Atypical Myoglobinuria

[IH Health]

Myoglobinuria

Also known as
Equine Atypical Myopathy, Atypical Myoglobinuria

What is it?
Myoglobinuria is a serious condition that can affect grazing horses in the spring and/or autumn. It is a generally unknown disease that is becoming more common in the UK. European countries seem hard hit by it.

Causes
The causes of AM are unknown making prevention difficult - however some techniques have been shown to be of some use.

Symptoms
Your horse may show signs of:
* Lethargy
* Apparent signs of colic but gut sounds are normal
* Stiffness and/or lameness
* Difficulty in urination
* General weakness / malaise
* Depression
* Excessive lying down / inability to stand
* Dark urine
* Difficulty in brething
* Muscle tremors

Diagnosis
Diagnosis of AM is normally through clinical examination and blood tests. If your horse appears unusually weak please speak to your vet immediately and discuss the possibility of AM.

Treatment
Treatment is done through treating symptoms as the cause is still not known. Treatments include attempting to stop muscular destruction, correcting electrolytic imbalances (sometimes through a drip), keeping the horse hydrated and supporting internal organs such as the kidneys. Your vet will be able to advise you in the best way forward for treatment. Please be aware that AM is a serious and often fatal condition.

Prevention
* Keep an eye on horses less than 3 year old (especially under 18 months) that are out on grazing. Older horses may also be affected.
* Horses in poor body condition could be more succeptible
* Vaccinate and worm your horse
* Some studies suggest stabling or reduced pasture grazing could be beneficial during autumn and/or spring
* Provide your horse with a mineral/salt block
* If your pasture has had a case of AM do not graze during spring/autumn
* Remove dead leaves from your pasture
* Keep an eye out for toxic plants/moulds/fungus
* Poo pick

Good websites
Equine Atypical Myopathy

Previous discussions (click on title for link)
Myoglobinuria
Atypical Myoglobinuria Hepatology and renal failure
Anyone heard of Atypical Myoglobinuria
Equine Atypical Myopathy

+ much more in the search section!

Please post below any information you have on this subject or of your experiences in diagnosis/treatment/aftercare. All information given is for reference only and does not constitute or should replace qualified veterinarian advice.

[jen526]

I went to a recent talk on Atypical Myopathy by Victoria Copas MA Vet MB Cert AVP (EM) MRCVS from Liphook Equine Hospital,
below is the information that was provided, it is very worth while reading. I had no idea about the Sycamore trees, our field is surrounded by very mature Sycamore trees on two sides....

SEASONAL PASTURE MYOPATHY (atypical myopathy, atypical myoglobinuria)

Victoria Copas MA Vet MB Cert AVP (EM) MRCVS
Resident in Internal Medicine
Liphook Equine Hospital
Tel: [phone]
Email: [e-mail]

The majority of equine myopathy cases are associated with exercise. Non-exertional myopathies are rarely recognised in horses but include postanaesthetic myopathy, polysaccharide storage myopathy, vitamin E or selenium deficiency, ionophore toxicosis and immune mediated myositis (Streptococcus equi equi). Additionally there are several reports from different countries (Europe and USA) which describe an unusual myopathy of unknown aetiology seen primarily in young, unexercised, turned-out horses, often following inclement weather. The condition has frequently occurred as an outbreak and often carries a poor prognosis for survival and recovery. Although recognised as long as 90 years ago, cases appear to be more common in recent years.

CAUSE
Multiple cases are frequently seen on the same premises, which suggests an infectious, toxic or nutritional aetiology although no evidence of infectious agents has been shown in affected horses and no consistent deficiencies have been demonstrated. The cause of seasonal pasture myopathy is therefore suspected to be due to a toxin, perhaps from fungi, plants or bacteria, although the exact aetiologic agent is not known.
Some evidence of association with toxins from Clostridium sordellii and bifermantans has been presented. The similarity, both clinically and pathologically, with ionophore toxicosis (eg monensin, lasalosid, salinomycin) is striking and it may be that a naturally occurring ionophore mycotoxin could be a causal factor. Association with maple/sycamore trees is common and might conceivably reflect a toxin directly from the leaves/seeds or associated with mycotoxins. Indeed several fungal species have been found on affected premises including Trichoderma, Alternaria, Cladosporium, Aspergillus and Penicillium.
Myocyte mitochondrial metabolic dysfunction is suspected to underly the condition, perhaps associated with a toxin-induced multiple acyl-CoA dehydrogenase deficiency (MADD).

