Category Archives: Equine health

Rethinking EPM or Wobbler Diagnoses: Signs of West Nile Virus in Horses

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Unfortunately, clinical signs of West Nile virus (WNV) aren’t unique, making it difficult for practitioners to suspect WNV above other neurologic diseases. For this reason, researchers from the University of Florida set out to closely scrutinize the clinical signs of WNV to see if any are particularly unusual. Records of 46 horses admitted to the hospital in 2001 with confirmed cases of WNV encephalitis were reviewed to try to find features that set this disease apart.

The most common clinical signs were weakness and/or ataxia (100% of horses), fever (65%), and muscle fasciculations (twitching; 60%). Fourteen horses (35%) became recumbent from the illness, and 10 of these had to be euthanized. The overall mortality rate was 30%, compared to a rate of 38% across the United States in that year. Importantly, 18 of the 46 horses (39%) had previously received one WNV vaccination, and one horse had received two vaccinations. The most relevant clinical findings were fever, which differentiates WNV from EPM (equine protozoal myeloencephalitis) and cervical myelopathy, and the consistent findings of weakness and/or ataxia, coupled with muscle fasciculations.

Porter, M.B.; Long, M.T.; Getman, L.M.; et al. Journal of the American Veterinary Medical Association, 222 (9), 1241-1247, 2003.

Wobbler Syndrome in Older Horses

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Wobbler Syndrome in Older Horses

By Erica Larson, News Editor

Mar 28, 2013

Wobbler Syndrome in Older HorsesThe gold standard for diagnosing CVSM is the meylogram (seen here), a procedure that involves injecting dye into the spinal canal before taking a set of radiographs to evaluate the spinal column’s width and to identify possible sites of compression.

Photo: University of Kentucky Gluck Equine Research Center

The neurologic condition cervical vertebral stenotic myopathy (CVSM, commonly known as wobbler syndrome) is much less common in older horses than it is in young, growing animals. But according to one clinician, this condition should be on all veterinarians’ differential diagnoses list when evaluating an aged horse presenting with neurologic signs and/or neck pain.

At the 2013 Western Veterinary Conference, held Feb. 17-21 in Las Vegas, Nev., Laurie Beard, DVM, MS, Dipl. ACVIM, associate clinical professor at Kansas State University’s College of Veterinary Medicine, presented a review of CVSM in aged horses.

Horses affected by CVSM essentially have a damaged spinal cord. The major causes of spinal cord damage include cervical (neck) vertebrae malformation or trauma.

“The exact pathogenesis of CVSM in older horses is unknown and likely different than younger horses,” Beard said. She said older horses are more likely to have lesions located in the caudal cervical vertebral column (near the base of the neck), between the vertebrae C5 and C6 or C6 and C7. She noted that some studies suggest biomechanical loading related to “wear and tear” could contribute to lesions. Additionally, she said, articular process osteophytosis (bony remodeling) is a common finding in older horses with CVSM.

Beard said common clinical signs associated with CVSM in older horses include:

  • Spinal ataxia (incoordination), generally symmetric with the hind limbs affected more than the front limbs. Beard noted that in some cases, however, mature horses with CVSM might appear more lame than ataxic;
  • Neck pain or stiffness;
  • Neck arthritis; and
  • Decreased appetite.

Beard said veterinarian frequently use standing cervical radiographs to diagnose CVSM in mature horses. However, if cervical radiograph results are inconclusive, a myelogram, considered the gold standard CVSM test, might be required. This procedure involves injecting dye into the spinal canal before taking a set of radiographs to evaluate the spinal column’s width and to identify possible sites of compression.

Treatment options for mature horses diagnosed with CVSM include:

  • Anti-inflammatory drugs (both steroidal and non-steroidal, depending on disease severity);
  • Natural vitamin E supplementation (Beard explained that vitamin E is an antioxidant that could act as an anti-inflammatory in horses with CVSM);
  • Cervical facet steroid injections (this procedure must be repeated every six months or so, but can reduce pain and soft tissue swelling); and
  • Surgical correction (which typically consists of fusing the affected vertebrae–the movement of which causes the spinal cord compression–together using a metal implement called a “basket” in a surgical procedure called cervical stabilization).

The prognosis for for return to work in mature horses with CVSM is variable and depends on the degree of ataxia present, Beard said.

“A horse with mild clinical disease that is a trail riding horse (or low-level performance horse) probably does have a reasonable chance of still performing,” she said. “However, higher level performance horses probably will not be able to perform at the level they were.”

Additionally, horses used for pleasure riding are more likely to have a good prognosis for full return to athletic function than higher performance athletes, she said.

Take-Home Message

Although it’s commonly thought of as a young horse disorder, Beard stressed that veterinarians should consider CVSM as a differential diagnosis in any horse with spinal ataxia. Prognosis for return to work depends on the degree of ataxia present, but many horses show improvement with medical management, she said.

Emerging Neurological Syndromes

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Emerging Neurologic Syndromes Discussed at World Equine Vet Meeting

“The more we look for neurologic signs, the more we discover new syndromes,” said I.G. Joe Mayhew, BVSc, FRCVS, PhD, Dipl ACVIM, ECVN, head of Equine Massey and professor of Equine Studies at Massey University in New Zealand, at the 2009 WEVA Congress. Mayhew gave several presentations, including an update on emerging neurologic syndromes.

“Over the last five years or so, we have learned much about existing and new (neurologic) disorders in horses from documentation of careful clinical observations and interventions, and from painstaking pathologic studies with special emphasis on clinicopathologic correlates,” he noted. “This paper will highlight a few of these disorders through which we have added to our understanding of anatomy, physiology, and clinicopathologic correlates–the building blocks for advancing equine neurology.”

Unintentional Parasite

Some nematode parasites that cause neurologic disease in wild and domestic ruminants have now been found to cause problems in horses.

Parelaphostrongylus tenuis is a lungworm that’s life cycle includes cervids (horned animals, such as deer) worldwide, including some in North America. This parasite passes through the host’s central nervous system (CNS) as part of its life cycle. In horses (although not a normal host for the parasite), it has been found to cause acquired cervical torticollis (“wry neck”) due to contraction of the cervical muscles that produce a twisting of the neck and an unnatural posture of the head.

“The scoliosis (curvature of the spine) was clearly argued to be due to loss of afferent cervical proprioceptive inputs because of the dorsal gray column lesions with some white matter involvement accounting for ataxia and weakness,” Mayhew said.

“These nematodes appear to be sensitive to various anthelmintics, such as fenbendazole and ivermectin, and such therapy has been successful when the cases have been treated soon after onset of clinical signs,” he continued.

Cervical Vertebrae Problems

Injury to the cervical vertebrae can affect the horse’s balance. “Special proprioceptive inputs from the cranial cervical vertebral ligaments and muscles pass via at least the C1-3 dorsal spinal nerve roots to ascend the spinal cord via the spinovestibular tract to the caudal vestibular nuclei,” said Mayhew. “These nuclei receive no other afferent inputs. Lesions involving these cranial cervical nerves or the vestibulospinal input to the vestibular apparatus can result in signs of vestibular disease (such as incoordination or loss of balance).”

He said confirmation that apparent neck stiffness and pain, or thoracic limb lameness, is emanating from specific arthritic vertebral articulations “requires radiographic and possibly scintigraphic (on bone scan) evidence of active arthritis and positive relief being achieved from intra- and peri-articular injection of local anesthetic agent.”

Electrodiagnostics

Mayhew reported on a “very sensitive and quite specific electrophysiologic test for disruption of somatic motor pathways in disease states” for horses with neurologic problems such as wobbler syndrome. “When used with the more elaborate, but error-prone, quantitative EMG investigations, this should allow more accurate identification of the presence and location of conduction blocks (electrical impulses to muscles), and, thus, functional lesions, in neurologic disease states such as wobblers and unusual hind limb gait abnormalities,” he explained.

Scandinavian Knuckling Horses

There have been reports of several individual cases and at least five “outbreaks” in groups of horses of a hind-limb knuckling syndrome. In one outbreak 24 cases occurred in a population of 75 animals. Only three of the 24 survived, and one of those three recovered fully.

Veterinarians have described another 75 cases of idiopathic (unknown origin) knuckling in horses in Norway, with no cause determined, but a frequent finding in the cases was poor feed in the form of low-quality baled silage. “Peripheral neurotoxins of plant or nonbiologic origin would be the most likely cause of these crippling syndromes,” said Mayhew.

Equine Motor Neuron Disease

“Acquired equine motor neuron disease (EMND) is a fascinating neuromuscular disorder of horses that does not appear to have existed prior to 1982 and was first described by the late John Cummings (DVM, PhD) and co-workers from Cornell University in 1993,” noted Mayhew. “Hundreds, if not thousands, of horses now have been definitively diagnosed with EMND in North America and from around the world.”

Clinical signs of EMND in horses depend on the stage of the disease, he said. Those signs in early cases often include weight loss in the face of a good to increased appetite, increased recumbency (inability to rise), and slight muscle tremors at rest. “The weight loss often precedes the onset of trembling by several weeks,” he noted. “Many animals display an extended tailhead position that appears to be due to selective involvement of dorsal sacrococcygeal (pertaining to both the sacrum and the coccyx, or the tailbone) muscles that are postural muscles containing a high proportion of Type 1 (slow-contracting muscle) fibers. Atrophy is followed by fibrous contracture leading to an elevated tail position.

“A short-strided gait is commonly seen that can show a rapid placement of the foot at the end of the protraction phase akin to that seen with fibrotic myopathy,” he described. “This also may well be due to fibrous contracture of affected muscles that in this case are caudal thigh muscles involved in stifle flexion and/or hip extension.

