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The usual suspects
The trials of diagnosing neurologic disorders.
It was the day before Christmas when a routine call came in about a horse that "didn't seem quite right."
Dr. X drove along thinking about possible causes such as viruses or mild impactions along with thoughts of scooping up those last-minute gifts. The mare in question, Rockett, was a Quarter horse used for barrel racing. Dr. X had vaccinated the mare, floated her teeth and seen to her relatively uncomplicated routine care for years.
On examination that day, however, something did seem wrong. Normally a friendly horse, Rockett was agitated and more reactive to handling. She did not stumble or drag her limbs or show any neurologic signs. The horse's cranial nerve functions were normal. All other parameters were normal as well (heart rate, respiratory rate, lung and gut sounds, temperature, ocular and oral examination findings), so Dr. X took blood samples to run a serum chemistry profile and complete blood count (CBC). While Rockett was still eating, her normal appetite had slowed over the last 10 days, according to her owners.
She had competed at a barrel event three weeks ago and had placed, but her time had been slower than usual and she had been harder to turn to the right. The owners had considered it was nothing more than a bad day at the time, but as time progressed she continued to show signs of slowing down, becoming less responsive and more anxious and irritated.
Dr. X watched as the owner turned Rockett out into the pasture. The mare kicked out as she ran off to find her pasture mates and did not look outwardly sick or uncomfortable. Letting the client know that he would call with the blood results the next day, Dr. X started to drive off. "Tomorrow is Christmas, Doc," said the owner. "I feel better that you looked at her and she's looking OK now, so let's just catch up the day after."
Dr. X drove home hoping the sinking feeling he had was not justified. He wasn't thinking about Christmas or the holiday season; he was mentally reviewing a list of the usual suspects.
Ruling out causes
Despite the fact that many cases of neurologic disease are still ultimately determined at necropsy, quicker and improved laboratory testing allows today's veterinarians a better chance at both diagnosis and treatment, if possible. Early intervention is crucial, but so is having a good grasp of the most likely diseases.
"The goals of initial stabilization in acute equine neurologic cases," according to Joanne Hardy, DVM, of The Ohio State University's College of Veterinary Medicine, "are to prevent further deterioration, initiate treatment of possible diseases as dictated by the exam, provide supportive care and facilitate transportation to a referral facility for further diagnostics and treatment."
Working through the differential diagnostic list with speed and caution is key, however, since treatment for some possible diseases is contraindicated for others.
The threat from rabies
Rabies is still encountered in horses. Because of the tremendous potential for disease transmission and disastrous outcome, it should always be considered in neurologic cases, and horses suspected of being infected should be handled appropriately (gloves, limited contact) until proven otherwise.
Rabies can present with a vast array of clinical signs, but, in many cases, colic is often the first one observed. Undulating fever, ataxia, visual deficits, hyperesthesia, hindlimb paresis, lameness, extraocular spasms, hyperactivity, aggressiveness and erratic behavior are all possible signs in cases of rabies.
Hydrophobia is not common in horses, and most rabies cases are acute with rapid deterioration and death in 24 to 48 hours. Antemortem diagnosis is based on clinical signs only.
EEE and WEE
Encephalitic diseases can present with many of the same signs, and their incidence has been increasing in various areas of the country recently. These mosquito-borne diseases have benefited from the wet weather through the southeastern states this past year, and they should always be considered in an equine neurologic differential list.
Eastern equine encephalitis (EEE) and Western equine encephalitis (WEE) are the most common diseases, although Venezuelan equine encephalitis (VEE) is also a possibility. VEE has not been reported in the United States since 1971 but has been reported in Mexico as recently as 1993. These diseases present with undulating fever (usually peaking at 103.5 degrees or higher), behavioral changes, head pressing, aimless wandering and blindness.
"WEE is a more mild form and may not progress beyond the acute phase of the disease, while EEE is much more severe and usually leads to death," says Eleanor Lenher, DVM, of Southern Pines Equine Associates in North Carolina. Acute and convalescent serum titers can be used for diagnosis in encephalitides cases along with complement fixation and cross-serum neutralization assays, cerebrospinal fluid (CSF) analysis and virus isolation.
West Nile virus can cause clinical signs that are similar to those of WEE and EEE. These horses tend to have more locomotor signs and are listless, uncoordinated, stumbling and weak with partial paralysis or ataxia, typically of the hindlimbs. They can be acutely recumbent as well. Serum or CSF analysis using a variety of tests is the best method of diagnosis.
EPM and herpesvirus
Equine protozoal myelitis (EPM) can present with recumbency, lameness and spinal cord signs. Equine herpesvirus (EHV1) can affect horses, producing weakness and ataxia primarily of the hindlimbs. These horses may exhibit urinary incontinence progressing to hind end paralysis and an inability to rise (classically known as the dog-sitting stance). While single cases of EHV1 are possible, this infection is usually associated with outbreaks and virus isolation, and pre- and post-convalescent titers are diagnostic.
