59       Bornaviridae

 

The family Bornaviridae contains a single genus, Bornavirus. The sole member of the genus is Borna disease virus (BDV). This enveloped virus, which has only recently been demonstrated by electron microscopy, is spherical, with a diameter of about 90 nm. The envelope surrounds an inner core, 50–60 nm in diameter. The genome consists of a single molecule of negative-sense, single-stranded RNA. Replication occurs in the nucleus of host cells with budding at the cell surface. This labile virus is sensitive to heat, lipid solvents and low pH values.

Borna disease

This fatal neurological disease of horses is named after Borna, the town in Saxony where a large outbreak occurred in 1895. The disease occurs sporadically in Germany, Switzerland and other parts of Europe. Sero-epidemiological studies, however, indicate a wide geographical distribution. Neurological disease attributed to BDV has been described in horses, sheep and cats. Serological evidence of infection has been recorded in other species including rabbits, cattle and ostriches. It is thought that virus may be transmitted through ingestion or inhalation. Most cases of Borna disease occur in spring and early summer; prevalence varies from year to year. There is evidence that rodents such as shrews may act as reservoir hosts. Persistent infections can be established experimentally in rats. It has been suggested that proventricular dilatation disease, a fatal disorder of parrots, is caused by an avian bornavirus. ‘Staggering disease’ in cats has been associated with BDV infection.

Following oronasal infection, the virus gains entry to the CNS by intra-axonal spread, either through the olfactory nerve or through nerves supplying the oropharyngeal and intestinal regions. Spread within the CNS and into the peripheral nerves also occurs within axons. A non-suppurative encephalitis with lymphocytic perivascular cuffing is largely confined to grey matter and neuronal degeneration is prominent. Borna disease has been described mainly in young horses. The incubation period, which is highly variable, ranges from weeks to several months. Factors which may influence the severity of clinical signs include the age and immunological status of the infected animal and the strain of infecting virus. On farms where infection in horses is present, clinical disease is usually confined to individual animals. Clinical signs include fever, somnolence and evidence of neurological disturbance. Ataxia, pharyngeal paralysis and hyperaesthesia may be present. The course of the disease is up to three weeks and mortality rates may reach 100%. Surviving horses have permanent CNS damage and may exhibit recurrent episodes of neurological disturbance.

Borna disease may vaguely resemble other neurological conditions in the horse. However, the distribution of lesions in the CNS differs from that in other equine encephalomyelitides and if eosinophilic intranuclear inclusions (Joest–Degen bodies) are present, they may be confirmatory. Viral antigen can be demonstrated in the brain by immunohistochemical methods. Demonstration of antibodies in serum or in cerebrospinal fluid by immunofluorescence, immunoblotting or ELISA may aid diagnosis. Reverse transcriptase-PCR for the demonstration of BDV-RNA is a valuable diagnostic tool. Control is difficult due to the sporadic nature of the disease. Although BDV does not appear to be readily transmitted by infected horses, seropositive animals should be isolated. Standard hygienic measures should be applied to suspect animals.