Dr. Murai Éva - Gubányi András szerk.: Parasitologia Hungarica 29-30. (Budapest, 1997)

virus.) Grigorievich and Tkachev were the first to demonstrate that mice inoculated with the brain suspension of a patient who had died of encephalitis succumbed to a disease that manifested itself in signs similar to those of the human disease. Initially it was believed that the virus was carried and infection was transmitted by healthy humans. It was thought that the pathogen colonised the throat and was transmitted by droplet infection and, thus, the disease could be prevented by rinsing the throat with permanganate solution. Excessive heat was also considered to be a predisposing factor: it was recommended that people should protect their body and especially their head from exposure to direct sunlight. This notion may have originated from the observation that the majority of cases occurred in the summer period. In 1937, a major expedition led by Silber started off for the taiga to elucidate the characteristics of the outbreaks. It became obvious already during the first expedition that the disease most frequently occurred in the spring, and infection was contracted exclusively by people working on the taiga. A substantial proportion of people affected by the disease had never met each other. It was soon found out that the seasonal activity of ticks indigenous in the region almost exactly corresponded to the seasonal fluctuation of encephalitis cases. There was an only two-week time difference between the two curves, which corresponds to the average incubation period. By that time it had already become almost certain that the Ixodes tick species indigenous in the area was responsible for transmitting the disease. The hypothesis of Silber was proved by Tchumakov, who successfully infected animals with the help of Ixodes ticks. Soloviev demonstrated that the virus remained viable for a long time in several rodent species which could thus act as reservoirs. As the last step of the investigations, the researchers successfully detected the pathogen by multiple methods. As a tragic consequence of the expedition, the newly discovered virus infected several researchers. Despite the strict precautions taken to prevent infection, three scientists died during the research. Soon afterwards it was found out that the disease occurred not only in Siberia but also on this side of the Ural Mountains. In Central Europe, the pathogen was first isolated in 1948 in Czechoslovakia, then in 1952 also in Hungary (Fomosi and Molnár 1954). THE CAUSATIVE AGENT Tick-borne encephalitis virus is a single-stranded positive sense RNA virus which belongs to the Flaviviridae family together with other human pathogens such as the causative agents of yellow fever, Japanese B encephalitis, and dengue. Its protein capsid has almost regular spherical shape. It is surrounded by a cell membrane like envelope. The virus is moderately resistant to environmental factors. Its resistance is markedly increased by protein-containing solutions. CLINICAL SYMPTOMS In typical cases the disease course consists of two phases. The characteristic temperature curve is referred to as two-humped or dromedary type. The first phase corresponds to the stage of viraemia, when viruses having multiplied at the site of the tick bite are disseminated in the organism. That phase is usually accompanied by fever. The clinical symptoms resemble those of influenza, and include moderately high temperature, headache, muscle pains, backache, sometimes abdominal pain, and malaise. Although the disease is not