Atypical Myopathy

In this episode of Current Vet, Dr. Lottie talks about equine atypical myopathy, how sycamore toxins disrupt muscle energy metabolism, why the condition is an EMERGENCY, the key clinical signs to recognise and how to manage affected horses and their co-grazers.

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Timeline:
00:00 Intro
00:45 Case
02:32 Aetiology & Pathogenesis
05:29 Clinical Signs
09:40 Diagnosis
15:11 Treatment
20:15 Prevention
22:02 Key Points
23:45 Outro

References

• Żuraw, A. et al. (2016) ‘Equine atypical myopathy caused by hypoglycin A intoxication associated with ingestion of sycamore maple tree seeds’, Equine Veterinary Journal, 48(4), pp. 418–421. Available at: https://doi.org/10.1111/evj.12460.
• Votion, D.M. et al. (2019) ‘Potential new sources of hypoglycin A poisoning for equids kept at pasture in spring: a field pilot study’, Veterinary Record, 184(24), pp. 740–740. Available at: https://doi.org/10.1136/vr.104424.
• van GALEN, G. et al. (2012) ‘European outbreaks of atypical myopathy in grazing horses (2006–2009): Determination of indicators for risk and prognostic factors’, Equine Veterinary Journal, 44(5), pp. 621–625. Available at: https://doi.org/10.1111/j.2042-3306.2012.00555.x.
• Sander, J. et al. (2016) ‘Rapid diagnosis of hypoglycin A intoxication in atypical myopathy of horses’, Journal of Veterinary Diagnostic Investigation, 28(2), pp. 98–104. Available at: https://doi.org/10.1177/1040638715624736.
• Fabius, L.S. and Westermann, C.M. (2018) ‘Evidence-based therapy for atypical myopathy in horses’, Equine Veterinary Education, 30(11), pp. 616–622. Available at: https://doi.org/10.1111/eve.12734.

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Host

Dr. Lottie Wilkinson

Creator and host of the Current Vet podcast

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Atypical Myopathy - Veterinary Vista
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[00:00:00] Hello, hello, and welcome back to Current Vet, the podcast that makes veterinary medicine simple. I'm your host, Dr. Lottie, and today we are talking about equine atypical myopathy. So atypical myopathy is an acute and potentially fatal musculoskeletal condition that occurs in grazing horses after they ingest toxic material from sycamore trees in Europe or box elder trees in North America.

So in this episode, we're gonna talk about what causes atypical myopathy, what the toxin does in the body, how these horses typically present, how we can investigate them, and then what treatments are possible. So let's start with our case It is a cold morning in late October, and you're called to see a four-year-old cob mare called Willow.

Willow lives out with two other horses on some quite bare pasture. The owner reports that all three horses [00:01:00] appeared completely normal the previous evening, but this morning Willow was found standing away from the others with her head held low. She's reluctant to walk and looks weak in her hind. The owner initially thought that she might have a little bit of colic because she was sweating and appeared quite uncomfortable.

When encouraged to take a few steps, Willow moves slowly and stiffly, and she has visible tremors over her shoulders and hindquarters. She has passed a small amount of dark reddish-brown urine. On exam, Willow is quiet but responsive. Her heart rate is 68 beats per minute. Resp rate is 36 breaths per minute, and her rectal temperature is 36.8 degrees Celsius.

Her mucus membranes are pink, but a bit tacky. She appears uncomfortable, and she's still interested in hay and attempts to eat when it's offered. When out in the field, you notice a couple of mature [00:02:00] sycamore trees around the field boundary, and a large number of their winged seeds have blown onto the pasture.

So at this stage, atypical myopathy is very high on a differential list, but some important questions to consider are going to be how stable is Willow? Is she safe to transport? What samples and tests are gonna be useful? What treatments can be started in the field? And then what do we do about the other two horses in the pasture?

Atypical myopathy is an acute non-exertional form of rhabdomyolysis. And rhabdomyolysis just means breakdown of skeletal muscle fibers. So the term non-exertional is important because unlike the traditional kind of tying up, affected horses do not need to have exercised before becoming affected. So in Europe, the disease is primarily associated with ingestion of [00:03:00] seeds or seedlings from the sycamore maple.

In North America, the condition is usually called seasonal pasture myopathy, and it's mainly associated with eating material from box elders. The condition is not infectious, so affected horses are not gonna transmit it directly to one another. However, several horses can become ill at the same time because they are sharing the same contaminated pasture and therefore eating the same toxic plant material.

Atypical myopathy is a genuine emergency. Many clinically affected horses either die or require euthanasia, and while those that survive the initial critical period can recover, the treatment is often quite intensive and full recovery takes weeks.

