Recent Equine Herpes Myeloencephalopathy
in North Idaho Facts About The Disease

Leah C. Gray, DVM, diplomate ACVIM
PRAIRIE EQUINE HOSPITAL, PLLC,
920 West Prairie Ave., Coeur d'Alene, ID 83858.
208-762-0930 * Fax: 208-772-3386

Of eight known equine herpesviruses (EHV), EHV-1 and EHV-4 have received the most attention because of economic losses associated with abortion, neonatal foal disease, paresis, and respiratory disease. Most horses are infected with EHV-1 and/or EHV-4 during the first one to two years of life. As with other herpesviruses, latent infections can occur; i.e. the virus lies dormant in the nerve ganglion and/or lymphoid tissue but can recrudesce under periods of stress, transport, or other systemic illness. Latency allows herpesviruses to be maintained even in closed herds. Disease of the equine neurologic system has been described as necrotizing myeloencpehalitis and meningoencephalomyelitis. The term myeloencephalopathy is used because the clinical syndrome is a result of ischemic damage to the central nervous system (CNS) secondary to vasculitis (inflammation of the vessels around the spinal cord) rather than direct toxic effects of the virus. The horse is left with an edematous, hemorrhagic spinal cord because of the vasculitis. Morbidity is variable but mortality is usually low.

History and Clinical Signs: Neurologic disease caused by EHV-1 may occur in a single animal or in multiple animals in a herd. A thorough history should be obtained to determine if affected horses have been in contact with other horses showing signs of EHV-1 infection (abortion, ataxia, and respiratory disease). A recent addition to the herd may be a source of EHV-1 infection. The range of clinical signs includes fever, anorexia, nasal discharge, cough, distal limb and scrotal edema, loss of libido, abortion, diarrhea, colic, and ocular lesions. Although fever is a common finding in horses infected with EHV-1, most horses are afebrile at the onset of neurologic disease.

Typically, the onset of paresis and ataxia is acute (sudden). The pelvic limbs are more severely affected than the thoracic limbs. The rear limb signs usually stabilize in the first 24-48 hours, however some horses will progress to recumbency and death. If not treated, the edema will migrate up the spinal cord to the brain and cause cranial nerve deficits.

Ocular lesions include serous ocular discharge, retinal lesions, and even blindness. Bladder dysfunction is common but bladder rupture is rare. Affected animals may dribble urine, and rectal palpation may reveal a distended bladder. Anal sphincter weakness, fecal retention, and decreased tail tone may all occur.

Diagnosis: A complete physical examination of a patient suspected of having EHV-1 should include palpation of the bladder per rectum because urinary dysfunction may be subtle. Difficult urination is probably caused by a combination of upper and lower motor neuron dysfunction resulting in a loss of detrusor muscle tone and voluntary control of urination. Consequently horses exhibit overflow incontinence or an inability to pass urine. Such horses may make frequent attempts to urinate but void little or no urine. A complete ophthalmic examination should be performed as well to evaluate ocular and retinal lesions.

A tentative diagnosis can be made based on history and physical examination findings along with cerebrospinal fluid (CSF) analysis. The xanthochromic (yellow color due to the breakdown of red blood cells) nature of the CSF is characteristic for EHV-1. Increases in protein can be dramatic, however a normal protein content does not rule out EHV-1. Furthermore, the increase in protein concentration in CSF does not necessarily correlate with the severity of signs or the outcome. Acute and convalescent serum samples should be taken 10-14 days apart to look for a four-fold increase in serum neutralization (SN) antibody titers. Care must be taken in interpreting titers because a positive could mean exposure, passive transfer from colostrum, or active infection. For approximately 12 days after infection, virus isolation can be obtained from nasopharyngeal swabs and from buffy coat smears of horses infected with EHV-1. However, appropriate handling of samples with special viral transport media is essential in recovering viable virus. Sero-typing the virus is important because EHV-1 has much more devastating ramifications than EHV-4.

Treatment: The beneficial anti-inflammatory effects of corticosteroids can be dramatic. These favorable effects must outweigh the possibility of immunosuppression, prolonged infection, delayed healing, and corticosteroid-associated laminitis. The advantages generally outweigh the potential risks. The use of dimethyl sulfoxide (DMSO) has been propagated in veterinary medicine but the efficacy has not been scientifically validated. Nonsteroidal anti-inflammatory drugs are indicated in the management of CNS vasculitis and soft tissue trauma associated with recumbency. Because of the possibility of pneumonia, cysititis, or infection of decubital ulcers, antibiotic therapy is indicated especially for patients receiving corticosteroids. More recently and based on human patients with CNS trauma, mannitol 20 % has been used with some success. It is an osmotic diuretic used to pull edema out of the spinal cord and has its own anti-inflammatory properties. Perhaps most important in patients with EHV-1 infection is good nursing care. This includes proper padding for a recumbent horse, rectal and bladder evacuation twice daily as needed, and prevention of urine scalding with petroleum based products. Use of an Anderson sling is beneficial especially if the horse can support weight.

The antiviral agent acyclovir has been used to treat human herpes simplex virus encephalitis. The agent has been used in horses with minimal side effects however the toxicity and pharmacokinetics of the drug has not been determined.

Prognosis: In general, affected horses that remain standing or can stand with assistance have a good prognosis for survival. Because recovery may occur during a period of weeks to months, euthanasia should not be performed prematurely.

Prevention: The currently commercially available EHV vaccines are not claimed to protect against the neurologic form of EHV infection. Outbreaks of the disease in vaccinated animals have been reported. Vaccination against EHV decreases the severity of respiratory disease. Although vaccinated horses may still become infected, nasal shedding of the virus is decreased and viremia may be less likely. Vaccination of affected horses is not recommended because of the potential immune mediated nature of the disease. The rationale for vaccinating unexposed horses during an outbreak is still debatable.

The control of EHV as it pertains to abortions applies to preventing myeloencephalopathy. In addition to vaccinating pregnant mares with killed rhino, important management practices used to prevent infection include reduction of stress, age segregation of the herd, and quarantine of new horses. Outbreaks of EHV are often attributable to an aborting mare or an addition of a new horse to the herd. Virus may be shed in nasal secretions for up to 3 weeks following infection. Cleaning facilities with disinfectants is recommended. Horses should not be moved on or off the farm for at least three weeks after the identification of the most recent new case. Serologic evaluation of all animals on the farm helps in identifying subclinical animals.

Leah C. Gray, DVM, DACVIM

 

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May 8, 2002 8:44 PM