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Full description of atypical myopathy

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01 October 2011, at 12:00am

MARION McCULLAGH presents the first in a series of reports on this year’s congress of the British Equine Veterinary Association, held in Liverpool last month

LIVERPOOL’s sparkling new Arena and Conference Centre provided a suitably grandiose setting for BEVA’s 50th congress last month. As usual, the association produced a programme which combined the esoteric and the practical, with a great deal of fun and good humour thrown in. Fran Henson chaired Monday morning’s session on “Muscle disorders” in which Dominique-Marie Votion of the University of Liege described “Atypical myopathy” (AM). This condition has appeared in Europe in all types of equidae including zebras  and donkeys. About 1,000 cases have been reported since the  year 2000 with 354 cases fully confirmed. It is a severe non-exertional rhabdomyolysis with a sudden onset: previously healthy horses are found ataxic or recumbent. It occurs seasonally, most commonly in autumn, with some cases in late summer, early winter and spring but the weather conditions of high humidity, heavy rain, high wind and little sunshine are predisposing. Outbreaks stop after heavy frost. It appears only in horses that are at grass (or those that have been removed from pasture up to four days before symptoms appear). The pasture is likely to be steeply sloping, have overgrazed areas, have a river running through it and have detritus from woodland on the ground. Affected horses are most commonly young (under three years old), not fat, not exercised, not fed concentrates and fed hay or silage from the ground. Changing the water supply to mains water lowers the disease risk. Spreading manure over the land increases the risk. Twenty-seven per cent of cases occur where deaths have happened before; one unfortunate horse was nursed through one episode of myopathy only to die of it six months later when returned to the pasture. Ninety per cent of cases are associated with debris from woods, 40% with high humidity. The search for a causal factor has ncluded looking at the lethal toxin of Clostridium sordellii which has been found in the skeletal muscle of affected horses and also considering mycotoxins. The immediate response to finding a suspect case of AM is to treat the patient but also to remove all companion horses from the pasture, stable them if possible, feed them high carbohydrate diet several times a day and observe them closely for five days. Prevention is the key to managing this disease as the mortality rate is 74%, though survivors recover rapidly. 

Clinical signs of AM 

So what are the clinical signs? The horse is suffering from necrosis of postural and respiratory muscles and sometimes the myocardium. It will have a good appetite, sometimes even ravenous, right to the end. Just over two-thirds (68%) of cases are unable to pass urine, so rectal examination and bladder catheterisation is a vital part of treatment and also of diagnosis as the urine will be dark, due to myoglobin, once the disease is established, though the urine will be clear in the very early and very late stages. Weakness, depression, tachycardia, tachypnoea (or dyspnoea), congested mucous membranes, moderate pain, stiffness, muscle tremors and recumbency dd up to a very compromised individual. A blood sample will show creatine kinase levels that exceed 10,000iu per litre, hypocalcaemia, hyperglycaemia and hyperlipidaemia. Necropsy reveals pale areas in postural and respiratory muscles and sometimes the myocardium. This is due to a process which mimics a multiple acetylCoA dehydrogenase deficiency so that mitochondrial fatty acid energy metabolism is disrupted. Muscle histology and analysis of acylcarnitines in blood or urine can be used to confirm the diagnosis of AM. Twenty-six per cent of AM cases do recover. Treatment starts with removal from pasture, regular bladder emptying, and general supportive care. High carbohydrate diet should be fed several times a day or, if the horse cannot eat, balanced intravenous glucose and electrolyte solutions are indicated. Drugs are used as for any form of rhabdomyolysis but aggressive therapy with antioxidants has been shown to improve survival rates. Horses that keep standing have a better chance of survival and if the horse keeps going for four days, recovery is likely. The Atypical Myopathy Alert  Group (www.atypicalmyopathy.com) exists for veterinary surgeons to record and analyse cases and so come to understand the disease. 

RER cases 

In contrast to AM, recurrent exertional rhabdomyolysis (RER) has a high incidence in two-year-old racehorses in training, especially in fillies. The big problem in its treatment is that if the horse is rested while its muscle enzymes (CK and AST) go down, it looses fitness and gets into a vicious cycle of increased training pressure leading to more incidents of ER as it comes back into work. The drug dantrolene (Dantrium) comes to the rescue. Charlie Schreiber, from Donnington Grove Veterinary Surgery, outlined the “Practical use of Dantrium”. It is a drug that has been used in horses for 20 years and it “always works in all types of horses”. It works by blocking the excessive release of calcium from its store in the sarcoplasmic reticulum of the cell. Once there is too much calcium free in the cell, excessive prolonged muscle contraction occurs. We recognise this as “tying-up”. The condition known as “malignant hyperthermia” in pigs and humans is very similar. Dantrolene is water soluble, it is readily absorbed through the stomach and the small intestine and it works fast. The stomach does not have to be empty. Dantrium comes in capsules which are dissolved in water and dosed orally, usually one to two hours before exercise, so that it is better for the patient to go out with the second or third lot. The dose used by Donnington Grove starts at 2mg/kg bodyweight; Charlie starts his horses on 12 capsules per day and reduces this by two  capsules every other day. If RER recurs, the rate of tapering off is reduced. The horse is kept in regular exercise, trying to work it more frequently and less intensely, and it is fed a diet low in starch and high in oil and fibre. Pre-race drug withdrawal is a big problem. Charlie suggests five days drug-free at the end of tapering off; DiMaioKynch’s 2010 research paper records elimination from plasma within 48 hours of administration but the drug was detectable in urine up to seven days after administration. 

  • It is reported that several horses in Cornwall suffered from atypical myopathy last autumn; one survived following intensive care.