Miscellaneous neurologic diseases in horses (Proceedings)


Overview of equine rabies, equine herpes virus-1, and parasitic infection of the CNS

Equine Rabies

Relatively uncommon, but probably underreported. Risk factors include: residence in endemic areas, 24 hour access to pasture, no vaccination history, and more common in younger horses. It may be more common in the fall.

Source: Foxes, raccoons, skunks, dogs, and coyotes. Bats not usually reported.

Pathogenesis: Bite wounds are not usually reported.

Phase 1: incubation period (ascending or centripetal phase- virus transported toward CNS) variable- days, weeks to months.

Phase 2: (period of multiplication of virus within CNS). This is characterized by extensive replication of the virus in the limbic system, adjacent parts of the brain and spinal cord. The extensive replication in the spinal cord in horses is different than in humans. Clinical signs occur during this phase. Average duration is 7 days, range of 5-10 days. Most horses are euthanized during this time; due to the severity of clinical signs horses rarely progress to phase 3.

Phase 3 (centrifugal or descending spread of virus): Is characterized by neuronal transport of virus into highly vascularized organs (including salivary gland).

Clinical signs: Clinical presentation of rabies is very diverse. Horse may present for "colic" or "lameness".

Paralytic/Spinal Cord Form: may be most common. Clinical signs include loss of tail tone, ascending ataxia/paresis, loss of anal sphincter tone.

Brainstem form: Clinical signs include dysphagia, pharyngeal paralysis, head tilt, blindness and drooling.

Cerebral (furious) form (least common): Clinical signs include aggressiveness, photophobia, hydrophobia, hyeresthesia, circling, and depression.

Diagnosis: Postmortem, immunofluorscent antibody test is the gold standard. Histopathology (negri bodies) are not always present. Cytology of spinal fluid- ranges from normal to mild increase in protein and a moderate lymphocytic pleocytosis.

Prevention: highly effective. Considered "core" equine vaccine.

Equine Herpes Virus 1 (EHV-1):

EHV-1 results in respiratory disease, abortion, neonatal death and neurological disease.

Signalment: Adult horses. Outbreaks occur more commonly in winter (overcrowding?)

Clinical signs: Neurological disease can be preceded by a fever. Ascending paralysis or paresis of the hindlimbs. Ataxia, weakness are present in varying degrees. Atonic bladder and decreased tail tone are often present. Cranial nerve disease can be occasionally seen.

Diagnosis: Suspect EHV-1 when 1) multiple horses develop neurological signs, 2) neurological disease and fever. Spinal fluid cytology is usually abnormal (normal WBC count, increased protein, and xanthochromia). Laboratory diagnosis is based on detection of virus which includes PCR of nasal swab or whole blood, or virus isolation. Virus shedding can occur for up to 14 days. Acute and convalescent antibody titers can be helpful. A single titer is not usually diagnostic.

Treatment: Anti-inflammatory drugs (including steroids) are often used. Supportive care includes catheterization of the bladder and antibiotics. Use of acyclovir has been used, questionable if absorbed. Quarantine for entire facility for at least 3 weeks after the last horse has had a fever.

Parasitic Infection of the CNS

Parasitic infections of the CNS are reported to due Halicephalobus gingivalis (Micronema), and Strongylus vulgaris. Other less common parasites include Hypoderma lineatum and bovis.

Halicephalobus gingivalis is the most common parasitic infection of the CNS in horses. This parasite is a free-living saprophytic nematode that is found in soil, manure and decaying humus. It was previously named Micronema, and Halicephalobus deletrix.

Infections are reported in masses of the face, mandible, kidneys, bone, testicles, eyes, skin and CNS.

Clinical signs are variable, and depend on neuroanatomic location. Most cases ataxia and encephalitic signs are reported.

Diagnosis: Most horses with halicephalobus infections have signs of infection in other parts of the body (masses of the head, renal infections etc). Spinal fluid analysis: non-specific signs of inflammation and eosinophils are rarely reported.

Treatment: There are no reports of horses surviving neurological disease due to helicephalobus. Suggestions on doses of anthelmintics include fenbendazole 60 mg/kg once to 50 mg/kg once a day for 2-3 days. Other recommendations include anti-inflammatory drugs (steroids or NSAID) and DMSO

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