West Nile fever - Causes, symptoms and treatment. MF.

West Nile Fever is an acute viral zooanthroponosis natural focal disease, with a transmissible transmission mechanism characterized by polyadenopathy, erythema and inflammation of meningeal membranes that occur against a background of febrile-intoxication syndrome.

The first epidemic outbreak was recorded in 1937 in the study of Japanese encephalitis. In the middle of the 20th century, another epidemic was recorded in Africa and Asia, later in the Mediterranean countries( especially in Israel and Egypt), Southern Russia, Belarus, Ukraine, Romania, the Czech Republic and Italy. In the future, a serological study was conducted confirming the presence of antibodies to the virus - in the Krasnodar Territory, the Omsk and Volgograd regions, in Belarus, Azerbaijan, Tajikistan and Ukraine - these studies raise the issue of endemic territories and confirm the transfer of the disease, even in the erased / subclinicalform. The urgency of this disease increased in 1999-2003, when the incidence began to increase in the Astrakhan Region, Volgograd and Krasnodar Territory.

The causative agent of the West Nile fever

RNA-containing virus belonging to the family of tobawiruses, the genus of flavoviruses - on the basis of this species affiliation, the structure of the causative agent explaining the clinical picture can be understood:

• Presence of capsular protein, protecting against phagocytosis;
• The presence of spinules in which the glycoprotein E1 is included with hemagglutinating activity( ie the process of gluing together red blood cells and their subsequent deposition on the vascular surface) - this explains the flushing of the face and mucous membranes of the mouth including the hard palate, the injection of vessels of the sclera.
• The presence of a soluble antigen, which has type-specific activity in the organs of the CMF( the system of monocytic phagocytes - connective tissue histiocytes, Liver cupper cells( stellate reticuloendotheliocytes), alveolar macrophages of the lungs, macrophages of lymph nodes, spleen, bone marrow, pleural and peritoneal macrophages, osteoclasts of bone tissue, microglia of the nervous tissue, synovial synovial membranes, skin cells of Langerhaus, pigmentless granular dendritic cells).
• Rapid genetic variability - this feature plays a big role in creating a protein membrane responsible for antigenic properties and for interacting with the cells of the body. Because of the high genetic variability, a sad prognostic picture develops - the more perfect the virus, the more severe complications it causes, this fact is based on scientific observation: old strains of the West Nile Fever isolated before 1990 - do not cause severe CNS lesions, but all other epidemicoutbreaks registered at a later date are associated with mass illnesses and severe CNS lesions.

Stability of the virus:

• Not stable at room temperature;
• It is stored at a temperature of -70 ° C;
• Inactivated by ether and deoxycholate-Na;
• Bends at 56 ° C for 30 minutes.

Susceptibility is high and depends on geographical location: so in hyperendemic areas( for example, in Egypt) are sick children of younger age, and in outbreaks with a low prevalence, adults are more likely to get sick. To the endemic areas are Volgograd and Astrakhan regions, Krasnodar and Stavropol Territory. Sexual limitations are not present. The prevalence is almost ubiquitous, since the disease is recorded on all continents, but with varying intensity. Seasonality is due to the activity of mosquito vectors and is associated with two types of cycle: rural( when active ornithophilous mosquitoes, ie those that feed on birds) and urban( the participation of synanthropic mosquitoes, ie, feeding on both birds and humans), so the seasonality is at the end of July and before the cold weather.

Causes of infection with Western Nile fever

Source and reservoir( keeper) - birds of the water-water complex, the carrier - mosquitoes. Ways of infection - transmissible( ie through the bite of mosquitoes).

Symptoms of West Nile Fever

The incubation period is the time from the onset of the introduction of the pathogen, to the first clinical symptoms and, in this case, it lasts 3-8 days on average, but can last up to 3 weeks. During this period, the pathogen passes its way from the moment of the mosquito bite, followed by the propagation of the pathogen at the site of the bite, which subsequently develops bacteremia and primary replication in the endothelium of the vessels and organs of the CMF( the system of monocytic phagocytes-everything that is referred to these organs is described above).

Once the pathogen reaches a certain concentration and exits from these target organs, where the primary replication occurred, secondary bacteremia occurs and this marks the onset of visible symptoms. Period of clinical manifestations - as soon as secondary bacteremia begins, there is an acute onset with a rise in temperature to 38.5-40 ° C and it increases for several hours, accompanied by general toxification symptoms in the form of: chills, headache localized more often in the forehead area, pain in theeyeballs, vomiting, generalized myalgia( muscle pain is especially noticeable in the neck and lower back), arthralgia( joint pain) and general malaise.

Appearance of the patient resembles a hemorrhagic fever - facial flushing, conjunctivitis, vascular injection of sclera, reddening and granularity of mucous cheeks and a hard palate. The next stage of the symptomatology will depend on the type of the affected strain( but in any case, the most commonly affected organs are the target: liver, brain, kidneys):