“Ophthalmic examination reveals varying degrees of a mosaic pattern with dark brown to yellow brown pigment deposited in the tapetal zone (the tapetum being the iridescent membrane of the choroid of the eye), coupled with a horizontal band of pigment at the junction of the tapetum and nontapetum,” Mayhew said. “A clinical truism for the syndrome is that affected horses move better than they stand.

“Overall study of this disease has given us a better understanding of syndromes of diffuse weakness in horses and particularly weakness involving Type 1 postural, slow-twitch muscles,” he said.

Equine Polysaccharide Storage Myopathy

Equine polysaccharide storage myopathy (EPSM) is an autosomal recessive disorder in Quarter Horse and related breeds and can result in rather exceptional susceptibility to recurrent exertional rhabdomyolysis, reviewed Mayhew.

“The disease EPSM thus refers to the clinical syndrome of muscle disease, particularly rhabdomyolysis, with amylase-resistant, sarcolemmal inclusions of acid mucopolysaccharides evident on muscle biopsy sample,” he said. However, to differentiate EPSM from other diseases of this type, “where there are clinical signs of myopathy (muscle disease or disorder), but histologic evidence of no or mild myopathic changes with excess aggregates or cores of sarcoplasmic (material in which the fibrillae of the muscle fiber are embedded), mostly amylase-sensitive polysaccharide (glycogen), then a distinguishing term such as polysaccharide-associated myopathy should be used.”

EPSM is seen particularly as a likely autosomal recessive trait in Quarter Horses and related breeds and in several other breeds including draft horses.

EPSM is one cause of exertional rhabdomyolysis, and glycogen-associated myopathy probably is also.

“Signs of a hypometric (short-strided) gait, reluctance to move, thoracolumbar lordotic (swayback), and kyphotic (hunchback) postures, and several movement disorders can be seen in association with these disorders,” Mayhew said. He added that “glycogen-associated myopathy is not the cause of most cases of the common postural and movement disorder known as shivers in draft horse and many other breeds.”

Hyperkalemic Periodic Paralysis

Veterinarians have reported the autosomal dominant disease known as hyperkalemic periodic paralysis (HYPP) in Quarter Horse and Quarter Horse-related breeds. Most affected animals are 2 to 3 years old and are male. Homozygous animals (having identical alleles on the paired chromosome) are more severely affected than heterozygotes (those having only one allele).

“The owner notices intermittent episodes of muscle trembling over the body or face, sometimes with intermittent projection of the nictitating membrane (third eyelid), that may lead to involuntary recumbency,” said Mayhew. “Other warning signs include yawning, lowering of the neck, swaying, and disinterest in food and water. During a mild episode the horse is alert, appears distracted and reluctant to move, and may stumble as if weak.” He said that in a full-blown episode, fasciculations (muscle tremors), particularly involving the flank, shoulders, neck, and sometimes the face, progress to staggering, buckling, marked muscle spasms, and paralysis of the limbs might precede involuntary recumbency.

“A severe episode, perhaps following forced exercise, results in severe tremor and tetany (spasming) of many muscles with recumbency and sweating,” he described. “This is followed by a state of flaccidity, possibly with depressed spinal reflexes. Attempts to move the patient result in further tremor and tetany, although the horse remains alert. An episode may last several minutes to hours, typically less than an hour, with full and usually rapid recovery occurring. Between episodes, affected, well-muscled Quarter Horses appear essentially normal.

He said most owners notice stridor (high-pitched respiratory noise) at some time in affected horses. Exercise and rest following exercise might precipitate episodes, which can occur daily or monthly. Stressors such as transportation, weaning, and anesthesia also can trigger episodes.

Stiff Horse Syndrome

Mayhew said a stiff horse syndrome–similar to stiff person syndrome–has been reported. Clinical signs appear to wax and wane and range from mild muscle stiffness to sudden and often violent muscle contractions. Generally, the onset is insidious.

“Between episodes the horse may appear normal, although generalized muscle stiffness may persist,” said Mayhew. “Stiff person syndrome (SPS) has been recognized in humans for some time. It is characterized by muscle rigidity and episodic and often violent muscle cramps.”

In horses, Mayhew described, “Exercise intolerance associated with mild to moderate muscle stiffness may be the only initial clinical sign. This may easily be attributed to a primary myopathy, with pain on muscle palpation, although serum muscle enzyme concentrations remain in the normal range. Components of the syndrome bear resemblance to such disorders as tetanus, equine motor neuron disease, hyperkalemic periodic paralysis, exertional myopathies, and especially the acquired channelopathies associated with the mycotoxicoses, such as perennial ryegrass staggers.

“The most useful diagnostic test is detection of antibodies against the enzyme glutamic acid decarboxylase (GAD) in serum and cerebrospinal fluid, and although some cases have had high anti-GAD titers, several strongly suspected cases have been negative on this test,” Mayhew noted. “It may be necessary to liaise with a human hospital for analyzing for GAD antibodies in the obtained samples. The test relies on cross-reaction with human antigens.

“The overall message really is that with the array of enigmatic movement and postural disorders encountered in equine neurology that appear to be variations on the themes of stringhalt, shivering, and claudication (cramping), a broad approach to delving into possible etiologic mechanisms should be taken that includes the possibility of immune-associated neurotransmitter derangements, such as SPS.”

Grass Sickness

Grass sickness (equine dysautonomia) has been described since the early 20th century, said Mayhew. “Since then it has had quite a devastating effect on equine populations in parts of Western Europe,” he added. “Horses of all breeds, as well as nondomestic equidae and camelids, can be affected, and dogs, cats, rabbits, and hares are affected by similar dysautonomias.”

Mayhew said this disease usually occurs in 3- to 8-year-old horses that are kept outside during late spring and summer, although cases occur year-round. The problem rarely is seen in stalled animals.

“The disease occurs commonly in Northern and Western Europe, particularly in Scotland and England,” he said. “More recently it has been recorded as an epizootic (a disease that appears as new cases in a given animal population, during a given period, at a rate that substantially exceeds what is “expected” based on recent experience) in Hungary, where 15 out of 55 1- to 3-year-old horses in one group succumbed to the disease over one summer, with only three surviving.

“An identical equine dysautonomia known as mal seco occurs in at least Argentina and Chile in South America, and grass sickness appears to now occur in the horse in North America,” stated Mayhew.

Clinical signs can range from acute colic with gastrointestinal stasis (slowing/stopping) and rupture, to anorexia with mild signs of colic and ileus, to chronic intestinal disorder.

“Moderate tachycardia (rapid heart rate), indifference to food, difficulty swallowing, excessive salivation, depressed gastrointestinal sounds, abdominal distension, and usually mild colic are very often present to varying degrees,” noted Mayhew. “Muscular tremor and patchy sweating may be primary signs or may reflect the dehydration, electrolyte imbalances, and colic that occur. Posturing with all feet close together as a weak patient does, ptosis (drooping eyelid), and especially rhinitis sicca (wasting of the mucous membranes and glands with no secretions) are very distinctive signs when present. No definitive clinical diagnostic test exists.”

Atypical Myopathy

Mayhew said several hundred cases of highly fatal, atypical myopathy or myoglobinuria (myoglobin in urine, causing it to appear red-tinged) have been reported in young adult grazing horses. Most of these have been reported in Europe, but they’ve also been detected in North America and Australasia.

“Horses may be found dead or more often showing various signs of reluctance to move, stiff and short strides, apparent sedation, and fine muscle tremors,” he noted. “They quickly become laterally recumbent and urine becomes dark with myoglobin staining, although more subacute cases do occur.”

Symptomatic fluid and analgesic therapy (given as clinical signs dictate) with attentive nursing care for severely ill and often recumbent patients is called for, but the mortality rate of the disease is around 90%.

“Outbreaks do occur, usually in the colder months, and can occur repeatedly on a property,” noted Mayhew. “Access to trees and inclement weather appear to be risk factors for the disease. Plant, bacterial, and fungal toxins have all been considered as possibilities, but the cause or causes remain completely unknown.”

He said preliminary results from one group of investigators suggested thatClostridium sordellii and Clostridium bifermentans toxins might play a role in what they term “pasture myodystrophy.”

Veterinarians with suspected cases are urged to log on to the atypical myopathy alert site (ivis.org) and complete the appropriate forms. This might help in the effort to unravel the epidemiology of this disease.

Lateral Digital Myotenectomy to Treat Stringhalt

Mayhew said stringhalt, also known as springhalt and Hahnentritt (“rooster kick”), is an anciently recorded disease that is characterized by a sudden, apparently involuntary, exaggerated flexion of one or both hind limbs during attempted movement.

“The hind limb motion may be as mild as a slightly excessive flexion to violent movements during which the fetlock or toe will contact the abdomen, thorax, and occasionally the elbow with attempted strides leading to a peculiar bunny hopping and plunging gait,” he described. “The form that usually occurs as outbreaks is seen in Australia, New Zealand, United States, Chile, and Japan, and will be referred to as bilateral, plant-associated stringhalt.”

Usually there is symmetrical or slightly asymmetrical involvement of the pelvic limbs in this syndrome, with prominent distal (farther away from the horse’s core) muscle atrophy in severe cases. The thoracic limbs are also affected in severe cases, with knuckling of the forelimb fetlocks, prominent extension of more proximal joints (those closer to the horse’s body), and atrophy of the distal musculature in association with prominent stringhalt in both hind limbs.

