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Not all diseases have cut-and-dried diagnoses. In this article, veterinarians walk us through actual cases of three tough-to-diagnose diseases: botulism, EPM, and Potomac horse fever.

Posted by Diane E. Rice | Dec 10, 2019 | Article, Botulism & Shaker Foal, Diseases and Conditions, Equine Protozoal Myeloencephalitis (EPM), Horse Care, Neurologic Disease, Potomac Horse Fever, Working With a Veterinarian

M urphy’s Law lives strong in the horse world.

If there’s one nail in a 40-acre pasture, unseen forces seem to inevitably draw your horse to it, resulting in a nasty gash. The one time you leave the feed room door unlatched, your horse escapes his stall and gorges on grain, resulting in a painful case of laminitis or colic. And if there’s a disease-causing organism within 50 miles, it’s as if it must hone in on your horse.

Some types of cases appear on your veterinarian’s call list almost daily: palpations, lacerations, lameness. But less-common diseases—including some that might manifest as more common ones—can come as out-of-the-blue surprises.

Knowing the realm of diseases your horse’s clinical signs might indicate could impact the information and urgency you convey when you call your veterinarian.

To help you build your knowledge arsenal, read on as veterinarians walk us through actual cases of three tough-to-diagnose equine diseases: botulism, equine protozoal myeloencephalitis, and Potomac horse fever. Familiarity with their signs could one day help save your horse’s life.

Treating veterinarian: Amy Johnson, DVM, Dipl. ACVIM, assistant professor of large animal medicine and neurology at the University of Pennsylvania School of Veterinary Medicine’s New Bolton Center, in Kennett Square

Five to 10 cases per year at the hospital.

Botulism due to Clostridium botulinum bacterial toxicity occurs when:

Vaccinate adult horses in C. botulinum-affected (-endemic) areas and all broodmares to protect their foals. Note, however, that the vaccine is only effective against botulism Type B—one of three major serotypes (A, B, and C) that exist in the U.S.

Type A is associated with soil and most common in the Western states. Type B, typically found in soil, accounts for about 85% of U.S. equine cases and is most common east of the Mississippi River, particularly in the mid-Atlantic states and Kentucky. Type C is seen sporadically across the U.S. and is associated with carrion.

Although the botulism vaccine falls into the risk-based category, Johnson considers it a core vaccine in her endemic area of Pennsylvania.

All the different toxin serotypes produce the same clinical signs, she says, but you can distinguish them in the lab if you submit blood for testing. That can be important for epidemiological purposes—studying disease incidence, distribution, and control—and for knowing whether the vaccine might be protective.

Other preventive measures Johnson suggests include:

Botulism frequently causes clinical signs similar to colic: lying down, not eating, and appearing distressed—sweating and shaking—while standing.

A 5-year-old Thoroughbred mare from a nearby race training facility presented with typical coliclike signs.

She was trembling, sweating, looking very distressed, and wanting to lie down. Her heart rate was high, 60-80 beats per minute, and she didn’t have very good gastrointestinal (GI) sounds when we listened to her. She had no fever, and when we passed a nasogastric tube, we didn’t obtain any reflux from her stomach (as you might expect to find in a colicking horse).

Related Content: Botulism: Deadly to Horses (Podcast)

Related Content: Botulism: Deadly to Horses (Podcast)

One of the first signs that led to our botulism diagnosis was that the horse had difficulty swallowing the stomach tube (affected horses typically don’t swallow well), she says.

The second clue was that when she lay down, she lay perfectly still. The sweating and shaking stopped; she looked much more relaxed. Horse with botulism are using all their energy reserves to recruit muscle fibers to keep them on their feet. When they lie down, they aren’t fighting gravity anymore and can relax.

Another clue was that because botulism causes weakness rather than pain, typical painkillers used for colic (sedatives such as xylazine or analgesics such as flunixin meglumine) won’t make a horse with botulism look or feel any better.

Once we have a clinical suspicion of botulism, we’ll typically do a tongue stress test—pulling the horse’s tongue out of his mouth to see how quickly he’s able to retract it.

We might also do a grain test where we offer 8 ounces of sweet feed in a pan to see if he’s able to eat any and how quickly he consumes it. A normal horse will almost always consume it within two minutes. But horses with botulism, even if they’re interested in the grain, will take a couple of bites and chew and chew, but because they’re unable to swallow will drop it from their mouth. It might even come back out through their nose.

Johnson describes her approach: The toxin binds to the part of the neuron—the lower motor neuron—that tells muscle fibers to contract. Once the toxin begins to take effect, you see increasing muscle weakness progressing to very flaccid paralysis. Every hour or two you wait, if the horse is still absorbing toxin from his GI tract, the disease will continue to worsen.