• When affected by "old" strains( ie those that were common before the 90syears) arises: scleritis, conjunctivitis, pharyngitis, polyadenopathy, rash, hepatolienal syndrome, dyspeptic disorders. But with these strains the current is benign.
• In case of infection with "new strains", the further picture of development may turn out to be slightly more sad, and the clinical manifestations are more variable and are associated with different forms of this disease:
- In subclinical form there are no clinical manifestations, diagnostics is possible only with the help of screening research - determinationIgM or an increase in the titer of IgG by 4 or more times.
- The flu-like form is the least studied, because people often do not consult a doctor because of nonspecific symptoms, referring to a cold. But as soon as the general condition worsens, no one connects it with the previous symptoms. With this form, deterioration of the condition is registered on 3-5 days and manifests itself in the form of increased headache, the appearance of nausea and vomiting, tremor, ataxia, dizziness, radicular pain, hyperesthesia of the skin, meningitis symptoms, prolonged fever - stably high temperature, which keeps about 10days. This symptom complex is more common for new strains.
- The meningic form is characterized by the emergence of cerebral symptoms in the first place( headache, dizziness, blocking, vomiting that does not bring relief, muscle tremor), and focal symptomatology - anisoreflexia, nystagmus, pyramidal signs - joins this clinic.
- Meningoencephalic form is the most severe form of the disease, because the cerebral symptoms are more pronounced with a gradual increase: confusion, agitation, nonsense, sopor often turning into a coma. Also not the last place focal symptomatology: convulsions, paresis of cranial nerves, nystagmus, paresis of limbs, respiratory disorders, central hemodynamic disorders. With this form, lethality reaches 50%, and in the recovered patients frequent complications are registered in the form of paresis, muscle tremors and prolonged asthenia.

Diagnosis of the Western Nile fever

Diagnosis is based primarily on epidemic data - consider staying in endemic areas, observe cases of influenza-like illness or neuroinfections in July-October and, in addition, try to conduct serological diagnostics. They also collect an anamnesis about mosquito bites, travel outside the city, availability of housing near open water bodies.

Lumbar puncture - the main and often the only indication for its conduct are positive meningeal symptoms. With LZN in the cerebrospinal fluid( lumbar) there are specific changes characteristic of a particular form of the disease: with influenza form - only the pressure of the cerebrospinal fluid increases and everything;with meningic form - also increased pressure, the cytosis varies from 15-1000 cells in 1 μl, but more often 200-300, often of a mixed nature. Often in the first 3-5 days of neutrophil cytosis - that is, in the cerebrospinal fluid neutrophils predominate, and this is attributed to the fact that a significant part of the neurons die. For the same reason, the sanation of the cerebrospinal fluid has been disrupted. Also, with this form, an increase in protein( 0.45-1.0 g / l) and glucose( upper limit of norm and above) is recorded.

UAC( general blood test) in the incubation period or at the beginning of clinical manifestations ↓ Lc( leukopenia), and at the height of clinical manifestations ↑ Lc( leukocytosis), HF and ESR, ↓ LF( lymphopenia).

OAM - proteinuria( protein in urine), cylindruria( presence of cylindrical epithelium in the urine), leukocyturia( white blood cells in the urine).

Serological diagnostic methods: RTGA( hemagglutination inhibition reaction), RSK( complement fixation reaction), pH( neutralization reaction), ELISA( enzyme-linked immunosorbent assay);With the help of PH and RNGA, a rise in antibody titer in paired sera is observed with a time interval of 10 days. RSK - is aimed at the detection of antigen-neutralizing antibodies and, if the result is positive, they speak about the last stages of the disease or about the recently transferred one. ELISA - is directed to the detection of specific antibodies - IgG( indicate the already transferred disease or to the end of the infectious process) and IgM( talk about the height of the disease).Serological methods should be performed up to 7 days from the onset of the disease( ie from the moment of clinical manifestations) and 2-3 weeks after the first sample was taken.

Genetic method - PCR( polymerase chain reaction) is aimed at detecting the genetic material of the pathogen. With this method, you can take the study of plasma, serum and cerebrospinal fluid.

Treatment of West Nile fever

Because all viral diseases are treated with viroids, West Nile fever is no exception, but none of the antiviral drugs produced the expected result and, at the moment, the treatment reduces only to symptom relief:

1) Whenhigh intracranial pressure - furosemide with potassium preparations or veroshpiron( it acts slower than furosemide, but potassium is saving).
2) With edema of the brain - mannitol followed by furosemide. If the edema of the brain is rapidly progressive, additionally prescribe dexamethasone.
3) Compensation for fluid volume - prescribe intravenous infusions of polyionic solutions( trisol) and colloidal solutions( albumin, reopolyglucin) - 2: 1
4) To combat hypoxia, oxygen inhalations are prescribed and transferred to mechanical ventilation by the following indications:
• dyspneabreathing increases 2 times or more from the norm);
• hypoxia( batch pressure O₂ <70 mm Hg);
• hypocapnia( CO₂ pressure & lt; 25 mmHg);
• hypercapnia( CO₂> 45 mm Hg), generalized convulsions or coma.
5) With cramps prescribe Relanium( Seduxen)
6) Sedative and antioxidants
7) Means improving the cerebral blood flow( pentoxifoline)
8) Antibiotic therapy for secondary bacterial infections, also appoint a balanced enteral-parenteral nutrition, a complex of vitamins and trace elements.

The duration of treatment is an average of 10 days, with complications from the central nervous system - up to 30 days and, only after the expiration of these terms, discharge patients( taking into account the normal temperature and regression of neurological symptoms).After discharge from the hospital, a dispensary observation by a neurologist is prescribed until the full recovery of work capacity and regress of neurologic symptoms.

Complications of West Nile fever

Complications are mainly observed from the central and peripheral nervous system - focal and obschevenrologic symptoms.

Prevention

Prevention is mainly non-specific and is aimed at reducing the number of mosquitoes, which is achieved by anti-mosquito treatments of mosquito breeding sites in the urban part and in nearby territories and recreation areas. Disinsection is subjected to the basement of residential buildings and public buildings in urban and rural areas. Consider an artificial decrease in the population of synanthropic birds( crows, pigeons, sparrows, etc.).During the season, we use clothing that protects against mosquito bites, and minimizes the time spent outdoors.

Consultation of a doctor

Question: Is a sick person dangerous for others?
Answer: no, but it is a potential threat if there are mosquitoes near

Question: Is immunity formed after the transferred disease?
Answer: yes, but it is strictly specific for a certain strain and short-lived.

Doctor therapist Shabanova IE