Bilateral stringhalt has been associated with exposure to several plants, notably related species of flat weeds: Hypochoeris radicata, Taraxacum officinale (the common dandelion), and Malva parviflora (mallow weed).

“It is interesting that size and age may be predisposing factors in at least bilateral stringhalt, in so far as older and taller horses tend to become affected in preference to smaller horses, such as ponies and native Chilean breeds,” noted Mayhew. “Although palliative, removing a section of the myotendinous region of the lateral digital extensor muscle relieves the syndrome quite spectacularly in many cases.”

Temporohyoid Osteoarthropathy

Temporohyoid osteoarthropathy (THO) with proliferative osteopathy (bone disease) involving the temporal bone, temporohyoid joint, and hyoid bone in the head, is reported only in adult horses, said Mayhew. It might be subclinical (undetectable) or can result in difficulty chewing or, more often, neurologic syndromes, notably various combinations of facial and vestibulochoclear (ear) nerve dysfunction. (The horse’s tongue lies on the floor of the mouth and is composed of a mass of muscle anchored by the hyoid bone and the bodies of the left and right mandibles–lower jaw.)

“Some of the cases have bilateral disease as determined by endoscopic and radio imaging studies, although the clinical signs are most often unilateral (on one side),” said Mayhew. “The cause of temporohyoid osteoarthropathy is unclear, although to this author a traumatic origin is most plausible in most cases with chronic otitis (ear) media/interna (inflammation of middle/inner ear structures) accounting for a select few cases.

“Regardless of the etiology of the osteoarthritis, clinical signs can occur from either the osteoarthritis itself or from fractures of the adjacent temporal bone and, rarely, basilar bones, due to partial or complete fusion of the joint,” he said. “Physical examination findings may include difficulty chewing, pain on external palpation of the parotid area, headshaking, and behavioral problems–especially when being ridden.

“Once the joint is partly fused, sudden forced head jerking, falling, teeth floating, nasogastric intubation, and sudden prolonged vocalization can cause periarticular fractures of the petrous temporal bone, resulting in combinations of an abrupt onset of facial and vestibular nerve dysfunction,” he noted. “Endoscopic examination of the guttural pouch is probably superior to plain radiographic imaging in confirming the presence of the disease by revealing enlargement of the proximal stylohyoid bone due to osteoarthritis when compared to the opposite side. “In acute or progressive cases having ill-defined endoscopic and plain radiographic imaging findings, gamma scintigraphy should be considered as a diagnostic aid.”

Mayhew said he was aware of several cases that improved over time, only to show further signs relative to facial and vestibular nerve dysfunction in weeks to months time. “These would seem to be ideal candidates for unilateral surgical disunion of the hyoid apparatus,” he noted. “Initial surgical disunion of the hyoid apparatus was performed by removal of a midshaft portion of the stylohyoid bone. To reduce the temporary difficulties in swallowing encountered and to reduce the possibility of other real and potential complications of this surgery, the technique of ceratohyoidectomy was proposed and used with success.”

He said that except for major cranial fractures and residual eye problems, the outlook for survival with residual neurologic deficits is quite good. “Of 33 cases of temporohyoid osteoarthropathy, 20 cases survived for which there were longer term follow-up details,” he reported. “Of these, 70% returned to previous level of use, although more than 50% of the 20 horses still had evidence of facial nerve deficits and/or vestibular dysfunction.

“Thus, in spite of some optimistic suggestions, if full athletic performance without neurologic dysfunction is required, then the prognosis with or without surgical intervention has to be fair to guarded for these cases,” he said. “Cases of THO have given us a better insight into the ability of horses to accommodate to vestibular dysfunction and to survive with degrees of facial paralysis.”

Post-Anesthetic Cerebral Necrosis

A newly defined, unexpected complication of apparently routine general anesthesia in some mature horses is diffuse and severe cerebral necrosis, resulting in signs of diffuse (not concentrated or localized) encephalopathy immediately or some hours to days after recovery from anesthesia, reported Mayhew.

There is cerebral edema (fluid swelling) and laminar neuronal cortical necrosis associated with generalized signs that predominantly consist of somnolence (drowsiness) to dementia, central blindness, wandering compulsively, pushing against objects, and ataxia.

“One patient with this tentative diagnosis that recovered showed prominent muzzle and ear twitching, very reminiscent of patients suffering from bacterial meningitis and from West Nile viral meningoencephalitis (inflammation of the brain and the meninges–the membranes that cover the brain),” he said.

Early Detection of Equine Arthritis?

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Is Early Detection of Arthritis in Horses Finally a Reality?

Is Early Detection of Arthritis in Horses Finally a Reality?Radiography’s ability to correctly identify joints without OA was 97%, meaning it had few false-positives, and that radiography was equal to or better than MRI for detecting early joint changes consistent with OA.

Photo: Kevin Thompson/The Horse

Osteoarthritis (OA) is a progressive deterioration of joint health with no known cure. Not only does OA negatively affect athleticism and quality of life but it is also a major cause of economic loss throughout the equine industry.

For years researchers have been trying to find ways to diagnose OA early in the course of disease to either slow or, better yet, arrest its progression. And although OA has proven a stubborn opponent, an international group of researchers recently found that radiographs (X rays) and low-field MRI appear to be useful tools for diagnosing OA.

“For our study we chose to use Icelandic horses, a breed that is known to have a high prevalence of OA and one in which a large number of older riding horses are culled due to the pain and lameness that result from the disease,” explained Charles Ley, BVSc, Dipl. ECVDI, PhD, from the Swedish University of Agricultural Sciences, in Uppsala. “Young horses without obvious lameness were used in the study in order to include horses likely to have a very early stage of the disease and normal horses. We chose to use two noninvasive and clinically available imaging techniques—radiography and MRI—to see if it was possible to detect early OA changes in the joints.”

Ley and colleagues collected 75 hock joint radiographs and MRIs from 38 Icelandic horses between the ages of 27 and 31 months. The team then used microscopy to classify joints as positive or negative for OA.

The team classified 42 of the 75 joints as OA-positive after they detected lesions on both radiography and MRI that corresponded with OA, including mineralization front defects and joint margin lesions. The team determined that radiography’s ability to correctly identify joints without OA was 97%, meaning it had few false-positives, and that radiography was equal to or better than MRI for detecting early joint changes consistent with OA.

“Radiography is a widely available, cost-effective, and repeatable method, and the high specificity and high frequency of the detection of mineralization front defects in radiographs suggests that this is a promising marker of early OA in the distal intertarsal joint (one of the middle hock joints),” Ley concluded. “Such a tool has a vital role in selecting horses for inclusion in long-term studies of how and why OA develops and evaluating early intervention and prevention methods for OA.”

The study, “Detection of early osteoarthritis in the centrodistal joints of Icelandic horses: evaluation of radiography and low-field magnetic resonance imaging,” will appear in an upcoming issue of the Equine Veterinary Journal.

I pray that gentle hands may guide my feet; I ask for kind commands from voices sweet; At night a stable warm with scented hay, Where, safe from every harm, I’ll sleep til day. -Author Unknown.

Today I met with a “new” vet, Vet7, who was Chance’s very first vet over 15 years ago, when he was vetted at purchase. She came out to do a chiropractic and acupuncture consultation, along with a general check-up. Vet7, while she has a more holistic approach to vetrinary medicinw, she also practices Western medicine.

Vet7 looked at Chance from head to hoof and took a thorough medical history, and ran some tests. She mostly did some balancing and acupressure type diagnostics, and declared that while Chance may have had EPM, she felt that his ataxia was due to his cervical spine….

She explained her reasoning:

1. EPM diagnostics are sub par at best. Even the spinal fluid testing. And, like I previously posted, about 50% of horses in the USA are EPM positive while only 1% are symptomatic.

2. Vet7 did a stretch test with Chance’s neck- to the left, while he compensated by bending at the top instead of the bottom, he showed little flexibility and increased ataxia while doing so. The right side bend was easier. Typically, horses with Cervical issues have issues with the hind-end on the opposite side. Chance has issues with his right leg.

3. Typically horses with EPM respond to treatment. Chance is on his second round of EPM treatment and while his symptoms have had moments where they are less noticeable, there are other moments when his symptoms are prominent; mostly at times of stress. (ie: trailering, new donkey friends, etc).

4. Vet7 put a needle in one of the points in Chance’s tail. He responded immediately showing that he has feeling and strength in his tail, which is something most EPM horses do not exhibit. Typically, an EPM horse will have weakness in his tail, and a times their tail is too weak to lift when they goto the bathroom resulting in having dried manure along their backside.

Vet7 made some adjustments and stuck Chance with a handful of needles. At one point he fell asleep with his head in my arms. She proceeded to inject different points along his cervical spine and hips with B-12.  She taught me some stretches and massage techniques, exercises he and I could do together to increase his hind-end and neck muscles, and gave me some weight gaining instructions.

Chance will have Rice Bran added to his feed beginning with 1 cup for a week and slowly increasing to 2 cups. This will aid in getting his weight up. Apparently, horses are able to tolerate up to 30% fat in their daily diets.

She also suggested adding a Probiotic to increase his Immune system since the gut is the control center. There were other supplements that she felt maybe helpful as well, Cervical Formula, to help with his neck flexibility and overall health.

As for the exercises, in conjunction with turning him out daily, he and I will do stretches to help increase his neck flexion and balance, and I will hand walk him. We will walk on flat land, up and down small hills, and do serpentines. Eventually, increasing to twice a day and adding ground poles and lunging. This will help to develop the muscles, increase his flexion, decrease the ataxia, and aid in his overall health.

acupuncture

Vet7 will come back out in two weeks to see how he is doing…I’m hoping that we have finally found some answers and are closer to a solution.