Once we’re convinced the clinical diagnosis is botulism, we give the horse a dose of antitoxin, a plasma product from another horse that has been hyperimmunized and built antibodies against the toxins.

The antitoxin doesn’t reverse clinical signs; it halts disease progression by attaching to botulinum toxin still circulating in the bloodstream and binding it before it can get to the lower motor neurons.

The mortality rate is high among horses exposed to a large amount of toxin and not treated quickly. And the critical treatment window varies with the type and amount of toxin consumed. The only thing that can clue you in is the rate of progression. If a horse ingested just a small amount of toxin, he might eat or drink abnormally for several days but still have the ability to walk around. He won’t spend much time lying down and will only have a little difficulty swallowing. But if the horse has ingested a lot of toxin, he can go from appearing totally normal to being recumbent (unable to rise) in less than 12 hours.

The good news is, if you can stop disease progression, horses can recover fully and return to their previous level of athletic performance, usually with no long-term effects.

Along with antitoxin, supportive care via a nasogastric tube, due to the horse’s inability to swallow, can maintain hydration and nutrition. Sometimes veterinarians give intravenous (IV) fluids. And sometimes, because of the horse’s weak swallow, aspiration pneumonia makes antibiotics necessary. Also, painkillers can alleviate discomfort from not being able to shift position while lying down.

Finally, if the horse doesn’t have a strong blink we can apply eye ­lubrication.

Usually it takes 10-14 days for a horse to regain full ability to swallow, so you might need to tube the horse or provide supplemental nutrition and hydration for as long as two weeks.

If the horse has lost his ability to get up, he might need the help of a sling for two, three, even four weeks until he’s regained that ability. Standing even for 15 minutes to an hour gets the blood flowing in all those muscle groups and prevents complications, such as limb contractures, that can come from recumbency.

Happily, the case mare recovered completely and is now a successful broodmare in Kentucky.

Treating veterinarian: Bill Gilsenan, VMD, Dipl. ACVIM, internal medicine specialist at Rood & Riddle Equine Hospital in Lexington, Kentucky

Rood & Riddle veterinarians see 25-50 cases of this neurologic disease per year. While exposure to its causative agents is fairly common, only a small percentage of horses develop clinical signs.

Two agents cause EPM: the protozoon Sarcocystis neurona (the most common) and Neospora hughesi. Opossums, the definitive host, shed infective protozoal sporocysts into the environment via feces. Secondary, or intermediate, hosts include raccoons, cats, skunks, and armadillos. Horses are dead-end hosts, unable to transmit the disease to other horses.

Horses ingest opossum feces in feed, in water, or while grazing, and while researchers aren’t exactly sure how sporocysts migrate from the GI tract to the central nervous system (CNS), they suspect they cross the blood-brain barrier through cell transport into the brain and spinal cord.

RELATED CONTENT | Update: EPM in Horses (Special Feature)

RELATED CONTENT | Update: EPM in Horses (Special Feature)

No immunization exists for EPM. However, management practices can help minimize exposure, including:

Unfortunately, it’s difficult to prevent EPM because the hosts, protozoa, and horses share environments.

Horses with EPM can exhibit signs similar to those caused by many other CNS diseases. Signs can be moderately acute (coming on quickly) or more gradual, which is one reason EPM can be so difficult to diagnose.

Both infective organisms cause the same clinical signs, but while N. hughesi can be found throughout the country, EPM cases caused by it seem more common on the West Coast.

A 15-year-old Warmblood gelding in Southwest Ohio suddenly lost body control and developed an abnormal gait. The signs were pretty dramatic, says Gilsenan—a Grade 3 of 5 neurologic. He could walk without risk of falling, but the veterinarians were worried he might fall on a circle or going down- or uphill. To the owner’s knowledge, the horse had no history of trauma to the skull or spine.

When the gelding came in, EPM was at top of the list of suspected diagnoses, Gilsenan said, but he and his colleagues needed to perform testing to confirm it.

When we do a neurologic exam, we try to localize the lesion and figure out what part of the nervous system is likely to be affected.

This horse’s attitude and cranial nerve reflexes were normal, but he had a really long-strided, almost stiff appearance to all four limbs. He also dragged his toes and, when you circled him, he’d swing his hind limbs out. At a stop he had a hard time standing squarely; all four feet pointed in different directions. Those findings led us to localize the lesions to the spinal cord—most likely in the neck, since that’s where neural pathways originate that affect the front and back limbs.

With signs of spinal cord disease, get neck radiographs to rule out:

This horse’s radiographs were normal.

