Vet notes
Within hours of eating sycamore seedlings, Peppercorn was dead. Heather Rea MRCVS gives the low-down on atypical myopathy and how to keep your horse safe
Atypical myopathy
PEPPERCORN WAS A HAPPY, healthy gelding. He was fit, in regular work and he loved to gallop — so much so that after a fast, exciting ride in the New Forest, his owner Jenny Crouch entered him for a local Boxing Day point-to-point. But Peppercorn didn’t live to see that day. That exciting gallop was his last. “The following morning, I went to the field to give the ponies their morning feed and he didn’t come over. I found him standing in the bottom of the field and it was clear he wasn’t right,” recalls Jenny. “He wouldn’t move. His head was low and he had a laminitic stance, leaning back slightly.” Jenny suspected laminitis or colic and phoned the vet immediately. During the 20 minutes it took for them to arrive, Peppercorn started to tremble and sweat. He remained totally silent, but was clearly in a lot of pain. Veterinary examination showed his gut sounds were normal, he passed droppings and was interested in his feed. However, the muscle on the topside of his neck was taught and his nostrils were dark pink. A bacterial infection was suspected. “This was 2009, prior to the known cause of atypical myopathy,” says Jenny. “We discussed a possible field injury — maybe a hip or shoulder fracture — and a muscle relaxant was given, bloods were taken and the vet left advising to keep him in a small area and update her in a few hours. As she departed, she did mention atypical myoglobinuria, but said it was very rare.” An hour later, Peppercorn was dead (see box, p72). Blood tests confirmed atypical myopathy. “Half an hour after the vet left, he tried to move, staggered and swayed, desperately trying to stay upright,” says Jenny. “He went down very quickly and I sat with him as he lay in the pasture, stroking him as he passed away. This happened within 2.5 hours of my arriving at the field that day.”
What is it?
Atypical myopathy or sycamore poisoning is a frequently fatal disease of grazing horses. Cases were first identified in the 1940s, but there’s been a marked increase in recent years. It’s caused by ingestion of hypoglycin A, a compound highly toxic to horses, which is found in sycamore seeds, seedlings and leaves (to a lesser extent) from sycamore trees (the Acer species). The amount of hypoglycin A within seeds and seedlings is variable and susceptibility to the disease varies between horses. Young horses are thought to be more vulnerable, but there does not seem to be any breed predisposition. The toxin leads to damage of muscle, specifically the muscles that help the horse to stand and breathe. Atypical myopathy is more common in autumn and can occur as outbreaks when large numbers of seeds have fallen down into the pasture grazed by horses. Smaller outbreaks have occurred in the spring when seedlings are present in grazing. Horses on sparse grazing are more likely to ingest seeds and seedlings.
Diagnosing the disease
In the event of a suspected case, your vet will perform a thorough clinical examination. Diagnosis of atypical myopathy is based on the clinical signs (see panel, above right) and evidence that the horse has been exposed to sycamores (seeds/seedlings/ leaves), as well as excluding other more common causes of these symptoms such as colic, choke and tying up (myopathy). The presence of red or brown urine is one of the most reliable signs of the disease. The dark colour is due to the presence of myoglobin, which is released by damaged muscle cells. Muscle damage can be confirmed by blood samples to measure the levels of muscle enzymes. Muscle enzymes are released into the blood when muscle damage is present, therefore increased levels would be present in cases of atypical myopathy (or other muscle injury). If blood samples are taken early on in the disease, then muscle enzyme levels may not show the true extent of the damage as it can take a number of hours for the levels to peak. Blood samples can also be sent to certain laboratories to measure levels of hypoglycin A in the horse’s blood to confirm a diagnosis of atypical myopathy.
Chances of survival
When a case of atypical myopathy is suspected, treatment usually begins immediately, often before confirmation of the disease to increase chances of survival. The mainstay of treatment is supportive: rehydrating or maintaining hydration using intravenous fluids and pain relief. The disease can be very painful. If the horse is unwilling to eat, then assisted feeding orally or intravenously may be instigated. Treatment can be intensive and often the horse is hospitalised. It is quite common in these cases that patients deteriorate before starting to improve, so transportation to a hospital should be considered early on while the horse can still be moved. The reported rates of survival range from as low as zero — this is a very serious disease — up to 60%. However, if the horse survives the first few days of treatment, then they often recover completely, although this may take several months. Middle-aged horses are reported to be more likely to survive than those under five years old.
“Outbreaks can occur when large numbers of sycamore seeds have fallen into the pasture grazed by horses”