IMG_2245  IMG_2249  11021196_860336367174_5928889682290861303_n  IMG_2226

Last night, I was mucking out Chance’s stall when suddenly I saw a little black fluffy creature skeet by followed by my dog.  I stick my head out of the stall, thinking (or hoping) it was the barn cat, only to see that my dog has cornered a skunk!  I yelled for her to “come”, but it was too late.

The pungent smell wafted towards me; it was so thick that I literally felt that the skunk had sprayed me in my mouth.  I grabbed Sadie, and with the help of the farm owner’s son, began to wash her.  I poured tomato juice all over her, followed by Dawn soap, and lots of water.  Thankfully, due to having her Rambo jacket on, she did not get much on her and the tomato and Dawn concoction worked!  The next thing was to tackle the corner of the barn where the skunk sprayed- tomato juice, Dawn, water, and due to the freezing temperatures, salt.

That was an interesting start to my evening at the barn!

The low temperatures has caused the 6+ inches of snow, surrounding the barn, to have a thick layer of ice on top.  Poor Chance has been stall bound for almost a week.  Even on a sunny day, when we try to let him outside or hand walk him, he goes straight back into his stall after a few laps.  However, his legs are looking good, he is full of personality, and his eyes are bright.

This week is his second week on the Marquis.  I have noticed that the twisting is not as prominent when I am walking him but that could be due to Chance concentrating more on walking due to the ice and snow- fingers crossed that it is due to the Marquis though.

I started him on a new blend of hay- an alfalfa mix- and he can not stop eating it.  I am hoping that the blend will help him gain some weight back especially since he is unable to access any grass right now.

I am hoping for some warmer days to melt this ice and enable Chance to get some exercise!

How To Prepare For An Equine Emergency

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Be Prepared for an Equine Emergency

You don’t want to waste time in an equine emergency! The American Association of Equine Practitioners (AAEP) offers these tips to keep you organized and calm in your horse’s time of need.

If you own horses long enough, sooner or later you are likely to confront a medical emergency. From lacerations to colic to foaling difficulties, there are many emergencies that a horse owner may encounter. You must know how to recognize serious problems and respond promptly, taking appropriate action while awaiting the arrival of your veterinarian.

Preparation is vital when confronted with a medical emergency. No matter the situation you may face, mentally rehearse the steps you will take to avoid letting panic take control. Follow these guidelines from the American Association of Equine Practitioners (AAEP) to help you prepare for an equine emergency:

    1. Keep your veterinarian’s number by each phone, including how the practitioner can be reached after hours.
    1. Consult with your regular veterinarian regarding a back-up or referring veterinarian’s number in case you cannot reach your regular veterinarian quickly enough.
    1. Know in advance the most direct route to an equine surgery center in case you need to transport the horse.
    1. Post the names and phone numbers of nearby friends and neighbors who can assist you in an emergency while you wait for the veterinarian.
    1. Prepare a first aid kit and store it in a clean, dry, readily accessible place. Make sure that family members and other barn users know where the kit is. Also keep a first aid kit in your horse trailer or towing vehicle, and a pared-down version to carry on the trail.First aid kits can be simple or elaborate. Here is a short list of essential items:
        • Cotton roll
        • Cling wrap
        • Gauze pads, in assorted sizes
        • Sharp scissors
        • Cup or container
        • Rectal thermometer with string and clip attached
        • Surgical scrub and antiseptic solution
        • Latex gloves
        • Saline solution
        • Stethoscope
        • Clippers

Many accidents can be prevented by taking the time to evaluate your horse’s environment and removing potential hazards. Mentally rehearse your emergency action plan. In an emergency, time is critical. Don’t be concerned with overreacting or annoying your veterinarian. By acting quickly and promptly, you can minimize the consequences of an injury or illness.

For more information about emergency care, ask your equine veterinarian for the “Emergency Care” brochure, provided by the AAEP in partnership with Bayer Corporation, Animal Health. More information can also be obtained by visiting the AAEP’s horse health web site, www.myHorseMatters.com.

The American Association of Equine Practitioners, headquartered in Lexington, Kentucky, was founded in 1954 as a non-profit organization dedicated to the health and welfare of the horse.

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Stem Cell Therapy

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Cutting Edge Cell-Based Therapies for Horses

Regenerative therapies, such as stem-cell therapy and platelet-rich plasma, can help speed up healing in equine tendon and ligament injuries and make the repairs stronger.

By Elaine Pascoe

Microscopic view of stem cells
Stem cells
Your horse has torn a major tendon in his leg, and the news from your veterinarian is not good. Even after months of rest and rehabilitation, she says, his tendon likely won’t be as strong as it was before the injury. It may limit what you can do with him. But then she mentions a new treatment: stem-cell therapy. It’s cutting edge?and costly. Could it help your horse?

Stem-cell therapy is one of several treatments that fall under the umbrella of regenerative medicine, a fast-growing field that’s creating major buzz in veterinary and human medical circles. These treatments use the body’s own repair tools with the goal of better healing. In this article you’ll find what you need to know about two regenerative treatments being used in horses, stem-cell therapy and platelet-rich plasma. For guidance we turned to Alison Stewart, DVM, an equine surgeon and stem-cell researcher at the University of Illinois, and Jamie Textor, DVM, an equine surgeon who is researching PRP at the University of California at Davis.

These treatments are exciting, but they are very much works in progress. Researchers are searching for the most effective ways to use them, and there are many questions about how?and how well?they work in different situations. They require specialized facilities and know-how that may not be available in every private veterinary practice. But they’re becoming more widely used, and if they live up to their promise, that trend will continue.

Stem-Cell Therapy
Stem cells are cells that have the potential to develop into some or many of the different specialized cells that make up body tissues, such as muscle, bone, blood and nerves. There are different kinds of these chameleonlike cells:

    • Embryonic stem cells are derived from fertilized embryos. Taken early enough they are totipotent?they can develop into any tissue type, Dr. Stewart says. They go through several stages, becoming less able to differentiate as they mature.
    • Induced pluripotent cells are adult cells that have been genetically reprogrammed in the lab so they behave like embryonic stem cells. Like embryonic stem cells, they proliferate readily and can differentiate into multiple tissue types. Researchers generated the first iPSCs less than five years ago and the first from horses only last year. They’re still exploring the potential of these cells.
    • Adult stem cells are found in many organs and tissues, typically in small numbers. They are multipotent?not as versatile as embryonic stem cells but able to differentiate into at least three specific cell types. These cells seem to remain at rest for many years until called on to generate replacements for cells that are lost through normal wear and tear, injury or disease. They also produce a range of bioactive proteins, including growth factors and other agents that help repair damaged tissue.

The commercial stem-cell treatments available for horses ?today make use of adult mesenchymal stem cells, or MSCs, which can differentiate into bone, cartilage, fat and fibrous connective tissue. The cells are autologous?derived from the horse being treated. (Experimental treatments have also been done using donor, or allogenic, stem cells.)

“The commercial treatments are ?mainly being used for soft-tissue injuries??tendons and ligaments,” Dr. Stewart says. They are used less for joint problems generally, although some veterinarians think that they can be helpful for stifle injuries that involve a lot of soft-tissue damage.

Tendons and ligaments have different functions?tendons transfer the action of muscles to the skeleton, while ligaments lash bone to bone and keep joints from wobbling. But both are made up mostly of organized networks of dense, elastic connective tissue, rich in a tough protein called collagen. And they basically heal in the same way?that is, slowly and often poorly, with disorganized scar tissue in place of organized collagen fibers. This leaves your horse prone to reinjury.

MSC therapy may allow better repair, with more organized collagen and less scarring, Dr. Stewart says. Your horse will still need a lengthy layup and rehab period, though. The therapy seems to help most when it’s given in the first few weeks after an injury, during the time when healing is getting underway. It’s much less effective for longstanding or chronic conditions.

MSC Treatment. If you and your veterinarian decide to try stem-cell treatment for your horse’s injured tendon, the first step will be to collect MSCs. The cells are harvested from bone marrow or fat, depending on the treatment method used. This is done with your horse standing and sedated, with local anesthesia.

    • For marrow-derived stem cells, a sample of bone marrow is aspirated (drawn with a special needle) from the horse’s sternum or hip. The marrow contains stem cells along with serum that’s rich in growth factors. It’s couriered to a laboratory where stem cells are extracted, cultured to expand the numbers, recombined with the serum and returned for injection. Usually 10 million cells are used to treat a tendon, Dr. Stewart says, and expansion can take two to three weeks. (VetCell, www.vetcell.com, a British company, developed the process and now offers it in North America through Equine Partners America, LLC, www.vetcellamericas.com.)
    • For fat-derived stem cells, the veterinarian makes an incision, usually near your horse’s tailhead, and collects a sample of fat tissue. The sample goes to a lab where it’s treated with enzymes and spun in a centrifuge to separate nucleated cells from the fat that makes up most of the tissue. The nucleated cell fraction (which may include MSCs and some adult fat cells) can be sent back for use within three days or kept and cultured to get a higher concentration of MSCs. (Vet-Stem, www.vet-stem.com, in Poway, California, is a leading provider of this service in the United States.)

Does it matter where stem cells are collected and how they’re processed? “Some would say yes, but there has been no head-to-head comparison of the long-term effects,” Dr. Stewart says. The various stem-cell products are handled in much the same way when they come back from the lab:

Stem cells being injected into an injured tendon
After stem cells are havested and processed, they are injected directly into the injury site.