Next, we did a spinal tap to help differentiate causes of disease. We tested the cerebrospinal fluid (CSF), which showed he had a really high proportion of CSF antibodies (against S. neurona) compared to those in his blood, and that allowed us to make the EPM diagnosis.

About 25% of horses with EPM recover fully, and about 80% improve at least one neurologic grade.

Gilsenan describes his approach: Because the horse’s prognosis depends on how soon treatment begins, your veterinarian will most likely start treating a suspect EPM case with any of several antiprotozoals before test results even arrive.

In most cases treatment lasts 28 days, with four weeks to see improvement. In some instances treatment might extend to two or three months. It can be difficult to decide when to finish treatment, as we don’t have a means of determining when the infection is completely cleared.

Adjunctive therapies that might help, at the veterinarian’s discretion, include:

This horse responded well to treatment. He returned to normal over four to six weeks. About 25% of horses fully recover, and about 80% improve at least one grade; these horses might return to being ridden safely. Visual effects (muscle wasting) resolve as the horse resumes exercise and regains strength.

Treating veterinarian: Bryan Waldridge, DVM, MS, Dipl. ABVP, ACVIM, internal medicine clinician at Park Equine Hospital at Woodford, in Versailles, ­Kentucky

The University of Kentucky reported 26 cases from Jan. 1 to Aug. 27, 2018, which is comparable to most years.

The causative agent is ­Neorickettsia risticii, a bacterium found in some fluke parasites that infect aquatic snails and larvae of aquatic insects such as mayflies.

Horses can ingest the infected insects (through grazing or eating hay and uncovered feeds) or possibly drink the flukes directly from streams and rivers.

Potomac horse fever becomes catastrophic when the horse also gets ­laminitis—inflammation of the sensitive tissues connecting the coffin bone to the hoof wall in the foot. Severe to life-­threatening laminitis occurs in about 40% of PHF cases, and it can occur anywhere in the disease’s course. It’s a side effect you must deal with long-term, says Waldridge. If the horse is infected by a strain likely to cause laminitis, there’s little veterinarians can do to prevent it, he says.

Decide, in consultation with your veterinarian and depending on your particular situation, whether to vaccinate your horse with the risk-based PHF vaccine. The downside is it’s made from one strain from one horse so, depending on what strain your horse gets exposed to, it might or might not be effective, says Waldridge. Other preventive steps include:

Loss of appetite, fever as high as 104-105 degrees F, diarrhea, and laminitis. Waldridge says he’s seen horses with all combinations of these clinical signs. Potomac horse fever tends to be a mid- to late-summer disease, though it began affecting horses in late spring in Kentucky this year, possibly attributable to abundant rainfall in April and record-breaking heat in May.

A 3-year-old Thoroughbred colt from a well-managed breeding farm. The horse had been vaccinated against PHF; he never drank water that wasn’t from the tap; and he had no exposure to natural water sources. Still, he got sick and suffered from the worst PHF signs Waldridge had ever seen. It turned out that a light mounted outside the barn near his stall attracted bugs carrying the bacterium.

We first take bloodwork, which indicated a low white blood cell count that goes along with gut disease. We also looked at serum chemistry (to assess liver and kidney function).

Definitive tests are polymerase chain reaction to determine the presence of N. risticii DNA in blood and in manure.

The IV antibiotic oxytetracycline is our first line of defense, and it’s pretty inexpensive. We might also use oral doxycycline. The sooner treatment starts, the better your horse’s prognosis.

Resolution depends on the strain to some degree. The really bad strains, like the case horse’s, cause animals to just get sick and die. But for strains that respond, usually by the end of 24 hours of treatment, the fever comes down and the horse goes back on his feed. Then in two to three days his manure starts to firm back up.

About 60% of horses respond to treatment. If they do respond and don’t develop laminitis, there’s no lasting effect.

This horse foundered and was euthanized.

While some diseases have cut-and-dried diagnoses, others can cause vague clinical signs or ones that can be confused with other disease’s symptoms. It’s imperative to work with your veterinarian to arrive at a speedy and accurate diagnosis. “If you don’t pursue the appropriate diagnostics, you may be unintentionally mis-treating a disease,” says Gilsenan.

Diane Rice earned her bachelor’s degree in agricultural journalism from the University of Wisconsin, then married her education with her lifelong passion for horses by working in editorial positions at Appaloosa Journal for 12 years. She has also served on the American Horse Publications’ board of directors. She now freelances in writing, editing, and proofreading. She lives in Middleton, Idaho, and spends her spare time gardening, reading, serving in her church, and spending time with her daughters, their families, and a myriad of her own and other people’s pets.

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