Epidemiology and transmission routes
The pathogen belongs to the Japanese encephalitis virus antigenic complex. The infection is reported as sporadic cases and outbreaks in Asia, Europe, and Africa. The risk group is predominantly rural populations; however, "duck fever" is known in France, contracted by urban hunters in the Rhône valley.
- Reservoir and sources: Wild and domestic birds (especially waterbirds and wetland birds) serve as the primary reservoir. Long-distance migrants, such as herons and waders, introduce the virus from African wintering grounds. In anthropogenic foci, the infection is maintained by pigeons, while in natural foci, it is maintained by corvids (jays, rooks, crows). Mammals (bats, rodents) also participate in the circulation, and epizootics in horses have been described.
- Vectors: Ornithophilic mosquitoes of the genus Culex are the main transmission vector. Ixodid and argasid ticks also play an important reservoir function in preserving the virus during winter.
- Modes of transmission: The vector-borne mechanism dominates. Additionally, vertical (intrauterine, via breast milk), artificial (in laboratories), and iatrogenic transmission are possible. The iatrogenic route via organ transplantation and blood transfusion is of high significance due to the widespread prevalence of the virus.
Pathogenesis and nervous system lesions
Dissemination of the virus in 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-term and of low intensity.
Severe central nervous system damage is the leading link in pathogenesis. The virus involves the meninges and the brain parenchyma, clinically manifesting through meningeal syndrome, focal, and general cerebral symptoms.
In unfavorable cases, thanatogenesis (causes of death on days 7–28 of the illness) is associated with the development of cerebral edema and swelling, neuronal death, and critical hemorrhages in the brainstem, leading to vital function failure.
Clinical presentation
The disease begins acutely. Fever reaches high values, can be biphasic, and lasts from 3 to 12 days.
The following basic syndromes are distinguished:
- General intoxication (severe headache, arthralgia).
- Exanthema (scarlatiniform rash).
- Lymphadenopathy (generalized polyadenitis).
- Catarrhal (pharyngitis, conjunctivitis).
- Hepatosplenomegaly (enlargement of the liver and spleen).
Most often, the infection runs a benign course (asymptomatic in many cases). Recovery is accompanied by a prolonged asthenic syndrome that can persist for up to a year or more. Immunity after the infection is solid.
Severe forms manifest as meningitis or meningoencephalitis with the development of paresis and paralysis, where case fatality reaches 50%. Elderly individuals are in a particularly high-risk group due to the phenomenon of antibody-dependent enhancement upon reinfection with a different serotype.
Principles of microbiological diagnostics
Since specific therapy and human vaccines have not been developed, accurate laboratory verification plays a crucial role.
- Serological method (main): ELISA, neutralization test (NT), complement fixation test (CFT), and hemagglutination inhibition test (HI) are used. Material: CSF and blood serum. The diagnosis is confirmed by detecting specific IgM in CSF, high titers of IgM in blood (marker of activity), or a 4-fold or greater rise in antibody titers in paired sera (in NT).
- Virological method: Involves isolating the virus from blood, CSF, or autopsy material using cell cultures or newborn white mice.
- Molecular biological method (PCR): Used primarily to confirm the diagnosis in fatal cases. In the acute period of fever, blood PCR often yields a negative result due to the low intensity of viremia.
Briefly: answers to topical questions
Which structural proteins form the virion of the West Nile virus?
- Capsid protein (C) — forms a capsid with icosahedral symmetry surrounding the genomic positive-sense RNA.
- Membrane protein (M) — located on the outer side of the virion's supercapsid envelope.
- Surface protein E (dimer) — a key glycoprotein of the outer lipoprotein envelope that determines cell tropism, carries virulence determinants, and serves as the main immunogen inducing virus-neutralizing antibodies.
What changes in the cerebrospinal fluid are observed in the neuroinvasive form of West Nile fever?
When the central nervous system is affected and the neuroinvasive form of West Nile fever develops, the following characteristic changes are found in the cerebrospinal fluid:
- Elevated protein content less than 150 mg/dL.
- Moderate pleocytosis less than 500 cells per µL.
- Predominance of lymphocytes in the cellular composition, although mixed pleocytosis may be observed in the early stages of infection.
With which infectious diseases is it necessary to differentiate West Nile fever?
To confirm the diagnosis of West Nile fever and exclude other pathologies, differential diagnosis is performed with the following nosological entities:
- Enteroviral meningitis
- Bacterial purulent meningitis
- Tuberculous meningitis
- Herpetic encephalitis
To memorize the reservoir and vector, imagine the chain: migratory bird (heron from Africa) → local urban bird (pigeon/crow) → Culex mosquito → human.
Class and exam questions
Why is blood PCR often falsely negative at the peak of the disease?
Viremia in West Nile fever is short-lived and has very low intensity, making it difficult to detect viral RNA in the bloodstream.
Why do elderly people suffer from the infection more severely?
High mortality in the older age group is associated with the phenomenon of antibody-dependent enhancement, which occurs upon reinfection with a different viral serotype.
What role do ticks play in the spread of the virus?
Argasid and ixodid ticks are not the primary vectors for human infection, but they perform a critically important natural reservoir function by preserving the virus during the winter period.
What else to study on this topic
- Mechanisms of antibody-dependent enhancement (ADE) in flavivirus infections.
- Features of thanatogenesis: mechanisms of brain edema and brainstem hemorrhage development.
- Japanese encephalitis virus antigenic complex: comparative characteristics of the pathogens.
- Iatrogenic transmission routes of the virus and methods for monitoring donor blood and organs.
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