West Nile fever

West Nile fever (West Nile encephalitis) is an acute viral zoonotic natural focal disease with a transmissible mechanism of pathogen transmission. It is characterized by an acute onset, pronounced febrile-intoxication syndrome and damage to the central nervous system.

ICD-10 code

A92.3. West Nile fever

Epidemiology of West Nile Fever

The reservoir of the West Nile fever virus in nature is birds of the aquatic-peri-aquatic complex, the carrier is mosquitoes, primarily ornitophilous mosquitoes of the genus Cilex. The virus circulates between them in nature, they determine the possible area of distribution of West Nile fever - from the equatorial zone to regions with a temperate climate. Currently, the West Nile fever virus has been isolated from more than 40 species of mosquitoes, not only in the genus Cilex, but also in the genera Aedes, Anopheles, etc. The significance of specific mosquito species in the epidemic process occurring in a certain territory has not been clarified. The work of Russian scientists has established the infection of argasid and ixodid ticks in natural foci of West Nile fever.

Synanthropic birds may play an additional role in the preservation and spread of the virus. The outbreak of West Nile fever in 1999 in New York was accompanied by a mass death of crows and exotic birds in a zoo; in 2000-2005 the epizootic spread throughout the United States. The epidemic in Israel in 2000 was preceded by an epizootic in 1998-2000 among geese on farms. About 40% of poultry in the Bucharest area in the fall of 1996 had antibodies to the West Nile fever virus. Together with "urban" ornitophilic and anthropophilic mosquitoes, domestic and urban birds can form the so-called urban, or anthropurgic, focus of West Nile fever.

Diseases of mammals are described, in particular epizootics of horses (from tens to hundreds of cases).

Due to the high incidence of West Nile fever in the United States in 2002-2005, there were cases of West Nile fever infection in blood and organ recipients.

In countries with a moderate climate, the disease has a pronounced seasonality, due to the activity of mosquitoes that carry it. In the northern hemisphere, the incidence is observed from the end of July, reaches a maximum in late August - early September and ceases with the onset of cold weather by October - November.

Human susceptibility to West Nile fever is apparently high, with a subclinical course of infection predominating. Once West Nile fever has been suffered, it leaves behind a pronounced immunity. This is evidenced by the fact that in hyperendemic regions (Egypt), children of younger age groups get sick, and antibodies are found in more than 50% of the population, while in countries from hypoendemic areas, the level of population immunity is below 10% and mainly adults get sick, in particular, in the southern regions of Russia (Volgograd and Astrakhan regions, Krasnodar and Stavropol Krai).

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What causes West Nile fever?

West Nile fever is caused by the West Nile fever virus, which belongs to the Flavivirus genus of the Flaviviridae family . The genome is single-stranded RNA.

Replication of the virus occurs in the cytoplasm of affected cells. West Nile fever virus has a significant capacity for variability, which is due to the imperfection of the mechanism for copying genetic information. The greatest variability is characteristic of genes encoding envelope proteins responsible for the antigenic properties of the virus and its interaction with tissue cell membranes. West Nile fever virus strains isolated in different countries and in different years have no genetic similarity and have different virulence. The group of "old" West Nile fever strains, isolated mainly before 1990, is not associated with severe CNS lesions. The group of "new" strains (Israel-1998/New York-1999, Senegal-1993/Romania-1996/Kenya-1998/Volgograd-1999, Israel-2000) is associated with mass and severe human diseases.

What is the pathogenesis of West Nile fever?

West Nile fever has been poorly studied. It is believed that the virus spreads hematogenously, causing damage to the vascular endothelium and microcirculatory disorders, and in some cases, the development of thrombohemorrhagic syndrome. It has been established that viremia is short-term and non-intensive. The leading factor in the pathogenesis of West Nile fever is damage to the membranes and brain tissue, leading to the development of meningeal and general cerebral syndromes, focal symptoms. Death usually occurs on the 7th-28th day of the disease due to disruption of vital functions due to edema-swelling of the brain tissue with dislocation of stem structures, necrosis of neurocytes, and hemorrhages in the brain stem.

What are the symptoms of West Nile fever?

The incubation period of West Nile fever lasts from 2 days to 3 weeks, most often 3-8 days. West Nile fever begins acutely with an increase in body temperature to 38-40 ° C, and sometimes higher for several hours. The increase in temperature is accompanied by severe chills, intense headache, pain in the eyeballs, sometimes vomiting, muscle pain, lower back, joints, and severe general weakness. Intoxication syndrome is expressed even in cases with short-term fever, and after normalization of temperature, asthenia persists for a long time. The most characteristic symptoms of West Nile fever caused by "old" strains of the virus, in addition to those listed, are scleritis, conjunctivitis, pharyngitis, polyadenopathy, rash, hepatosplenic syndrome. Dyspeptic disorders (enteritis without pain syndrome) are common. CNS damage in the form of meningitis and encephalitis is rare. In general, West Nile fever is benign.

How is West Nile fever diagnosed?

Clinical diagnosis of West Nile fever is problematic. In the region where West Nile fever is endemic, any case of influenza-like illness or neuroinfection in June–October is suspected of being West Nile fever, but can only be diagnosed using laboratory tests. During outbreaks, diagnosis can be made with a high degree of certainty based on clinical and epidemiological data: association of the disease with mosquito bites, trips out of town, residence near open water bodies; absence of repeated cases of the disease in the outbreak and association of the disease with consumption of food products, water from open water bodies; increase in the incidence of neuroinfections in the region during the warm season.

How is West Nile fever treated?

West Nile fever is treated with syndromic therapy, since the effectiveness of antiviral drugs has not been proven. To combat cerebral hypertension, furosemide is used in adults at a dose of 20-60 mg per day, maintaining normal circulating blood volume. With increasing symptoms of edema-swelling of the brain, mannitol is prescribed at a dose of 0.5 g / kg of body weight in a 10% solution, administered quickly for 10 minutes, followed by the introduction of 20-40 mg of furosemide intravenously. In severe cases (coma, respiratory failure, generalized seizures), dexamethasone (dexazone) is additionally prescribed at a dose of 0.25-0.5 mg / kg per day for 2-4 days. Detoxification and compensation for fluid loss are carried out by intravenous infusions of polyionic solutions (solution "trisol"). polarizing mixture and colloidal solutions (10% albumin solution, cryoplasm, rheopolyglucin, rheogluman) in a ratio of 2:1. The optimal daily volume of administered fluid, including oral and tube administration, is 3-4 l for adults and 100 ml/kg of body weight for children.

How is West Nile Fever prevented?

West Nile fever is prevented by measures aimed at reducing the number of mosquitoes, which is achieved by carrying out anti-mosquito treatments of mosquito breeding sites within the city limits and in adjacent territories, as well as in areas near country recreation centers, health centers, and children's camps. Basements of residential and public buildings in urban and rural areas are subject to disinfestation treatment. Treatment can be carried out outside the epidemic season to destroy mosquitoes that overwinter in the imago stage. It is recommended to reduce the population density of synanthropic birds (crows, jackdaws, sparrows, pigeons, seagulls, etc.). Public prevention measures for West Nile fever are carried out according to epidemiological indications based on regular epidemiological surveillance and examination of the territory.

Non-specific individual prevention measures include the use of repellents and clothing that protects against mosquito bites during the epidemic period (June-October), minimizing the time spent outdoors during the peak mosquito activity (evening and morning), screening windows, and choosing places with the fewest mosquitoes for rest. In endemic regions, health education work among the local population and visitors is of great importance.