So the main toxin involved is called hypoglycin A. Hypoglycin A is a naturally occurring amino acid found in certain plants. [00:04:00] It's often described as a protoxin, which just means that the compound ingested by the horse is not the final toxic molecule. So the body metabolizes it into compounds that then become toxic, and they interfere with normal mitochondrial function.

The highest risk period is typically when sycamore seeds are out during autumn or when seedlings are out during the spring. But it is important to remember that not every sycamore tree produces the same amount of toxin, and then concentrations of that toxin can differ between the seeds, the seedlings, the leaves in individual trees, and between different years for the same tree. So the presence of sycamore does not mean that we can predict exactly which horse is gonna become ill or how severe the disease will be.

Horses are more likely to ingest seeds or seedlings when their normal pasture is sparse. So if [00:05:00] supplementary forage is inadequate or seeds have blown into heavily grazed areas or overgrazed pasture, they're more likely to be eaten. That said, atypical myopathy can still occur on fields that appear pretty well-managed, but the key point is basically that any horse with access to potentially toxic sycamore material may be at risk.

To understand the clinical signs, we need to look quickly at how muscle cells generate energy. So muscle fibers can use several different fuels, including glucose and fatty acids. Fatty acids are broken down inside the mitochondria in a process called beta oxidation, and the mitochondria are essentially the energy-producing structures within cells. During oxidation, several enzymes called acyl-CoA dehydrogenases help break fatty acids [00:06:00] into smaller components that can then be used to generate ATP. And then ATP is that immediate energy source that's needed for muscle contraction and normal cell function. So once hypoglycin A, that toxin in sycamores, is ingested, it is converted into a toxic metabolite called methylene cyclopropylacetic acid, or MCP.

The metabolites inhibit several acyl-CoA dehydrogenase enzymes, which then produces a condition known as multiple acyl-CoA dehydrogenase deficiency. So basically, in simple terms, the horse loses the ability to use fatty acids efficiently as an energy source, and muscle fibers with a high dependency on aerobic metabolism are gonna be particularly vulnerable to then subsequent energy depletion.

So these are gonna include postural muscles, which help keep the horse standing up, respiratory muscles, which drive ventilation, and then sometimes [00:07:00] cardiac muscle as well. As energy production falls, lipid compounds accumulate within the muscle cells, and the fibers then begin to degenerate and die. The damaged muscle then breaks down and releases substances in the bloodstream, including creatinine kinase and myoglobin.

Myoglobin is that oxygen-binding pigment found within muscles, and when large amounts of it enter the circulation, the kidneys filter it into the urine, producing that dark red-brown color. Myoglobin can also contribute to renal tubular injury, particularly if the horse is dehydrated or also has poor renal perfusion. So atypical myopathy is not just a muscular condition. It can then cause weakness, recumbency, respiratory failure, cardiac abnormalities, electrolyte disturbances, and secondary kidney injury.[00:08:00]

Okay, so what clinical signs are we going to see? Clinical signs in atypical myopathy can develop really quickly. One of the earliest signs we're gonna see is reluctance to move. Owners can report that the horse is a bit stiff, weak, or unusually quiet. We can see fasciculations or trembling, and then some horses can also sweat quite heavily. Affected horses can have that lowered head position that we saw in Willow, and they may be struggling to support their body weight, so maybe we're seeing increased recumbency or increased weakness. Urine is often that dark red or brown color because of the myoglobinuria, and tachycardia and tachypnea are also common.

The increased respiratory rate may not just be because of respiratory muscle fatigue, it can also be because the horse is painful, stressed, there are [00:09:00] metabolic disturbances, but obviously there's progressive damage to the respiratory muscles is also going to impair ventilation. Some horses can develop dysphagia because muscles involved in swallowing are affected. And then cardiac muscle injury and electrolyte abnormalities can cause arrhythmias as well. So for Willow, that combination of the acute weakness, muscle tremors, tachycardia, pigmenturia, and then we know that they have access to fallen sycamore seeds, makes atypical myopathy very likely.

But how do we work these horses up in practice? So diagnosis of atypical myopathy is usually based on three main things: a compatible history, that characteristic clinical presentation, and then third thing is lab evidence of muscle injury if that is possible. So [00:10:00] we need to start by working out whether the horse has had potential access to the toxin.

So important questions for the owner are gonna be: Has the horse been grazing near sycamore or near box elder trees? Do we know if there are fallen seeds present, particularly if it's autumn? Are seedlings emerging during the spring? Has the pasture been overgrazed? Is it quite sparse? Has there been drought or other causes for the pasture to become poor quality?