CLINICAL PRESENTATION
Affected cases generally demonstrate sudden onset of weakness and stiffness, perhaps with tremors and sweating, which may then progress to recumbency. Myoglobinuria is frequently observed. Rapid progression to death may occur in 80-90% of cases over the course of 6-72 hours. Profound weakness with low head carriage and head oedema is sometimes seen. Some cases may be found dead with no previously observed clinical signs. Pyrexia is uncommon and appetite is variable. Tachycardia is common and occasionally arrhythmias may be detected. Respiratory distress is a poor prognostic sign and probably reflects intercostal muscle and diaphragm damage. Apparent head-tossing behaviour, mild diarrhoea and choke may sometimes also be seen.
The number of affected animals in outbreaks has been variable. Single cases are reported although it is more common for two or more to occur on the same premises within a few days of each other. One outbreak in Germany resulted in the death of 111/115 horses. Where single clinical cases are seen, blood testing often reveals many subclinically affected herdmates. Recurrence on the same premises in subsequent years has been reported.
Reported mortality rates of clinical cases have ranged from 33% to 100% and may vary from year to year but is typically around 80-90%. Most terminal cases have succumbed within 48 hours although some have survived as long as a week. Most cases still alive at 5 days are most likely to recover. In cases which have survived, recovery has sometimes been slow and incomplete.
DIAGNOSIS
Measurement of serum or plasma CK reveals rapidly increasing levels but has no prognostic relevance. Prompt sampling might not reveal very high CK levels but further increases within 4-6 hours will be seen. Cardiac troponin I may be increased in some cases.
Low arterial oxygen and high lactate levels may be useful prognostic indicators reflecting poor respiratory function.
Hyperglycaemia, hypertriglyceridaemia and hypocalcaemia are also very commonly seen.
In addition to myopathy, there is often biochemical evidence of hepatopathy.

Box 1. Useful laboratory tests in blood samples

Urinary dipsticks will reveal myoglobinuria (“blood”-positive) where not grossly obvious and glycosuria is also common.

POST MORTEM EXAMINATION
Muscle abnormalities are not always obvious at post mortem although pallor and haemorrhage is reported in some cases especially in intercostals, diaphragm, neck and shoulder muscles as well as occasional cardiac involvement. Myoglobinuria may be detected on examination of the bladder.
Histopathologic changes are found in type I rather than type II muscle fibres. They are most consistently found in the diaphragm and intercostal muscles. Oil red O staining indicates marked lipid accumulation within myocytes.

RISK FACTORS

Individual characteristics
No breed predisposition has been demonstrated although unworked young horses and females turned out to pasture are most commonly affected. The majority of affected cases are less than 3 to 4 years old but any age may be affected. The high incidence of the condition in young horses may be as a consequence of a primary age-susceptibility (e.g. related to immunity, deficiency, toxicity), different ingestive behaviour or the fact that young horses may be more likely to be turned out. The apparent predisposition in females, may result from them being more likely to be turned out also (eg broodmares) in comparison with stallions and geldings. Additionally, horses in poor body condition that have not received regular prophylactic healthcare (vaccines and deworming) may be predisposed.
Field characteristics
Fields with access to a river, stream or pond, sloping pasture and the presence of dead leaves have all been recognised frequently in outbreaks. Presence of maples and sycamores are common in affected fields.

Season
A strong seasonal incidence is apparent. About 75% of reported cases have occurred in the autumn with the majority of remaining cases occurring in spring with a few in the winter (virtually none in summer).

Weather
Weather has generally been severe leading up to outbreaks, including cold, cloudy, strong winds, increased humidity, rain and sometimes frosts.

TREATMENT
Treatment for suspected cases of seasonal pasture myopathy is largely supportive:

Analgesia
Many cases show extreme pain that is unresponsive to NSAIDs, opioids and alpha-2 agonists and probably warrant euthanasia in such cases. Cases showing just stiffness and weakness and minimal pain are more likely to survive. NSAIDs may not be ideal where dehydration and nephrotoxic myoglobin is also causing renal insult.

