Sycamore poisoning in horses: signs & treatment | KBIS

Atypical myopathy (also known as sycamore poisoning) is a severe and potentially fatal muscle disorder of horses caused by eating sycamore ‘helicopter’ seeds and, to a lesser extent sycamore leaves, that fall onto pasture in the autumn & winter or sycamore seedlings which grow in the Spring. The Horse Health Programme explains the signs to look out for, current treatment options and how to reduce the risk in your horse’s grazing.

 

The seeds and seedlings of sycamore trees contain a toxin known as hypoglycin A (HGA). The toxin slows or stops energy production in muscle cells and particularly affects the heart and the muscles which enable the horse to stand and breathe.

 

The sycamore tree is a member of the Acer family and research indicates that it is mainly the sycamore that contains HGA. There are over 25 species of Acer tree but not all of them have HGA in their seeds. However, it can be difficult to distinguish between the different species. The amount of the toxin in sycamore seeds varies and it is not understood how many seeds have to be eaten before a horse may show signs of atypical myopathy.

 

Atypical myopathy, which has a rapid onset, can affect individual horses or several horses in the same group. It appears that some horses may be more susceptible to the toxin than others and this may be due to genetic differences or differing gazing habits. Cases often follow a sudden adverse change in weather conditions, such as a frost or heavy rain.

 

Horses and ponies of any age, breed, sex and height can develop atypical myopathy although there is some evidence which suggests that young horses might be more severely affected, possibly because they typically spend more time outside and grazing, and thus have an increased chance of eating the sycamore seeds or seedlings.

 

The survival rate in affected horses is around 30-40% and is highly dependent on rapid diagnosis and treatment.

In some horses, the rectal temperature, heart rate and respiratory rate may be normal.

 

Atypical myopathy is not contagious.

Diagnosis is confirmed based on a clinical examination, grazing history and a variety of laboratory tests.

 

As a confirmation of diagnosis may take several days, if atypical myopathy is suspected then treatment is often started before confirmation has been received. Unfortunately, there is no anti-toxin, but some medications can be used to help stop the absorption of the toxin from the intestinal tract. Severely affected horses often need to be admitted to a specialist equine hospital for round-the-clock intensive care including intravenous fluid therapy and anti-inflammatory medication.

 

If horses survive the first few days of treatment, they usually recover completely, although this may take several months.

 

When a case is suspected or diagnosed, field companions should be removed from the pasture and have blood samples taken for muscle enzyme analysis.

There are practical measures you can take to minimise the risk of atypical myopathy to your horses:

 

Even if your pasture contains sycamore trees and has been grazed by horses for many years without a problem, this does not mean it is safe. For reasons unknown, some horses do not seem to be affected by the toxin even though they are potentially exposed to it. Unfortunately, there is no way of knowing which horses these are.

 

If you have any concerns that your horse may show signs of atypical myopathy, please call your veterinary surgeon immediately.

On the Tuesday before Christmas 2022 on a dark, rainy evening, I was sitting at my desk at home when I got a phone call from my partner (Tony) “Bridget is really poorly, the vet is on the way, can you come and help”. At that point, I was, of course, worried but I had no idea what was in store.

Bridget (2yo WB x riding horse), the first of our homebreds had sycamore poisoning and was incredibly unwell. A couple of hours later we then realised that Barry (5 month old WB x riding horse) also had the same condition. I have been lucky enough to have horses for nearly all of my life and prior to working at KBIS spent several years working in racing and as an event groom, but never in all that time have I seen a horse as sick as Bridget was. The next five days were hell for all of us, especially Bridget and Barry.

Bridget and Barry were turned out in a large field with their mother and their sister (1yo TB x riding horse) both of whom did not succumb to the illness. There were no sycamore trees in the field and had been plenty of grass. The weather had been cold and the ground frozen, so we were feeding haylage in the field. We believe the sycamore seeds had blown in and the horses had been foraging because of the cold weather.

We were lucky enough to be able to use some stables belonging to a kind family in the village and there we set up camp (quite literally). We had all four horses in stables with Bridget and Barry on drips. We thankfully manged to be able to do this at home rather than admitting them to hospital. Our wonderful vet, Helen, came multiple times a day to administer some of the stronger pain relief and we were able to manage their pain the rest of the time. We set up a bed in the tack room and I set up my office there too. We took it in turns with Tony sleeping up there and me working from there during the day so that between us, we were constantly monitoring them and were there to change drip bags and administer pain relief.

Bridget seemed to suffer the most, we think that as Barry was not fully weaned and had a smaller muscle mass he was not affected as much despite having equally high levels of muscle enzymes in the blood, similar to a horse that has tied up much higher.

The first three days were the hardest for all, they almost seemed to get worse before, thankfully, getting better. Bridget could go from looking reasonably fine to on the ground groaning in pain in the space of ten minutes and then return back to seemingly well in just as quick a time.

Initially, Bridget spent a lot of time laying down during the day but whenever she was checked she got up and looked fine. The first obvious symptoms she showed were very similar to colic combined with ataxia. This improved with pain relief and fluids after around 48 hours but the low head carriage, laboured breathing and trembling lasted nearly a full five days. They were on fluids and pain relief for five days and we kept them in for around three weeks to make sure they had recovered fully. It was a very slow process but they have both made a full recovery and are back out (in a different field!).

We are incredibly grateful to our vet Helen and her team at VT vets for everything they did to save our lovely little homebreds, without her quick reactions and expert knowledge Bridget and Barry would not be here today. We are hoping to back Bridget (now three) this summer and hopefully never witness this horrid condition again.

Article originally posted by B&W Equine Vets. For more knowledgeable vet advice take a look at the Vets View section of our blog next.