Borna Disease
Basic Information 
Definition
• Borna disease virus (BDV) is an enveloped, single-stranded RNA virus that causes polioencephalomyelitis in horses.
• Transmission most likely occurs through contact with infected nasal, lacrimal, or salivary secretions with viral ascent through the olfactory (and possibly trigeminal) nerve. The incubation period is extended, and infection appears to be restricted to the central nervous system (CNS).
• Affected horses present with alterations in behavior, sensorium, and consciousness that may progress to cranial nerve abnormalities, spinal cord abnormalities, and death. There is no effective treatment or vaccine. The prevalence and incidence of the disease worldwide are unknown.
Epidemiology
Contagion and Zoonosis
• The route of transmission of BDV is unknown. The virus has been detected in nasal, lacrimal, and salivary secretions of affected animals, so it is postulated that direct and indirect contact with infected horses can spread the virus.
• Whether BDV is a zoonotic agent that causes overt illness in humans is unknown. It does appear that humans can be affected by either the Borna virus or a Borna-like virus. Seroprevalence studies have revealed BDV antibodies in humans with psychiatric disorders and in humans without disease (similar to horses). However, the exact pathology of the virus in humans, whether it is transmitted to humans from horses, and whether it is a causative agent of disease in people, is unknown at this time.
• Veterinarians should take universal precautions when handling and performing necropsies on horses with any neurologic disease.
Geography and Seasonality
• Clinical BDV has been recognized in horses in Germany, Switzerland, Liechtenstein, and Austria. Seroprevalence studies in Germany reveal that there is a large discrepancy between the incidence of disease (low) and the prevalence of BDV-specific antibodies (11%–20% normally; 55% during outbreaks). New occurrences of disease may occur anywhere from 2 months to several years after the initial outbreak. There is no seasonal trend to the virus.
• BDV is not likely restricted to Europe. Seroprevalence studies have revealed BDV antibodies in horses worldwide, including Europe, Turkey, the Middle East (Israel and Iran), Asia (Japan and China), Australia, and the United States. However, the incidence of disease caused by BDV infection in these countries is unknown.
Clinical Presentation
Physical Exam Findings
• Initial clinical signs involve changes in personality and sensorium. Movements are deliberate and slow and include general hypokinesia, postural unawareness, and slow eating or chewing with no food in the mouth. Many horses demonstrate rhythmic or repetitive movements and often yawn frequently and head press. Changes in personality and mental status, including hyperexcitability, fear, aggression, lethargy, somnolence, and stupor, may also occur. Loss of the cutaneous trunci reflex may also be noted early in the disease. A fever refractive to nonsteroidal antiinflammatory drugs may also occur.
• As the disease progresses, neurologic deficits increase. Cranial nerve abnormalities are often seen, including alterations in cranial nerve (CN) III (strabismus and miosis), CN V/VII (bruxism, trismus), CN VII/XI (nystagmus), CN VIII (head tilt), CN IX/X (dysphagia, pharyngeal paralysis), and CN XII (tongue paralysis). Spinal cord abnormalities are also present, including ataxia, imbalance, abnormal postures, hyporeflexia of spinal reflexes, and proprioceptive deficits. Changes in personality may progress.
• In the latter, end stages of BDV, the horse appears extremely unbalanced and often stops eating or drinking. Neurogenic torticollis accompanied by dystonia of the neck muscles with or without circular walking is often present. Head tremors, convulsions, head pressing, loss of the pupillary light reflex, and comatose states occur.
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