In most cases the veterinarian injects the stem-cell product directly into the injured tissue, using ultrasound to guide the injection into the lesion. The treatment also can be delivered into the blood supply around the site (regional limb perfusion), but this may not be as effective. “A study comparing the two methods found many more MSCs at the lesion when they were injected directly at the site than when ?injected using regional limb perfusion,” says Dr. Stewart.

The cost varies. “In most cases, from harvesting to reinjection, you’re looking at $1,200 to $2,000 to treat a tendon ?injury,” Dr. Stewart says.

Side effects are rare. As with any injection, there’s a small risk of transient inflammation or infection. But with autologous cells there should be no immunogenic reaction?that is, your horse’s immune system won’t target the cells as foreign and try to destroy them. “Even with cells from another horse, MSCs should be less immunogenic than adult cells,” Dr Stewart says. “But studies are still being done on this.”

Will It Help? Stem-cell success stories abound, but there’s not much peer-reviewed scientific research comparing outcomes with stem cells and traditional treatments. Researchers have done postmortem tissue studies that show good results in tendon and ligament injuries, ?including better alignment of fibers and less disorganized scar tissue?but benefits are hard to track in living horses because of individual differences in their injuries and care, Dr. Stewart says.

Ultrasound Scans of Injured Tendon
Four ultrasound sacans of an injured superficial digital tendon. You can see a large lesion in the scan at the time the bone-marrow aspiration takes place. There is some degradation a month later when the stem cells are implanted and then clear improvement two and four months post-implantation as the tendon regenerates.A recent follow-up study showed lower rates of injury after MSC treatment. Dr. Roger Smith, a professor of equine ?orthopedics at the Royal Veterinary College in Britain and developer of the VetCell technique, reviewed outcomes in 113 racing Thoroughbreds with core lesions in the superficial digital flexor tendons and found that treatment with marrow-derived MSCs cut reinjury rates by more than half. Horses who returned to training after stem-cell treatment and were followed up for three years had a reinjury rate of 27 percent, compared to 57 percent in conventionally treated horses. No comparable follow-up study has been done with fat-derived cells, Dr. Stewart says.

Stem cell therapy is evolving, and researchers are still trying to determine exactly what the cells do after they’re ?injected. “Early research evaluated MSCs for their potential to replace damaged tissue,” Dr. Stewart says. “More research now is directed at their ability to modulate inflammation and encourage healing.”

How long they hang around the injection site varies with the cell type and the tissue. “In tendon, bone-marrow-derived MSCs seem to be present up to two weeks, and then the numbers drop off. We don’t know if they’ve migrated somewhere else, died or divided so that the dye marking them no longer shows up,” Dr. Stewart says. “Embryoniclike stem cells seem to persist longer at the site of injection and travel farther, but they’re not yet commercially available.”

The cells don’t always behave as ?expected. Veterinarians at Cornell University tracked bone-marrow-derived MSCs injected into the fetlock or stifle joints of healthy and arthritic horses. They hoped the stem cells would migrate into damaged cartilage, where they might help repair it. Instead, the cells went to the synovial membrane, which surrounds the joint.

Platelet-Rich Plasma

Platelet-Rich Plasma
Platelet-rich plasma is blood plasma that has been enriched with platelets. PRP contains and releases several types of growth factors that stimulate soft-tissue healing.PRP is plasma (the straw-colored liquid portion of blood) with a high concentration of platelets, small cell fragments that circulate in the blood. Platelets are best known for their role in helping blood clot, but they also release high concentrations of growth factors that encourage healing. Injected into injured tissue, the premise is, PRP delivers a potent cocktail of these healing proteins to help stimulate tissue repair. This treatment has been used in dentistry for jaw repair and in human sports medicine. In horses, it’s being used primarily for tendon and ligament injuries, both alone and along with MSC therapy.

“We think acute lesions are most likely to benefit from PRP,” says Dr. Textor. “Chronic, degenerative tendon conditions are less likely to respond.” The ideal time for treatment isn’t known, she adds, “but three to four weeks after an injury is probably a good target.”

PRP has been tried as a way to spur wound healing in horses, but it doesn’t appear to help and may actually increase proud flesh formation, Dr. Textor says. It has also been tried as an equine joint treatment; but another blood-derived treatment, IRAP, is more often used there. (IRAP stands for interleukin-1 receptor antagonist protein, a substance that blocks a specific inflammatory agent involved in the erosion of cartilage.)

PRP Treatment. If you opt for this treatment, the PRP will be prepared in the clinic from your horse’s own blood.

A sample of blood is drawn and spun in a centrifuge to separate the plasma and platelets from the red blood cells and most of the white blood cells. The plasma is then concentrated so it contains higher-than-normal blood levels of platelets.

It’s ready for injection into the injury the same day, often in less than an hour.

The cost of a single treatment typically ranges from $400 to $1,000, depending on the veterinarian’s preparation method, Dr. Textor says.

As with stem-cell therapy and any other injection, there’s a small risk of infection or a brief flare of inflammation?but because PRP is derived from your horse’s own blood, the risks of an immunogenic reaction to the treatment are low.

Will It Help? PRP has several advantages?it’s easy to collect and prepare, the turnaround time (from harvest to reinjection) is short and the treatment is cheaper than stem-cell therapy. Those plusses are helping PRP gain acceptance in the horse world.

As with stem cells, though, there’s little published research on effectiveness. In a study of horses with experimentally created tendon lesions, Dutch researchers showed that a single PRP injection resulted in improved healing and increased tendon strength at six months. In a clinical study of racing Standardbreds with severe suspensory ligament lesions, Ohio State University researchers found that one PRP injection helped horses recover and return to racing. On the other hand, some studies in human medicine have cast doubt on PRP’s effectiveness in shoulder and Achilles tendon injuries.

The reasons for different outcomes may emerge with answers to some of the many questions about how the treatment works and how it should be given. For example:

    • Do tendon injuries benefit from more than one injection? “We don’t know,” Dr. Textor says. “Many vets are using multiple injections.”
    • Do injected platelets stay at the injury site after injection, pumping out growth factors as they do when activated naturally? They might be quickly cleared from the site by macrophages, the cells that “eat” other dying cells or tissue debris, Dr. Textor says. “We are looking into this question now to find out whether the physical presence of platelets is required at the site or whether we can just administer the growth factors derived from them.”
    • How do different preparation and treatment methods affect outcomes? “There is so much variety in methods of PRP use, both in humans and in horses, that the results are becoming more and more difficult to interpret,” Dr. Textor says. For example, the platelets must be activated to release growth factors. That can be done in different ways?by exposing them to the clotting protein thrombin or to calcium, or by freezing and thawing, for example.

“The main focus of my research is in trying to identify all the variables that go into PRP preparation and administration and figuring out what is the best way to do things so we can standardize our methods and be consistent as practitioners,” Textor says. “It may be that better results are achievable once we figure out how to maximize the benefit of PRP.”

Looking Ahead
Here’s one thing that seems certain: There will be new developments in this rapidly growing field.

    • “Researchers will continue to work on treatments for soft-tissue damage,” Dr. Stewart says. They’ll explore different preparation and delivery techniques and look for ways to prove the action and ?retention of stem cells in injured tissue.
    • Cell-based therapies also hold promise for use against osteoarthritis, in which the cartilage lining the joint surfaces breaks down. So far stem-cell therapy has been less ?effective than hoped for this problem, Dr. Stewart says. Researchers are still investigating how to coax the cells to stimulate cartilage repair. One technique being ?explored combines them with PRP. Research is also being done on the use of stem cells for fracture repair, but practical treatments aren’t yet available for that.
    • Also on the horizon?or maybe a bit beyond it?are potential regenerative treatments for other diseases, including laminitis. “Studies haven’t been done yet, but there are some reports of successful laminitis treatment with high doses of MSCs. There’s interest, so it’s likely that research will be done,” Dr. Stewart says. “There is also interest in looking at MSC use in neurologic conditions.”
    • New sources of stem cells may come into use. For example, MSCs can be ?obtained from the umbilical cord ?moments after a foal is born. These cells are not yet used commercially, but forward-thinking horse owners can bank foal cord blood and tissue at the UC Davis Regenerative Medicine Laboratory.

Interest in human regenerative medicine is helping to fuel (and fund) a lot of the research into cell-based treatments for horses. People, like horses, heal slowly and often poorly after damage to tendons, ligaments, cartilage and bone?so the horse is an excellent research model for these treatments. That means research underway now may one day benefit you as well as your horse.

Learn more about tendon and ligament injuries.

Reprinted from the February 2012 issue of Practical Horseman magazine.

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USEF Equine Drugs and Medications Program

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Understand the USEF Equine Drug Testing Rules

If you compete in rated shows, here’s what you need to know to keep your horse healthy and maintain a level playing field.

By Elaine Pascoe

Drugs and medications
Your trainer meets you at the out-gate and starts to critique your round as you hop off your horse. That’s when a total stranger walks up and says, “Hi. I’m with the U.S.Equestrian Federation, and your horse has been selected for testing.”

If you’re like 99 percent of horse-show competitors, you don’t dope your horse. But you can’t help gulping when you hear those words?it’s like being called to the principal’s office in junior high. Did you or your trainer make a mistake? Are you in trouble?

The USEF regulations for drugs and medications can seem complicated, and changes this year may affect you. In this article Stephen Schumacher, DVM, chief administrator of the USEF Equine Drugs and Medications Program, explains the changes and tells you how to make sure you stay on the right side of the rules.

