Meningitis in Children - I.V. Bohadelnykov 2005

Serous meningitis in children. General overview
Serous meningitis of viral etiology
Poliovirus-induced meningitis

Poliomyelitis meningitis is a non-paralytic form of poliomyelitis characterized by pronounced infectious-toxic and moderately severe meningeal syndromes, a favorable course, and benign outcomes.

Etiology. The Fundamental properties of polioviruses are similar to those of other enteroviruses. The genus *Enterovirus* (polioviruses) includes 3 types that share identical physical and biological properties. Type 1 virus is considered to possess the highest virulence.

Each viral particle of poliovirus consists of a capsid comprising 60 subunits and containing 4 Polypeptides (VP1–4) that determine its immunogenicity. The antigenic Structure of polioviruses is quite stable. Polioviruses exhibit a particular tropism for the motor Neurons of the anterior horns of the Spinal Cord and the Medulla Oblongata.

Epidemiology. Polioviruses are globally widespread. Humans are the natural host, although experimentally, the virus is capable of adsorbing onto the Cells of certain monkey species. The disease is most frequently registered in temperate Regions of the Northern Hemisphere. The causative agents are highly contagious. The source of infection is a sick individual or a virus carrier.

The primary transmission mechanism is fecal-oral, with alimentary or waterborne routes of infection. Contact transmission via nasopharyngeal secretions and contaminated bodies of Water is also possible. A characteristic feature is seasonality, with an increased incidence during the summer and autumn months, associated with the spread of the agent via feces (an infected person sheds the virus for 5 weeks or more). The highest morbidity is observed in children under 4–5 years of age.

Pathogenesis. The portal of entry for the poliovirus is the mucous membrane of the nasopharynx and the digestive tract. Primary viral Replication occurs in the epithelium of the Mouth, Pharynx, Small Intestine, as well as in the lymphoid Tissues of Waldeyer's ring and Peyer's patches in the intestine. From there, the virus enters the systemic Circulation (primary viremia) and subsequently spreads to various Organs, excluding the CNS, because during this phase of infection the poliovirus is unable to cross the Blood-Brain barrier (BBB). If serum Antibodies are present by this time, further dissemination of the virus is halted (abortive form). If antibodies are scarce, secondary viremia develops, and the pathogen penetrates the CNS via the BBB or perineurally (in 1% of cases). In such instances, an isolated involvement of the Meninges may occur without spreading to the brain tissue and without affecting the anterior horns of the spinal cord—namely, the non-paralytic (meningeal) form of poliomyelitis develops.

Pathological anatomy. In the acute phase of poliomyelitis, plethora of Internal Organs is observed, along with Changes in the lymphoid tissue of the Tonsils, the Cytology/cytology/61.html">Lymphatic follicles of the small intestine, and the Spleen. With The Development of meningeal syndrome, edema and infiltration of the brain meninges are detected.

Clinical presentation. The disease has an acute onset characterized by fever, general intoxication symptoms, catarrhal signs, or dyspeptic disorders. After 2–3 days, body Temperature drops to normal, and the patient's well-being improves. However, 1–3 days later, the body temperature rises again, and against this Background, meningeal symptoms appear within the very first day, manifesting as severe headache and vomiting. Among the meningeal signs, neck and back Muscle rigidity are most frequently observed, while Brudzinski's and Kernig's signs are less common. Changes in superficial and deep Reflexes are characteristic. Initially, superficial reflexes (abdominal, cremasteric) decrease or disappear; 10–20 hours later, deep tendon and periosteal reflexes also change (becoming hyperactive or depressed).

Occasionally, a pronounced radiculomeningeal syndrome is noted, typically characterized by radicular pain alongside positive tension signs such as Lasegue's and Neri's signs.

Lumbar puncture yields clear CSF flowing out under normal or slightly elevated pressure, revealing moderate pleocytosis (50–300 cells per 1 µL)—predominantly neutrophilic in the first few days and lymphocytic after 3–5 days—alongside normal or slightly elevated protein and glucose levels.

The clinical course of poliomyelitis meningitis is benign and typically proceeds without complications.

Main diagnostic Criteria for the meningeal form of poliomyelitis:

1. Epidemiological history: contact with a patient or carrier, occurrence predominantly in early childhood, summer-autumn seasonality, and sporadic (less frequently epidemic) character of the disease.

2. Acute onset of meningitis with the infectious-toxic syndrome predominating over the meningeal syndrome.

3. Meningeal symptoms appear on the 1st day of the secondary temperature spike, or on the 2nd–3rd day of elevated body temperature in cases of a single-wave fever curve.

4. Concomitant radiculomeningeal syndrome is frequently detected.

5. Benign course of meningitis without complications.

Laboratory Diagnostics. In the complete blood count, the formula may remain normal, or a moderate neutrophilic leukocytosis may be revealed.

Virological examination. Materials for examination include blood, CSF, feces, and nasopharyngeal swabs. Isolation of the pathogen is performed in primary tissue cultures (embryos, surgical waste) or in Cell lines such as HeLa, Hep-2, SOC, etc. Identification of the agent is carried out via the cytopathic effect and its neutralization by type-specific antisera.

Serological testing involves the determination of antibodies in serum and CSF. The detection of high IgM titers or a 4-fold increase in antibody titer in paired sera indicates the presence of an infection.

CSF examination. In the first days of illness, a moderate (50–300 cells per 1 µL) pleocytosis with a predominance of neutrophils is detected. Protein and glucose levels are normal or slightly elevated (cell-protein dissociation). After 3–5 days of illness, lymphocytes predominate in the CEREBROSPINAL FLUID.