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Atypicalmyopathy

During the autumn, vets see a significant rise in this often fatal disease. Equine internal medicine specialist Victoria South, from the Liphook Equine Hospital, takes us through the latest research and explains how to reduce the risk

essential facts

Rustler was too weak to

stand, so he had to travel

to the hospital lying down

A frequently fatal muscle disease, atypical myopathy affects horses in the UK and northern Europe. This unpleasant disease results in destruction of

respiratory, cardiac and postural muscles. Affected horses show signs of weakness, muscle trembling and pain, and may be recumbent (lying down). Even with intensive veterinary treatment, severely affected horses may die. Several horses from one location can be affected and outbreaks most commonly occur in the autumn.

Clinical signsAtypical myopathy is a degenerative disease of muscle that is associated with grazing. Although recognised 90 years ago, cases have become more common. Affected horses cannot metabolise fatty acids (the major energy source of muscle), so there is widespread destruction of muscle cells.

Predominantly, the postural muscles are affected, so horses show signs of muscle soreness, stiffness and lethargy, which progress to muscle tremors, profound weakness and increased recumbency. Some horses will be reluctant to move but will whinny and toss their heads, which may be a sign of distress. A few affected horses will show signs of choke (oesophageal obstruction), leading to dropping saliva and food material from the nostrils.

Opposite are the main signs of atypical myopathy. If you suspect your horse may have this disease, contact your vet as a matter of urgency.

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ital Case study

Six-year-old American Paint Horse, Rustler, was struck down with atypical myopathy and was too weak to stand. He was carried into the lorry and taken to Liphook equine Hospital, where he was given strong painkillers, antioxidant medication, intravenous nutrition and fluid therapy. After only three days, he’d made a fantastic recovery and is now back in the show ring.

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Respiratory distress is a poor prognostic sign and reflects damage to the respiratory muscles, including the diaphragm. The majority of cases will have a fast heart rate and some will have an irregular heart rhythm (arrhythmia), caused by damage to the cardiac muscle. Rapid progression to death occurs in the majority of cases over a period of six to 72 hours, but some cases may be found dead with no previously observed abnormal signs.

Reported mortality rates range from 40% to 100% and vary from year to year. Most affected horses who are still alive after five days are likely to recover. Initially recovery is slow, but most affected horses are healthy in the long term and will return to their pre-illness level of work.

Multiple casesThe number of horses affected in an outbreak has been variable. Single cases are reported, although it is more common to see several animals affected on the same premises. When a single case is identified, it is sensible to blood test all other horses on the same premises, as many others may be affected to a lesser extent without showing clinical signs (known as subclinical disease).

■ Muscle soreness■ Stiffness■Muscle tremors■Weakness■Lethargy ■Choke ■ Increased vocalisation ■Head tossing■ Increased recumbency■Tachycardia (fast heart rate)■Arrhythmia (irregular heart rhythm) ■ Respiratory distress (difficulty breathing)■Red-brown urine■Sudden death

The main signs

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For several years, vets noticed that horses with atypical myopathy were often kept on sparse pastures that were surrounded by trees with an accumulation of dead leaves and seeds, and that they were often not fed any supplementary hay or feed. This pattern of pasture characteristics, and the fact that groups of grazing horses can be affected, led vets and researchers to suspect that an ingested toxin was cause of the disease.

In the past few years, international research has revolutionised our understanding of the cause of this horrifying disease. Researchers have discovered that horses suffering from atypical myopathy and seasonal pasture myopathy (the American version) have an impaired ability to produce energy from fatty acid and amino acid metabolism in the mitochondria (energy factories) of muscle cells.

A toxin called hypoglycin A has been detected in the blood and urine of American horses suffering from seasonal pasture myopathy, and the seeds of the box elder tree (Acer negundo) are the likely source of this toxin for horses in the USA. Researchers investigating the cause of atypical myopathy in the UK and Europe found the same toxin in the blood of European horses suffering from atypical myopathy.

How UK horses acquire the toxinBox elder is not native to Europe, but the European sycamore (Acer pseudoplatanus) is in the same tree family. Sycamore trees have

consistently been found on atypical myopathy-affected pastures for many years.

A scientific study published by researchers in Switzerland identified high concentrations of

hypoglycin A in sycamore seeds (also called samaras) in the autumn from pastures in which atypical myopathy had occurred previously, as well

as control pastures where it had not been previously diagnosed. This study indicates that ingestion of seeds from the sycamore tree is the most likely

source of the toxin to UK horses. It is not yet known why

horses develop atypical myopathy in the spring. It could be due to access to old seeds or ingesting sycamore seedlings as they pop up in the pasture. At

this time, though, it is not known if the sycamore seedlings contain hypoglycin A – further studies investigating this possibility are underway, including samples from UK pastures.