The goal of the USEF program is to protect horses from abuse and maintain a level playing field, so no competitor gains an unfair advantage through chemistry. And it’s working, Dr. Schumacher says. Of the 10,000 to 12,000 horses that the USEF tests annually (not a huge number, considering how often horses compete and the number of disciplines that the federation oversees), anywhere from 50 to 100 may test positive in a given year?1 percent or less.

“The low rate of positives doesn’t mean the program isn’t needed,” Dr. Schumacher says. “The numbers are low because the program is there?deterrence is its main effect. We would rather educate than adjudicate.”

Education starts with understanding what is and isn’t legal. It’s all spelled out in the USEF Rule Book.

Read All About It
General rules 401 through 413 outline the procedures for testing and enforcement and explain in general what is and isn’t permitted. These rules are carefully (and sometimes densely) worded but definitely worth the read. Anyone who signs an entry form at a USEF-recognized show needs to understand them because that person (usually the trainer, acting as the agent of the owner) has the primary responsibility for making sure the rules are followed. The separate “2012 Guidelines for Drugs and Medications,” available on the USEF website or in a pamphlet from the federation, provide a roadmap for staying out of trouble.

The rules allow different breeds and divisions to adopt different standards for permitted medications; endurance horses, for example, are subject to strict “no foreign substances” requirements. Here we’ll focus on the rules and guidelines that apply to hunter, jumper, eventing and dressage ?divisions. These rules don’t give you a list of every substance that is and isn’t allowed, although they do mention some specifics. New drugs are always being developed, and there will always be a few people willing to try new ways to gain an advantage.

To cover all cases, the rules classify substances based on their actions and uses. Permitted substances, which are not regulated by USEF, include vitamins, minerals, electrolytes, dewormers and most antibiotics (except procaine penicillin?penicillin is OK, but procaine is a local anesthetic that can linger in the horse’s system). They can be given to a horse at any time, including at a competition. Other drugs are sorted into two groups, restricted and forbidden.

Restricted Substances
These drugs can be used for therapeutic reasons?that is, to treat an injury or disease?but they’re subject to strict limits on the amount of the drug or its metabolites (breakdown products) that can be in blood or urine at the time of competition, as set out in Rule 410. They include the muscle relaxant methocarbamol (Robaxin), the corticosteroid dexamethasone (Azium) and seven nonsteroidal anti-inflammatory drugs: phenylbutazone, flunixin meglumine (Banamine), ketoprofen (Ketofen), meclofenamic acid (Arquel), naproxen (Equiproxen), diclofenac (Surpass, a topical) and firocoxib (Equioxx). Theobromine, a metabolite of caffeine and related substances, is also in this category; the limit is just enough to account for any the horse might get through diet.

You should know:

    • The “2012 Guidelines for Drugs and Medications” provide detection times for restricted substances, to help you judge when blood and urine levels are likely to be within legal limits. For example, if your horse breaks out in hives and you give him oral dexamethasone at the dosage listed in the guidelines, his blood levels should be OK in six hours.
    • The times listed in the guidelines are recommendations, not rules, and the drug clearance times vary with dosage rates, the form of the drug and how it’s delivered. If your horse tests over the limit, he’s in violation whether or not you followed the guidelines.
    • Compounded medications (made up to order by compounding pharmacies) call for special care because ingredients may vary more than they do in manufactured drugs.

New this year:

    • Only one NSAID can be present in a sample; previously the rules allowed two. “This is probably the most significant change this year,” Dr. Schumacher says. The change, which took effect December 1, 2011, was made to end the potentially harmful practice of “stacking” these drugs.
    • With just one NSAID allowed, detection times have been reduced from seven days to 72 hours for these drugs. If your horse has been getting two NSAIDs, you need to stop one of them at least 72 hours before competing. Only one can be administered in the 72 hours before a competition, and that one must be within the limits set by the rules.
    • Although only one NSAID is allowed, there’s a new emergency provision for therapeutic use of Banamine (flunixin meglumine) for colic or eye problems, conditions for which this drug is particularly helpful. Suppose your horse was given phenylbutazone before a competition and you stopped the drug to allow for the recommended withdrawal time. Then, at the show, he colics. Under the new rule, he can have Banamine?a single dose, limited quantity?and return to competition in 24 hours. “Under the old rules he couldn’t have Banamine unless he waited seven days to compete, so the change is an improvement.” Schumacher says. “The caveat is that you must have a veterinarian administer the drug and submit a medication report to show officials.”

Forbidden Substances
These are drugs that can affect performance, give an unfair advantage, pose a danger to your horse or interfere with drug testing by masking the presence of other drugs. They include stimulants, ?depressants, painkillers and local anesthetics, and tranquilizers and psychotropic drugs, such as reserpine and fluphenazine. Prednisolone, bethamethasone, triamcinolone acetate (Vetalog, often used in joint injections) and other corticosteroids except dexamethasone are in this category. So are NSAIDs other than the seven listed in the restricted group. Although many of these drugs have legitimate therapeutic uses, they should not turn up in a horse-show drug test.

You should know:

    • Some of these drugs can still be ?detected weeks after the last dose; reserpine and fluphenazine can persist for 90 days. The guidelines list detection times for a number of the drugs, and the USEF Equine Drugs and Medications Department can provide times for more.
    • Herbal and other supplements sometimes lead to positive drug tests, so be sure you know what’s in a product ?before you feed it to your horse. ?”Natural” doesn’t mean drug-free?plants are the source of many potent drugs, and some can produce metabolites like those of forbidden substances. For ?example, the herb rauwolfia (Indian snakeroot) is the source of reserpine.

New this year:

    • USEF has changed the way it handles some forbidden-substance violations in the eight disciplines governed by the ?International Equestrian Association (FEI), including dressage, eventing and show jumping. See the box on page 57 for more about this change.
    • Anabolic steroids have been added to the “forbidden” list for all USEF disciplines; previously they were banned only in some halter divisions for Arabians, Half-Arabians and Anglo-Arabians. These drugs have therapeutic uses?they can help in recovery from colic surgery and in cases of muscle wasting, for example?but they’ve been widely misused in race training as a short-cut to building muscle mass and stamina in young horses. They’re not widely used in sporthorses, according to Dr. Schumacher, because such shortcuts aren’t needed, and the drugs can produce undesirable behavior.

“We’ve run surveillance across the ?disciplines and never had an issue with anabolic steroids. But we’ve made them forbidden and provided withdrawal guidelines for the most commonly used ones to recognize their potential for ?unfair use and to be consistent with other groups,” he says. “We are actually the last horse-sport group to abolish their use in competition.”

Bending the Rules
The USEF rules are clear: If you give your horse something to calm him or make him less sore in competition, you’re in violation?even if the same something might be permitted for a legitimate therapeutic reason. But intent can be hard to judge, so it’s not always clear when someone steps over the line.

For example, you might see dexamethasone in horse-show medicine chests. Some competitors administer “dex” in the belief that it will calm a nervous horse, although the rules expressly forbid that use and there’s not much evidence that it works.

“Based on work done years ago, the level permitted under the rules would not be expected to sedate a horse,” Dr. Schumacher says. “Some people feel differently. I don’t think there’s any peer-reviewed scientific literature to support that, but there’s a racetrack mentality?people think it works so they use it.” The USEF Drugs and Medications committee will likely be reviewing the guidelines and recommendations for dex, he adds.

Magnesium is also used to quiet horses, something that Dr. Schumacher says is based on a misconception. ?”Hyperexcitability is a sign of hypomagnesia?magnesium deficiency?and giving therapeutic doses of magnesium corrects it. Based on that, some people conclude that giving any horse more magnesium will make him calmer even if he isn’t deficient, but there’s no evidence for that,” he says. Even if it were so, oral magnesium is not a concern because it’s unlikely that a horse could consume enough orally to be affected, he notes. But some competitors administer magnesium sulfate intravenously, which is dangerous. “Given this way, magnesium can affect cardiac rhythm and have a depressant effect, and it’s a horse-welfare issue,” he says.

As of this writing, USEF had no prohibition on magnesium, although the substance is on the association’s radar. One problem is that magnesium is naturally present in horses and in all animals. “To regulate it, you first have to establish a threshold level that’s acceptable. It’s a different situation with drugs like NSAIDs that aren’t naturally present,” Dr. Schumacher says. Nevertheless, he adds, injected magnesium sulfate has been added to the FEI prohibited list this year, and administration will no longer be permitted at FEI show treatment areas.

If Your Horse Is Tested
How likely is your horse to be tested? The choice is pretty much random. “We test at 20 to 25 percent of competitions each year,” Dr. Schumacher says. “There is a focus on upper levels, where more is at stake and violations may be more likely to occur, but we test lower levels as well.” He selects the shows and then asks one of the veterinarians who works with the program to test perhaps one day out of four, at his or her convenience. The odds of being tested are greater for horses who display unusual behavior or place in the top five of their classes, but anyone can be selected. For example, in a dressage class, horses are picked randomly as they leave the ring before the placings are decided.

If your horse is tapped, be polite and take him promptly to the testing area. Arguing or stalling (by cooling out, bandaging and other delays) may be considered “noncooperation,” as much a violation as a positive test. Be helpful as the veterinarian draws blood and the technician working with the vet collects a urine sample.

The samples are handled according to standards set by the World Anti-Doping Agency. Both blood and urine are separated into A and B samples; the A samples are sent to the designated USEF lab for testing, and the B samples are held. If the A samples test clean, the B samples are discarded. But if the test is positive, the trainer (or whomever is responsible) has the right to have the B sample tested to confirm or disprove the result.

