadful feeling inside me just got worse. By the early hours I called the vet back. He went to give Barnaby another dose of paraffin but as the stomach tube went in a whole load of fluid came back out of it. That was it - he was rushed to the Vet Clinic in Oakham, his stomach completely pumped out and he was put on an intravenous drip.
[The late] Mike Seckington was very matter-of-fact, which did not help me in my distraught state, but said Barnaby's only chance of survival was an operation. Whilst various tests were carried out (at this stage there were several other things that could be wrong) they kept pumping out his stomach to keep Barnaby as comfortable as possible but each time it became harder for the stomach tube to be inserted down his throat; the muscles were slowing becoming paralysed. Barnaby was then taken into the operating theatre.
That night I received a call giving promising news. Yes, there was a severe impaction but now that was removed the gut was working again. There was a lot of long standing worm damage evidenced by thickening of the walls of the digestive tract which would have aided the severity of the impaction (I remembered that after an azoturia attack shortly after I became Barnaby's owner my vet at the time put him on a 5-day worming course because of a very high worm count. Things appeared to be making sense. I spent another sleepless night, morning couldn't come quickly enough; I was desperate to see Barnaby as soon as possible. Next morning I raced to Oakham and, despite the angry shouts of the head girl, leapt over the gate to the stable yard and went to find my horse. He wasn't in the stable I'd left him in the previous day. "Never mind" I thought, "that's because he's had an op and is in one of the internal boxes for closer observation". More fool me. I raced into the barn and although I knew Barnaby would look pretty rough having been cut open throughout the entire length of his body, nothing, but nothing could have prepared me for the sight that met me. Barnaby was stood with all 4 feet bunched together as if tied up, his head was on the floor, his eyes were sunken and barely open, his ears hung out sideways, his abdomen was tucked right up and every bone stuck out through taught, dull, dry skin, there was not an ounce of flesh on him yet 3 days before he was well-filled and rounded from having had 5 weeks at grass, he was completely lifeless, already "dead". That image has remained with me and is as vivid today as it was that day. Barnaby did not respond at all to my presence and as I went to stroke him his mouth opened and drools of saliva fell out. I wanted to cry out but gathered myself, I had to remain in control for Barnaby. Mike and Michael [Gibson] came in but before they could say anything I looked at them and nodded; I was too choked to speak.
Barnaby was led to the indoor school. I couldn't watch because I felt so guilty that he was being asked to move when he obviously felt so wretched but he could not be put to sleep in the stable as he was coming home for burial.
I made a fuss of him, but Barnaby was oblivious to my presence as the needle went in. Then suddenly a surge of life went through his body; he pulled back and I shall never ever forget the expression on his face; it was a look of complete bewilderment as to what was happening to him. If he could have spoken I'm sure he would have said exactly that - "help, what's happening". I knew it just the effect of the anaesthetic but nonetheless it was heartbreaking - I ran out and sank to the floor; a few seconds later Mike came out, put his hands on my shoulders and pulled me up - "it's over" he said, "Barnaby's o.k. now. You thought a lot of the horse, we can see that" he said and then led me back into the school. I sat down beside my once beautiful horse and stroked his neck. Michael put his hand on my arm for a moment and then walked away to leave me with Barnaby and my thoughts……
Rowena
(Equine Management and Training)
Barnaby is buried with a couple of his pals; he is at peace but my quest for answers goes on. I had many, many questions which no-one could answer for me then and sadly, even today most of them still remain that way. We must all do whatever we can to help put an end to this indiscriminate killer. There are typical signs to look out for but remember that Barnaby did not exhibit any of these until he was very close to death, so don't rely on them as a diagnosis.
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