Is supplementary forage being provided? Do they have other sources of feed? Has it potentially been really windy and the wind has blown seeds into the pasture even if the trees aren't in the pasture? Are any other horses on the pasture showing similar signs? And has the horse exercised recently so we can rule out causes of exertional rhabdomyolysis?

We then combine that history with a good clinical exam to identify those key clinical signs that we mentioned before, so the muscle stiffness, the weakness, [00:11:00] tremors, tachycardia, tachypnea, and then increased respiratory efforts, and perhaps checking that urine color, too. If we do suspect atypical myopathy, we shouldn't be repeatedly walking the horse to assess the gait because movement is gonna increase muscular energy demands and can worsen the muscle injury. The clinical exam also needs to determine whether the horse is safe to be transported. So a standing horse that can swallow and can be loaded with minimal walking may benefit from referral to a hospital so they can be hospitalized. But a horse that is repeatedly falling over, severely dyspneic, or unable to remain standing may require stabilization in the field before we can even consider transport, if it's possible at all.

If we do pursue blood work and the case isn't too critical, the most useful routine lab test is going to be a serum creatinine kinase, or CK. So CK is concentrated [00:12:00] inside muscle cells, and then when the muscle cell membranes are damaged, CK leaks into the bloodstream. So in atypical myopathy, CK levels are often markedly increased.

We can also check AST and lactate levels. They may also increase. AST rises more slowly than CK and remains elevated for a longer time. So the relationship between CK and AST can sometimes help clinicians to determine whether muscle injury is continuing or if it is beginning to resolve. A full biochemistry is useful for assessing renal function, potentially if we suspect secondary renal injury from that myoglobinuria, the hydration level, electrolyte levels, blood glucose, acid-base status, and then, as we kind of said, evidence of secondary injuries like that renal injury as well.

Urinalysis helps to confirm a pigmenturia [00:13:00] rather than hematuria, and is also useful for monitoring renal involvement in injury. So if we do a urine dipstick test, even with pigmenturia, they can come up as positive for containing blood, even if a cytology shows very few blood cells. And this is because dipsticks read myoglobinuria as hematuria.

So in order to differentiate between the two, we need to spin down that sample and see if there are red blood cells present within it to make sure that we have a true hematuria or we have a myoglobinuria and a pigmenturia. We should also be monitoring urine output because reduced urine production can indicate dehydration, poor renal perfusion, or acute kidney injury and early-onset renal failure.

If the horse is hospitalized, we should be using an ECG to monitor any tachycardia or any [00:14:00] arrhythmias, but we can also measure cardiac troponin. So troponin is released when cardiac muscle cells are damaged, so an increased level is gonna indicate myocardial damage. But neither ECG or troponin is required to diagnose the condition, but they can both help the monitoring and guide prognosis in those critically affected horses.

Hypoglycin A and its metabolites, those toxic metabolites, can be measured in blood or urine samples. So specialist labs may test for their metabolite compounds, which indicate that Hypoglycin A has been metabolized within the horse, and these tests are obviously gonna provide good evidence of toxin exposure, but they are specialized. They're only available from labs that do these tests, and the results are not gonna be available immediately, so treatment should not be delayed while waiting for confirmation in these cases. These tests are more to guide future [00:15:00] management, making sure that owners are aware that their horses have been exposed to this toxin, and that they are able to put measures in place to prevent future episodes.

There is no specific antidote for atypical myopathy, so treatment is supportive, and we're gonna be making sure we're maintaining good circulation, good kidney function, respiration, providing good nutrition, and keeping that horse comfortable while the toxin is eliminated and they start to recover. The first priority is going to be to stop further exposure.

Removing the horse from the contaminated pasture, but also minimizing movement as much as possible. We should not be forcing the horse to walk long distances because that exercise is gonna increase muscle energy demand and can worsen rhabdomyolysis. So that next decision is gonna be whether the horse is safe to transport.

A horse that's standing, as we said before, swallowing normally, able to [00:16:00] load with minimal walking, can be referred and can be hospitalized for monitoring and continued care. But if that horse is falling over, severely dyspneic, or just unable to stand, they're likely to require stabilization in the field as they're not gonna be able to be moved anywhere.

Any co-grazers in the field should also be removed from the pasture immediately, even if they appear clinically normal, just so we're making sure that they aren't being exposed to the toxin as well So then we have supportive care. IV fluids are gonna be used to correct any dehydration, support circulation, and maintain good renal perfusion.

This is so important because myoglobin released from those damaged muscles can then cause renal injury. Carbohydrate support may also be used because fatty acid oxidation has been impaired. So if the horse can swallow safely, making sure we offer frequent small feeds. [00:17:00] Analgesia is really important for comfort, but we should be using NSAIDs, non-steroidal anti-inflammatories, with caution in our dehydrated or azotemic patients because of the risk of further renal injury.