Confirming the disease is essentialVets may suspect a diagnosis of atypical myopathy on the basis of their clinical examination and the horse’s recent grazing history. Suspicions can be confirmed by measuring concentrations of muscle enzymes in a blood sample – such as creatine kinase (CK) – which become markedly increased due to the presence of severe muscle damage. Very early sampling might not show the extent of the damage as the peak levels of CK may take several hours. Some horses also have high concentrations of a marker of cardiac muscle damage called cardiac troponin.

Urine will be very dark red or brown, due to the presence of myoglobin (muscle protein). There are high concentrations of myoglobin in the blood when the horse has a muscle disease, and this is filtered by the kidneys

into the urine. This gives a positive result on a urine dipstick for ‘blood’ (there is not blood in the urine, just myoglobin, but it reacts with the dipstick nonetheless).

A post-mortem examination is strongly recommended in any horse that is suspected of dying from the disease to confirm the diagnosis of atypical myopathy. This confirmation is important as it helps horse owners make a confident decision on whether to graze horses on a particular pasture for the rest of the autumn or spring, and may encourage blood testing of other horses that may be affected subclinically.

At post-mortem, abnormalities of the muscle may be mild (pale muscles with haemorrhage) and might not be apparent to the naked eye. Muscle samples are taken from the postural and respiratory muscles, such as the diaphragm and intercostals (the muscle layers between the ribs). When the muscle tissue is examined under the microscope, the pathologist will see fatty accumulation in the muscle cells, a classic sign of atypical myopathy.

The likely cause

Sycamore trees have consistently been found on atypical

myopathy-affected pastures

To confirm diagnosis, the concentration of muscle enzymes in the blood is measured

Dark red urine

Sycamore seedlingsSycamore

seeds could be the cause

of atypical myopathy

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➤ turning out horses for only short periods rather than extended periods of the day (ideally less than six hours).

➤ hoovering up/picking up sycamore seeds.➤ fencing off areas where sycamore seeds have

fallen from trees.➤ regularly inspecting fields

to ensure seeds have not blown in from sycamore trees nearby.

➤ supplying extra forage (hay or haylage) especially where pasture is poor.

➤ reducing stock density so there is plenty of palatable grazing for every horse.

When a case is seen or suspected, field mates should be removed from the pasture and blood tested for muscle damage. Just because they are not showing signs does not mean they are not affected. Provision of antioxidants (eg, vitamin e) and B vitamins may be worthwhile in these cases.

The concentration of hypoglycin A in sycamore seeds varies between seeds in the same pasture and even from the same tree. It is likely that the most important factors contributing to horses being poisoned by hypoglycin A are the availability of the seed (and possibly seedlings in the spring) in the field combined with a lack of adequate grazing or supplementary forage. It should be noted that sycamore seeds are the only confirmed source of hypoglycin A toxin in grazing pasture to date. There could be other sources of the toxin (other tree species/seeds) yet to be identified.

The recent scientific research helps to provide specific advice to reduce the risk of horses contracting atypical myopathy. In practical terms, horses’ ingestion of sycamore seeds in the autumn could be reduced by...

Care of the affected horseTreatment is supportive and may be best in a hospital environment where high-quality nursing care, and round-the-clock veterinary monitoring and treatment can be provided.

Many cases show signs of severe pain that may require multiple types of pain-relieving medication, including non-steroidal anti-inflammatory drugs such as phenylbutazone (bute), opioids (such as morphine) and sedatives. Another drug called lidocaine is a potent pain-killing, anti-inflammatory and antioxidant medication that can be given as a constant drip. Lidocaine might also help reduce the chance of the horse developing heart rhythm disturbances.

Fluid therapy (given intravenously) is an essential part of treatment. It reverses dehydration, protects the kidneys from the damaging myoglobin and corrects electrolyte abnormalities. Many hospitalised horses may also

receive intravenous nutrition to provide the muscle

cells with an alternative source of

energy in the form of glucose.

Supplementary vitamins and minerals have

been shown in one study to be helpful in the treatment of atypical myopathy. In particular, carnitine, vitamin B1 and B2 might support the function of muscle cells’ mitochondria (energy factories), and vitamin C might be a useful antioxidant. Some cases have been shown to be deficient in vitamin E and selenium, so these might also be given.

For more information

If you would like further advice on reducing the

risk of your horse contracting atypical

myopathy, please contact your vet. Further

information can also be obtained from Atypical Myopathy Alert Group,

myopathieatypique.fr/en/la-maladie/

Horses are best cared for in hospital so they can receive intensive treatment

After three days of intensive care in the

hospital, Rustler made a superb recovery

Supply extra forage

protect against poisoning

Fluid therapy is an essential part

of treatment

Ask a vet