A positive test leads to an investigation and a decision on whether the rules were violated. The trainer usually has the choice of accepting an administrative penalty or responding at a hearing before a USEF committee, with or without legal representation. If the committee finds a violation occurred, it will weigh several factors?the type and (for drugs covered by Rule 410) the quantity of drug found, prior violations and how similar cases have been handled. Violators forfeit winnings and any points earned, and under USEF rules they face penalties that include fines ($750 to $5,000) and suspension (one to six months). The violation and the penalty are published, in itself a strong deterrent.

There are trends in violations, Dr. Schumacher says, like a recent spike in reserpine positives. “Medications pop up, but after a few positives, word gets around and the use tails off,” he says. Still, the most common violations ?involve NSAID levels over the limits set by the rules.

“These are ?speeding ticket’ violations, not as serious as, say, doping the horse with an antipsychotic medication,” Dr. Schumacher says. “In most cases we can identify the reason for the violation, and it’s a mistake. Maybe a groom dosed the horse, and the trainer was unaware and gave a second dose.”

To guard against such mistakes, he suggests, make sure your horse’s treatment program is secure, defined and documented:

    • Lock up medications and restrict access to them, at home and at shows.
    • Be sure only designated people (for safety, just one person at a competition) can give medications to your horse.
    • Write down the treatment program and document every dose.
    • Clean out the feed buckets (they could harbor traces of medications or supplements), and don’t swap buckets among horses.

Last fall, the American Association of Equine Practitioners published a set of guidelines for veterinarians treating nonracing performance horses, and they included several tips that may also help you stay out of trouble:

    • No medication should be administered to a horse within 12 hours of a competition.
    • Nontherapeutic or nonprescribed medications or substances should not be administered to performance horses by anyone.

Maybe some competitors will always be ready to bend the rules (or ignore accepted ethics), even when doing so puts a horse’s health at risk. But statistics suggest these folks are a very small minority. Care and common sense will keep you out of their group.

This article originally appeared in the April 2012 issue of Practical Horseman magazine.

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Early Recognition of Neurological Disorders May Save Your Horse

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Recognize the Signs of Equine Neurological Disorders

Recognizing the signs of equine neurological disorders and starting ?treatment early will give your horse his best chance of recovery from these diseases.

By Elaine Pascoe With Debra Sellon DVM

The tail pull is one of the diagnostic tests veterinarians commonly use to assess a horse's strength, balance and reaction time.
The tail pull is one of the diagnostic tests veterinarians commonly use to assess a horse’s strength, balance and reaction time. | ? Dusty PerinYour horse hesitates and steps awkwardly when he walks downhill. He’s dragging his toes, too, and a few times he has even stumbled while trotting in the ring. He doesn’t seem sore, and your trainer and farrier don’t see anything wrong with his feet?but you know he’s not right. Could he have one of several equine neurological disorders, like equine herpesvirus type 1 (EHV-1) equine protozoal myeloencephalitis (EPM) or West Nile virus?

Owners dread equine neurological disorders, such as equine herpesvirus type 1, equine protozoal myeloencephalitis or West Nile virus, and no wonder. Many of these problems are hard to diagnose and hard to treat, and they can damage a horse’s nervous system in ways that leave him unsafe to ride. But every neurologic case doesn’t end badly, and quick action?recognizing signs, getting a diagnosis and starting appropriate treatment?can give your horse the best chance.

If you think your horse might have a neurologic problem, it’s time to call your veterinarian. What exactly will your vet do, and what disorders might she find? In this article, we’ll walk you through a standard neurologic exam, tell you what else may be needed to make a definitive diagnosis and give you an overview of the most common problems.

Sorting Out the Signs
Signs of neurologic problems in horses run the gamut?seizures, abnormal behavior, abnormal gait, facial paralysis and more, says Debra Sellon, DVM, professor of equine medicine at the Washington State University College of Veterinary Medicine. “The most common neurologic problem equine veterinarians see in the United States is an abnormal gait,” Dr. Sellon says. “Affected horses are usually ataxic and weak, meaning that they walk with a staggering or drunken type of gait. They may drag their toes, stumble frequently or sway back and forth when they walk.”

Disruptions in a horse’s command and control system create these problems. For normal movement, nerve signals must flow from his brain along his spinal cord to the nerves that govern his muscles?and nerves must signal back to his brain, reporting where his limbs are. If the signals don’t get through, your horse may become uncoordinated or develop abnormal gaits.

Many neurologic disorders can disrupt the signals. In most parts of North America, Dr. Sellon says, the most common are equine protozoal myeloencephalitis and cervical vertebral malformation (“wobbler syndrome”). But there are plenty of others, including injuries, several viral diseases and degenerative conditions, such as equine degenerative myeloencephalopathy, which has been linked to vitamin E deficiencies in young horses.

“Veterinarians use a fairly standard ?approach to determine a diagnosis for horses with neurologic disease,” Dr. Sellon says. The process begins with gathering information on your horse’s history. When did he begin to stumble or show other signs? Has he fallen? Information on your horse’s age, breed and use is important ?because some neurologic problems are more common in certain groups of horses.

Step two is a thorough physical ?examination. This exam may reveal soreness or other non-neurologic causes for your horse’s signs, or it may turn up signs of an injury or a disease that produces neurologic problems. As she examines your horse, your vet compares the right and left sides of your horse’s body, looking for asymmetry and loss of muscle mass (atrophy) that may develop when muscles go unused, as happens in some neurologic conditions. She may check the range of motion in his neck by encouraging him to bend to each side, using a carrot or another treat as a lure. Limited range of motion may mean an injury or even fractured vertebrae in his neck (the cervical spine).

Neurologic Exam
The third step is a detailed neurologic examination. “The goal is to determine, to the best extent possible, the site in the nervous system that is affected,” says Dr. Sellon. By finding out which functions are impaired, your veterinarian can figure out which nerves are involved. The process, called lesion localization, typically ?includes these steps:

General assessment: Your veterinarian observes your horse’s mental status and behavior. Is he alert or ?lethargic? Standing or down? Wandering aimlessly, circling or showing other odd behaviors or postures?

Basic reflexes: This part of the exam starts at the head with tests of the cranial nerves, which are involved in functions like hearing, vision, swallowing and facial sensation and muscle control. To test ?vision, for example, the vet quickly moves a hand toward your horse’s eye to trigger the menace reflex; your horse should blink and perhaps jerk away.

Along your horse’s neck and back on each side of his spine, your vet uses a ballpoint pen or similar object to touch your horse’s skin. A light but firm touch should trigger the panniculus reflex, the skin twitch you see when your horse is pestered by a fly. Lack of a reaction in any area suggests a problem with the nerves that supply that region. At the hind end, the vet checks muscle tone by lifting the tail; a limp tail may be a sign of a spinal cord problem. When his anus is gently stimulated, it should pucker and your horse should clamp his tail.

Maneuvers in hand: These tests show if your horse has control of his limbs and knows where his feet are. The vet watches as your horse is backed and turned in very tight circles in both directions to see how he places his feet. A normal horse keeps his rhythm and steps under his body, while a horse with a neurologic problem may interfere, take confused steps, swing a hind leg wide or pivot on one leg.

On a slope: Your vet may ask to see your horse led up and down a slope, to see if he stumbles, drags his toes or shows other gait abnormalities. Repeating this test with your horse’s head raised sometimes makes the signs more obvious.

Tail pull: This helps your vet assess your horse’s balance, strength and reaction time. As a handler leads your horse forward, your vet grasps his tail and pulls it firmly to the side. A normal horse will resist the pull; a horse with a neurologic problem may be tipped off balance. The test is repeated on the other side.

Foot placement: These tests help determine your horse’s awareness of his limb position. Your vet takes each foot in turn and places it over its opposite number?left front over right front, right front over left front, and the same behind. A normal horse will immediately put each foot back where it belongs; a horse with a neurologic problem may leave one or more feet out of place for a time.

By the end of the exam your veterinarian should know whether your horse’s problem is neurologic and, if so, what areas of his nervous system are ?involved. She may not have enough information for a clear diagnosis yet because many neurologic disorders have variable signs. “Horses with EPM can show a wide variety of signs, ranging from ataxia and weakness, to individual nerve paralysis, to seizures, to problems with urination or defecation,” Dr. Sellon says. “The vast majority of wobblers present for examination with ataxia and weakness of all four limbs. That means a horse with EPM often looks different from a wobbler but sometimes looks just the same.”

Still, your veterinarian will have enough information to make a list of the diseases or disorders that are most likely the cause and then choose the most appropriate diagnostic tests to confirm or rule out the items on that list. Here’s what you can expect for three common conditions.
EPM
This disease is common in most parts of the United States, Dr. Sellon says, but diagnosing it can be problematic.

Cause: Microscopic protozoan parasites (Sarcocystis neurona) invade the horse’s central nervous system, damaging the spinal cord and/or brain. S. neurona is mainly carried by opossums, which shed sporocysts (dormant protozoa) in their feces. The horse ingests the sporocysts in contaminated feed or water. (Another protozoan, Neospora hughesi, has been reported in a small number of cases.)

Signs: Depending on the area of the central nervous system that’s affected, signs may include loss of coordination, loss of muscle mass, difficulty swallowing, abnormal gait or lameness, seizures or paralysis. Signs are often more pronounced on one side of the body, Dr. Sellon says.

Diagnosis: Blood and spinal fluid can be tested for antibodies against the EPM parasite, and a negative result rules out the disease. But a positive test doesn’t necessarily mean that your horse has EPM?just that he was exposed to the parasite at some time and mounted an immune response to fight it off. In some regions, 30 to 60 percent of horses have antibodies, but only a small fraction ever show signs of disease. Some new tests have been reported to give a clearer picture of antibody levels. But, Dr. Sellon says, a panel of experts has agreed that test results alone are not enough?it’s important to rule out other possible diseases as well.