Fluids and electrolytes
Fluid therapy (preferably iv) is essential to provide routine hydration, to protect the kidneys from myoglobin, and to facilitate correction of electrolyte abnormalities (especially hypocalcaemia). Initial fluid rates of around 2-5 mL/kg/hour (1-3 L/hr for 500 kg) should suffice.
Normal ionised calcium concentration is approximately 1.5 mmol/L (total calcium 3.0 mmol/L). Attempts to calculate a calcium deficit using available formulae often fail in this author’s experience and it is suggested that empirical supplementation followed by rechecking calcium status is the most practical method of correction. Most calcium deficits seen in horses can be corrected with provision of around 100 mL 40% calcium borogluconate which can be given subcutaneously or added to iv fluids, followed by repeat administration if required. Subsequently, routine supplementation of 5L fluid bags with 50 mL 40% CaBGC (ie 10 mL per litre of fluids) should account for ongoing calcium requirements.
Glucose/dextrose addition to iv fluids has been advocated, in view of the finding of lipid accumulation in myocytes, as a possible means of stimulating carbohydrate metabolism although this has not been critically evaluated. Given that most cases are already hyperglycaemic, this generally requires insulin infusion alongside.

Vitamins and minerals
Vitamin E and selenium have been administered empirically or following discovery of low serum concentrations in a few cases. Vitamin E requirements should be ensured (approx 1 IU (0.7 mg) per kg per day). Vitamin C might also be a useful antioxidant. Supplementation with carnitine, vitamin B1, and B2 is might also support mitochondrial function.

PREVENTION
Autumnal outbreaks are often followed by further problems the following spring warranting planned management changes.

• Housing horses (especially younger stock not in work), for at least part of the day, in the autumn during and after inclement weather may reduce the incidence of cases. Where this is impractical then forage should be provided, perhaps in association with restricting the turnout area
• Fence off areas near trees with dead leaves/seeds on the ground. Remove leaves/seeds from pasture.
• Fence off areas near streams/ponds etc… and provide tap water
• Reduce stocking density
• Access to a salt/mineral block may be helpful along with general healthcare including regular vaccination and deworming.
• Manure spreading may pose a risk and should be discouraged. Conversely dung collection from pasture may be helpful.
• When a case is seen or suspected then herdmates should be removed from the pasture and CK measured as subclinical cases are common. Provision of antioxidant supplements (e.g. vitamin E 1.0 IU (0.7 mg) per kg BWT daily) may be worthwhile.
• Stable (for part of day at least) following bad weather in autumn
• Watch for alerts from Atypical Myopathy Awareness Group

[Deleted]

Thanks for the update Jen, it's a scary subject when you start reading up but something we all should be aware of.

[jen526]

Vets are more aware these days too. We have had one fatality and one survivor. An informed owner and rapid treatment is the only hope a horse has with this, scary how quick it kills. xx

[jen526]

Admin, this information needs updating from the start. Much more is known by scientists over the last few years. The symptoms have not changed but the rest is very out of date. Im happy to provide the information, or feel free to take it from my notes pages on my facebook page "equine atypical myopathy myoglobinuria" please email me if you would like me to help x

[jen526]

To update the IHDG: please do visit my facebook page too, Equine Atypical Myopathy myoglobinuria, on the notes pages you will find all the latest research, links and management of affected pasture, questions answered and much more. this is the link to one of the notes pages from that site: www.facebook.com/notes/equine-atypical-myopathy-myoglobinuria/most-common-questions-asked/801628693246274

The Cause
Hypoglycin A, is, today considered the toxin responsible for Atypical Myopathy, being present in the seeds, leaves and seedlings of some Acer such as Acer pseudoplatanus (= maple/Sycamore tree)

Risk Season: Autumn & Spring are peak seasons. Rain/showers and wind, Acer/Sycamore seeds, leaves or Seedlings on the pasture.

Areas at Risk: : Any paddock with Sycamore/Maple trees on or near the paddock, the wind can blow the seeds upto 500 meters. Remove the seeds and fallen leaves in the autumn and look out for/remove seedlings in the Spring. The most commonly affected animals are the younger ones out at grass 24/7, not in work. Those not immunized, rugged, fed supplementary feed or provided with shelter are also higher on the risk list.

Warning Signs: Atypical means “no typical scenario”, warning signs could be one or more of the following:
Lethargy, reluctance or inability to move
Head held low, an almost laminitic type stance (if still standing) Can look similar to colic, gut sounds often normal
Decrease in appetite, will still eat and pass Urine/droppings
Quarter muscles tense, possibly with some trembling, shoulders the same, the trembling seems to come in waves
Red nostrils
Vocal
Depressed
Dark Urine
Increased respiratory rate

IF YOU SUSPECT ATYPICAL MYOPATHY, CALL YOUR VET IMMEDIATELY.
For further information: www.facebook.com/pages/Equine-Atypical-Myopathy-myoglobinuria/184297444979405
For updates on research, cases, alerts:
labos.ulg.ac.be/myopathie-atypique/the-disease