Epidemiology and Transmission Routes
The pathogen belongs to the Japanese encephalitis virus antigenic complex. The infection is registered as sporadic cases and outbreaks across Asia, Europe, and Africa. Rural populations are predominantly at risk, although urban hunters can contract the infection through vector exposure in river valleys.
- Reservoir and Sources: The primary reservoirs are wild and domestic birds (especially waterbirds and wetland species). Long-distance migratory birds, such as herons and waders, introduce the virus from wintering grounds. In urban settings, pigeons maintain the cycle, while corvids (jays, rooks, crows) serve as natural reservoirs. Mammals (bats, rodents) also participate in circulation, and epizootics in horses have been described.
- Vectors: The primary transmission vector is ornithophilic mosquitoes of the genus Culex. Ixodid and argasid ticks play an important reservoir function by preserving the virus during the winter.
- Transmission Routes: The vector-borne mechanism dominates. Additionally, vertical (transplacental, via breast milk), accidental laboratory, and iatrogenic transmission are possible. The iatrogenic route via organ transplantation and blood transfusion is highly significant due to the widespread distribution of the virus.
Pathogenesis and Nervous System Involvement
Dissemination of the virus throughout the body occurs via the hematogenous route. The primary target of the pathogen is the vascular endothelium, leading to microcirculatory disorders. Viremia during the febrile period is characterized as short-lived and of low intensity.
Pathogenetically, the leading feature is severe central nervous system damage. The virus involves the meninges and brain parenchyma, clinically manifesting as meningeal syndrome, focal neurological deficits, and diffuse encephalitic symptoms.
In unfavorable cases, thanatogenesis (cause of death on days 7–28 of the illness) is associated with brain edema and swelling, neuronal death, and critical hemorrhages in the brainstem, leading to vital function failure.
Clinical Presentation
The disease has an acute onset. Fever reaches high values, may be biphasic, and lasts from 3 to 12 days.
Basic syndromes include:
- General intoxication (severe headache, arthralgia).
- Exanthem (scarlatiniform rash).
- Lymphadenopathy (generalized polyadenitis).
- Catarrhal (pharyngitis, conjunctivitis).
- Hepatosplenomegaly (enlargement of the liver and spleen).
Most commonly, the infection follows a benign course (frequently asymptomatic). Recovery is accompanied by a prolonged asthenic syndrome that can persist for a year or more. Immunity following the infection is solid.
Severe forms present as meningitis or meningoencephalitis with paresis and paralysis, where case fatality rates can reach up to 50%. Older adults are at a particularly high risk, which is linked to the phenomenon of antibody-dependent enhancement upon reinfection with a different serotype.
Microbiological Diagnostics
Since specific antiviral therapy and human vaccines are not widely available, precise laboratory verification is critical.
- Serological Method (Primary): ELISA, neutralization tests (NT), complement fixation (CF), and hemagglutination inhibition (HI) are used. Samples include cerebrospinal fluid (CSF) and blood serum. The diagnosis is confirmed by detecting specific IgM in CSF, high IgM titers in blood (markers of acute activity), or a 4-fold or greater rise in antibody titers in paired sera (via NT).
- Virological Method: Involves isolating the virus from blood, CSF, or autopsy material using cell cultures or newborn mice.
- Molecular-Biological (PCR): Used primarily to confirm diagnosis in fatal cases. During the acute phase of fever, blood PCR is frequently negative due to low viremia intensity.