Treatment: Drugs used to fight EPM include pyramethamine/sulfadiazine (or sulfamethoxazole) combination (paste, from compounding pharmacies) and ponazuril paste (Marquis, from Bayer). There’s also a pelleted medication, diclazuril (Protazil, from Intervet International), which can be top-dressed on feed if you’re sure your horse will consume the full dose. All the drugs are expensive, and treatment lasts weeks or months.

Be guided by your veterinarian in choosing what’s right for your horse, Dr. Sellon says. “The advertisements for some new diagnostic and treatment procedures may sound very exciting, but they may not have solid science backing them up.”

Outlook: Without treatment your horse will get worse. Medication can halt the progression of the disease, but his recovery depends on how badly nerve tissues have been damaged. If your horse is diagnosed and treated promptly, he may recover fully; but a severe or longstanding case may cause lasting neurologic deficits.

Prevention: So far no vaccine has proved effective against EPM, although research continues. You can take other steps to reduce your horse’s risk:

    • Minimize stress. Stress?from showing, shipping, training and the like?seems to increase the risk of developing this disease, perhaps by suppressing your horse’s immune response.
    • Discourage opossums. They’re scavengers, so cover grain and garbage tightly. Clean up spilled grain and dispose of dead animals, including birds and ?rodents. Keep water troughs and buckets clean and filled with fresh water to prevent contamination.

Wobbler Syndrome
Wobbler syndrome usually appears in young, growing horses. It’s the most ?common noncontagious cause of neurologic problems.

Cause: The bones of the spine (vertebrae) have a central canal that lets the spinal cord pass through. A wobbler has a structural narrowing of the canal in vertebrae of the neck?a cervical vertebral malformation (CVM) that squeezes the spinal cord and damages nerve tissue. The pressure may be constant or occur only when the neck is flexed or extended. Rapid growth, a diet excessively high in nutrients and imbalances of various minerals have been blamed. The condition can ?affect any breed but is especially common in Thoroughbreds, and genetics may play a role. An injury to the spine may worsen the problem.

Signs: Your horse is incoordinated and weak behind and, often, in front as well. Usually both sides of your horse are affected equally. The signs may creep up gradually or appear suddenly, and the ?severity may vary from time to time.

Diagnosis: X-rays of the neck can help rule out a fracture, Dr. Sellon says, but confirming that your horse is a wobbler usually requires a myelogram. This is a set of specialized X-rays taken while your horse is anesthetized. A dye is ?injected into the space around his spinal cord, and the X-rays are taken with your horse’s neck in various positions to see if the bones impinge on the spinal cord.

Treatment: A wobbler may improve with rest, but the underlying condition doesn’t go away. In some cases a surgeon may be able to fuse the affected vertebrae to reduce pressure on the spinal cord.

Outlook: Most wobblers are not candidates for athletic careers. Successful surgery may improve the condition enough for your horse to be ridden, though.

Prevention: There’s no sure way to prevent CVM, but correct nutrition will help any young horse develop well.

Trauma
Injuries to the skull or spine can produce severe neurologic problems.

Cause: These injuries typically ?occur when a horse falls or collides with a solid object. For example, a horse who pulls back in cross-ties, panics and flips over backward may strike his poll, sometimes with enough force to fracture his skull or the first few vertebrae of his neck. An event horse who doesn’t clear an obstacle and flips or plows headfirst into the ground may fracture vertebrae farther along the spine.

Signs: Head trauma may knock your horse unconscious, make him temporarily blind or disoriented or kill him instantly. But signs don’t always show up immediately?pressure from internal bleeding in the skull can build slowly, so you won’t know initially how serious the injury is. Signs of spinal injury depend on the location. Your horse may have difficulty rising, lack coordination and show other abnormalities.

Diagnosis: Your horse’s history and signs generally point to injury. X-rays can identify fractures in the skull and spine, but some sites are difficult to image.

Treatment: If a fracture leaves your horse paralyzed or severely incoordinated, not much can be done. Treatment for milder injuries focuses on reducing the inflammation and swelling that put pressure on nerve tissue. Your vet may put your horse on anti-inflammatory medications, perhaps intravenous DMSO, a cortico?steroid or a nonsteroidal anti-inflammatory such as phenylbutazone, depending on the case. Your horse will need a period of rest, followed by reevaluation.

Outlook: No two injuries are the same, so the outlook is different in each case. A horse with soft-tissue injuries ?obviously has a better outlook than a horse with a fractured spine.
Prevention: Accidents happen, but you can minimize your horse’s risks by being sure that he’s fit and ready for his sport and by avoiding situations in which he’ll fight head restraint. If you can’t tie him safely, don’t tie him.

Mosquitoes transmit viral diseases, such as West Nile Virus and Eastern and Western encephalomyelitis, through bites.
Mosquitoes transmit viral diseases, such as West Nile Virus and Eastern and Western encephalomyelitis, through bites. | ? Joseph Berger/Bugwood.org

Viral Threats
Several viral diseases can attack your horse’s central nervous system. Rabies, always fatal, may be the most devastating?but, fortunately, it can be prevented with vaccination and is fairly rare. These are more common.

West Nile Virus. West Nile is one of several mosquito-borne viruses that cause neurologic disease in horses. In the United States, the others are Eastern and Western encephalomyelitis. Another, Venezuelan encephalomyelitis, hasn’t occurred north of the Mexican border since the 1970s. Here are the basics:

    • Mosquitoes transmit the virus to horses when they bite. If the virus invades the central nervous system, it can cause encephalitis?swelling around the brain and spinal cord. The virus does not spread directly from horse to horse or from horses to people.
    • Lack of coordination, weakness or paralysis of the hind limbs, muscle twitching, impaired vision, head pressing, aimless wandering, convulsions, circling and coma are some of the severe neurologic effects. Horses typically have non-neurologic signs, too, such loss of appetite and a depressed attitude. Some develop a fever. Lab tests can confirm the diagnosis.
    • Your horse should have supportive care, including anti-inflammatory medication and IV fluids, if needed, but there’s no specific treatment.
    • West Nile is fatal in 20 to 40 percent of cases. Horses who pull through may have lingering neurologic deficits, but that’s not always the case. Other forms of equine encephalitis have somewhat higher death rates and less chance of full recovery.

EHV-1. Equine herpesvirus type 1 usually causes a flu-like illness or, in pregnant mares, abortion. But in some cases, the virus damages blood vessels in the brain and spinal cord, producing a deadly neurologic disease (equine herpesvirus myeloencephalopathy).

    • Neurologic signs may include lack of coordination, hind-end weakness, diminished tail tone or unwillingness to rise. Fever, nasal discharge and other respiratory signs may appear first. But, says Dr. Sellon, “Most of the EHV horses we see at WSU do not have nasal discharge or respiratory disease signs that have been recognized by owners or trainers,” Dr. Sellon says. “If you depend on those signs, I think you might miss a lot of horses with EHV infection.” Your veterinarian can send a nasal swab and blood sample to a lab to confirm the diagnosis.
    • Supportive care can help your horse weather the infection. Antiviral medications may help if given before neurologic signs appear.
    • The virus spreads easily from horse to horse; isolation, quarantine and other biosecurity measures will help keep the disease from spreading through the barn.
    • Horses who remain able to stand usually recover. The outlook is not so good for those who go down and can’t rise.

All these viral diseases are widespread in the United States, so take steps to protect your horse:

Vaccinate:

    • Vaccines against WNV, EEE and WEE are effective, and they’re ?considered “core” for practically all horses in the United States. Boosters are usually given annually in spring, giving your horse time to build immunity before mosquito populations peak in summer. Where mosquitoes are active year-round, horses may need more frequent boosters.
    • No vaccine is labeled effective against the neurologic form of EHV-1, but vaccination can help protect your horse from other forms of the disease. There’s some evidence that a modified live virus vaccine (Rhinomune MLV, from Boehringer Ingelheim Vetmedica) offers better protection against the neurologic form, but more research is needed.

Reduce Risks:

    • Limit your horse’s exposure to mosquitoes. Keep him in at dusk and dawn, when mosquitoes are most active, and use fly repellents labeled effective against these insects.
  • Take precautions at shows and other places where many horses come together and contagious diseases like EHV-1 often spread. Don’t share water buckets or let your horse rub noses with strangers.

– See more at: http://practicalhorsemanmag.com/article/recognize-the-signs-of-equine-neurological-disorders-11614#sthash.sZkgPlCk.dpuf

Weight Gain- The Good Kind

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While Chance’s hind-end is still sunken, especially on the right side, he is looking much better than he did almost a year ago.  In the last year, he has gained a significant amount of weight (and still needs to keep gaining) and muscle mass.  This was achieved by upping his feed to 4 quarts and adding hay stretcher with each meal, along with Chance walking up and down small hills during the day.

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Chance 6 months ago (August 2014) Pre-EPM diagnosis or treatment.

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February 2015: Second round of EPM treatment and 6 months of upped feed with higher fat and protein content.

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The weather has been unrelenting over the last week. We got about 7 inches of snow and another 7+ inches 4 days later, with low temperatures and hail to boot! Poor Chance has been stall bound due to the slippery conditions. Some days it has even been too icy to hand walk him.

Regardless, Chance has been in good spirits and his back legs look great! He hasn’t stocked up and he is putting weight on the back right hind. I’m hoping that when he is able to go outside, his back right twist will have disappeared! Maybe wishful thinking, but I can still hope.

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