Additional diseases that should be present but further down on the neurologic differential list are:
> Fungal encephalitis (rarely seen)
> Botulism (inability to swallow, muscle weakness, tremors)
> Equine motor neuron disease (more slowly developing muscle wasting and weakness)
> Brain or spinal cord tumors (usually progresses slowly but can be variable in presentation depending on location)
> Brain or spinal cord abscesses (generally diagnosed with clinical signs and CBC and CSF results)
> Equine polysaccharide storage myopathy (breed-related muscle wasting and weakness that may at times appear neurologic; diagnosed based on muscle biopsy results)
> Hyperkalemic periodic paralysis (Quarter horse breed-associated muscular disease that can cause tremors, collapse and paralysis and may be confused with neurologic conditions)
> Gene-based diagnosis
> Lyme disease (joint stiffness/swelling that can appear to be neurologic at times because of changing presentation and often severe lameness; diagnosed with serum titer tests)
> Parasitic nematode migration (Parelaphostrongylus tenuis migration in the spinal cord of horses is uncommon but has been reported and is associated with wry neck conditions; CSF analysis is diagnostic)
> Pituitary adenomas (Cushingoid horses; can present with blindness, seizures and other neurologic signs).
Christmas passed with a return of unremarkable blood work results and a report that Rockett was not better, but no worse. The next day, however, an emergency call came in, and Rockett was now collapsed and wedged into a space in the corner of the pasture. On arrival, Dr. X found her standing in the yard. She was minimally responsive and blind. "She was quiet for a while," explained her owner. "Then she got anxious, bolted forward into the fence and went down. She laid that way for a bit, then got anxious and got up again."
A physical examination now revealed severe cranial nerve deficits, severe ataxia and rapidly progressing disease. Rockett had two more similar "episodes" within a short time, and it was obvious more aggressive care was needed. For a while, Dr. X and the owners struggled to get Rockett to step into a trailer. She could no longer see and could not control her limbs. Rockett was referred to a nearby equine hospital at a veterinary college. She was unable to rise on arrival, with even more progressively worsening signs during the trip of less than two hours. Humane euthanasia was elected for Rockett, leaving Dr. X to ponder his differential list.
Photo 1: The cerebellum and the brainstem of a horse affected with cryptococcal meningoencephalomyelitis. The granulomatous aspect of this disease process can be appreciated by the diffuse nodular appearance of the cord.
Necropsy results revealed that Rockett had severe, chronic pyogranulomatous meningoencephalomyelitis due to an infection with Cryptococcus neoformans (Photos 1-3). Far from a "usual suspect," this infection is a rare condition in horses with only a small number of reported cases in the literature outside of Western Australia, where it is endemic and carried by certain bird species. Most reported cases in the United States involve the respiratory tract and sinuses, and it is thought that this fungal infection is acquired by breathing in the cryptococcal yeast spores. The horse in this case, however, showed a complete lack of any respiratory or sinus involvement, and there was no indication about the mechanism of infection.
Photo 2: The spinal cord, seen with its myelin covering reflected, is also noted to be diffusely nodular. The extensive nature of the cryptococcal infection in this horse is also unique given that no respiratory or nasal sinus source of the organism was found during necropsy.
"The prognosis for horses with cryptococcal infections is not well defined because of their seemingly infrequent occurrence and the low number of reported cases," says Allen Morris, DVM, regarding a case report and literature review of cryptococcal meningitis in the horse.
Photo 3: CSF taken from the horse in this case shows large blue cryptococcal yeasts present throughout the slide.
"In order for treatment (fluconazole at 14 mg/kg PO loading dose, then 5 mg/kg PO q 24 h x 6 weeks) to be instituted in a timely fashion," Morris explains, "a definitive diagnosis of Cryptococcus infection at an early stage is probably critical to a positive outcome." Drs. Riley, Mills, Bolton and Thomas of the School of Veterinary and Biomedical Sciences at Murdoch University in Western Australia made this comment in their review of seven cases of cryptococcosis: "Cases of equine cryptococcosis carry a poor prognosis and treatment was not attempted in any of these cases."
Similar clinical signs and generally poor prognoses make neurologic diseases a diagnostic and treatment challenge for equine veterinarians. A broad differential list should be considered. Even though most cases will be caused by the usual suspects, clinicians should always be open to other more unique and obscure causes. As more cases of fungal encephalitis are described and possibly considered earlier in the disease process, greater numbers of cases may be treated with potentially better results.
Dr. Marcella is an equine practitioner in Canton, Ga.