We can use some antioxidant supplements for support, so things like vitamin E, selenium, vitamin C, and then riboflavin can be used in these cases. It's not certain what their exact clinical benefit is, so they should definitely be thought of as adjunctives rather than specific treatments. And then within supportive care, making sure that we're monitoring the cardiac rhythm, the respiratory efforts, electrolytes, renal function, and then urine output really closely.

In hospitalized patients and those that are hypoxic or severely dyspneic, oxygen can be provided, but oxygen isn't going to [00:18:00] correct respiratory muscle failure. It's just going to aid respiration. In our weak or recumbent horses, good nursing care is gonna make a big difference as well, so providing a deep, well-padded bedding so we're preventing development of muscle sores and compartment syndrome, regularly repositioning the horse, protecting the limbs with bandages if they're needed, monitoring again that urine output and bladder function, and making sure that the horse has easy access to uncontaminated forage and then fresh water.

So Willow is able to be transported, and she is taken to the referral hospital where her CK levels are measured. Her urine dipstick is strongly positive for blood, but sediment exam shows that she has very few red blood cells, so we actually suspect a myoglobinuria. She is a bit dehydrated, she has [00:19:00] some electrolyte abnormalities, although her renal values are currently within normal limits.

Her ECGs shows tachycardia, but no arrhythmias. Willow is started on IV fluids, analgesia, and frequent small meals. She's monitored closely, especially with her respiratory efforts and her muscle weakness. By day two, she is still weak, but she remains standing. She's urinating normally, and she has not developed any severe respiratory compromise.

Her two co-grazers in the pasture are removed and examined as well. Neither of them show any obvious clinical signs, but blood samples are collected to measure CK because those apparently healthy horses can still have subclinical muscle injury. In any case of possible exposure, make sure these horses are removed from the contaminated pasture immediately, kept calm, they're not exercised, make sure they're examined for any signs of [00:20:00] weakness, stiffness, or pigmenturia, and measure the CK whenever possible.

Prevention of atypical myopathy depends entirely on reducing exposure to the toxic plant material. So the first step is identifying any trees on and around the pasture. Remember that the tree does not need to actually be inside the pasture, inside the field. Sycamore trees can travel quite considerable distances in windy weather, so neighbors' trees can still contribute to contaminating land.

Inspecting fields quite carefully is really important, especially in those high-risk periods, so maybe during autumn when there is seed fall, after a particularly windy or stormy weather, and then during spring when seedlings are starting to emerge Areas containing seeds or seedlings should be fenced [00:21:00] off or horses should be moved to a lower risk pasture.

We make sure we're providing adequate supplementary forage, particularly if the pasture is quite sparse. And then avoiding overgrazing, avoiding high stocking density to reduce the chance that horses are going to eat less desirable plant materials. If we can, physically removing any seeds and seedlings is really important, and then making sure we inspect any hay or forage to make sure it's not contaminated as well.

If we do have a suspected case, all co-grazers should be removed from the pasture whenever possible. So basically, the safest prevention principle here is gonna be that if there are sycamore seeds or seedlings present, don't just rely on horses choosing not to eat them. Prevent their access to them completely.[00:22:00]

Okay. So if you remember nothing else from today's episodes, make sure you remember these key points. Atypical myopathy is an acute non-exertional rhabdomyolysis, mainly caused by ingestion of toxins from sycamore maple in Europe and the box elder in North America. The main toxin or the protoxin is hypoglycin A, and then toxic metabolites from that hypoglycin A inhibit mitochondrial function and cause muscle energy failure.

Typical clinical signs include sudden onset weakness, muscle tremors, sweating, tachycardia, rapid breathing, recumbency, and then dark red-brown urine caused by myoglobinuria. Diagnosis is usually presumptive and based on the clinical signs, that pasture history, and then we can also check serum CK [00:23:00] activity.

That specialist toxin test can also be used, but waiting for results should never delay treatments. There is no antidote to the condition, so treatment is gonna focus on intense supportive care, minimizing movement, fluid therapy, nutritional support, analgesia, and then close monitoring of the horse throughout treatment as well.

And then finally, prevention is going to focus on identifying sycamore or other toxic trees, inspecting the pasture, especially during those high-risk periods, providing adequate safe forage, and then preventing access to seeds and seedlings as much as possible. And that is atypical myopathy. Thank you so, so much for listening.

If you found this episode helpful, follow or subscribe wherever you get your podcasts, and share it with a friend or colleague who might find it useful as well. As always, if there's a topic you'd like [00:24:00] covered in a future episode, let us know in the comments or come and find us on Instagram or TikTok @veterinaryvista.

I'll see you next time.