Tick-borne meningoencephalitis

Overview
Tick-borne meningoencephalitis or Tick-borne encephalitis is a tick-borne viral infection of the central nervous system affecting humans as well as most other mammals. The virus can infect the brain (encephalitis), the membrane that surrounds the brain and spinal cord (meningitis) or both (meningoencephalitis). It is transmitted by the bite of infected deer ticks or (rarely) through the non-pasteurized milk of infected cows. Sexual transmission has been documented in mice with vertical transmission to progeny. Sexual transmission with humans has never been documented.

Etiology
The responsible virus, Tick-Borne Encephalitis Virus (TBEV), is a member of the genus flavivirus. Other close relatives include Omsk hemorrhagic fever virus, Kyasanur forest disease virus, alkhurma virus, louping ill virus and the langat virus.

TBE virus has two subtypes: (a) European subtype (Tick vector: Ixodes ricinus) (b) Far Eastern subtype (Tick vector: Ixodes persulcatus)

Russia and Europe report between 10-12,000 human cases annually. The disease is incurable once manifest, but the virus can be inactived and prevented by vaccination. In humans, the disease is lethal in approximately 1.2% of cases and leaves 15-20% of its survivors with permanent neurological damage. The former Soviet Union did a great deal of research on all tick borne disease including TBE viruses.

Diagnosis
The TBE virus may be present in a seronegative strain or subtype. In such cases a marker for TBE infection is elevated IFN-g in CSF.

Treatment
There are four main catgeories of treatment for TBE:
 * Phosphrenyl, both a therapeutic and prophylactic agent for TBE
 * interferon treatment (like interferon for Hepatitis C)
 * antibiotic treatment for possible tickborne coinfections
 * phytotherapy

Antibiotics
Although the TBE virus cannot be eradicated from the body, it can be inactivated. It can also be activated. Unfortunately, certain antibiotics activate the TBE virus while others have no effect. This is important because the TBE virus may be a coinfection with a Borrelia Burgdorferi infection, Lyme disease, which needs treatment with antibiotics. The Russians studied this matter for years and their findings were as follows: gentamicin exerts no activating effect while streptomycin and ten other antibiotics activate the virus. They also found that some herbs inactivated the TBE virus almost completely in mice, as follows: ledum, motherwort and blackcurrant.

Progressive form and Amyotrophic Lateral Sclerosis
The TBE virus is a slow virus; it can take decades to become fulminant. This is termed Progressive Form of the TBE Virus (PFTBE). In 1983 in Russia a follow-up study was done of patients with acute TBE 2-22 years later. 68% developed PFTBE, the "overwhelming majority" of these developing ALS, Amyotrophic Lateral Sclerosis. The first isolation of a TBE virus connected with ALS was in 1975 when 70% of the ALS cases in Hamburg, Germany were found to have contact with this virus. In 1978, ALS was reproduced in laboratory animals by inoculation of the Schu virus, a TBE flavivirus, taken from the CSF of a patient with ALS. In regard to the sexual and vertical transmission of the TBE virus, it is thought provoking that conjugal and familial ALS have both been documented.