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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