Poliomyelitis

Etiology and Epidemiology

The causative agent of the disease is an RNA-containing virus belonging to the genus enteroviruses (Enterovirus). There are three distinct poliovirus serotypes. The pathogen is highly stable in the environment, but is rapidly destroyed by ultraviolet radiation (UVR), boiling, as well as contact with iodine and chlorine-containing disinfectants.

Poliomyelitis is a strict anthroponosis, meaning the reservoir and source of infection is exclusively human (a patient with clinical manifestations or an asymptomatic virus carrier).

Mechanisms of infection transmission:

• Primary: fecal-oral.
• Additional: airborne droplets (occurs only in the first days of the disease).

The virus is excreted from the nasopharynx during the incubation period and in the first 5–14 days of the illness, while fecal excretion continues for a prolonged period—on average about 30 days. The highest-risk group consists of young children (aged 1 to 4 years).

Pathogenesis of the infectious process

The development of the disease directly depends on the state of the host immune system and goes through several successive stages:

1. Portals of entry: the virus invades the epithelium of the gastrointestinal tract and nasopharynx.
2. Abortive course: with high host resistance, the infection is aborted at the portal of entry stage.
3. Primary viremia: if local immunity is insufficient, the virus multiplies in the lymphoid tissue, crosses the epithelium, and enters the systemic circulation without involving the nervous system.
4. Secondary viremia: against the background of serum antibody deficiency (in approximately 1% of cases), the pathogen breaches the blood-brain barrier (BBB).

The virus exhibits specific tropism for motor neurons of the anterior horns of the spinal cord and cranial nerve nuclei. Pathomorphologically, neuronal cell death has a patchy and asymmetric pattern, which determines the specific nature of the resulting paralysis.

Clinical presentation of paralytic forms

All forms of poliomyelitis are divided into atypical (without CNS involvement) and typical. The development of the typical paralytic form strictly goes through four periods:

• Preparalytic period (lasts from 3 to 6 days). Manifests with fever, dyspeptic and catarrhal syndromes, accompanied by headache and neurological symptoms. A specific prognostic sign is pronounced myalgia. Precisely the muscles that exhibit pain will subsequently undergo paralysis.
• Paralytic period (from several days to 2 weeks). Flaccid paresis and paralysis develop with complete preservation of sensation. The involvement is asymmetric, more commonly affecting the lower extremities; pelvic organ dysfunction is possible. Severity depends on the topography: involvement of the cervicothoracic region carries a high risk of respiratory disorders, while the bulbar form is accompanied by swallowing disorders, nasal voice, and hypersalivation. Severe forms develop predominantly in unvaccinated individuals.
• Convalescent period (lasts up to 1 year).
• Residual period. Characterized by persistent residual effects: muscle atrophy, paralysis, and the formation of contractures, leading to delayed motor development. Cognitive functions remain completely intact.

Diagnostic methods

A clinical diagnosis is established in the presence of an acute onset with fever and rapid (up to 6 days) development of flaccid paralysis without loss of sensation. Laboratory and instrumental methods are used for confirmation:

• Virological method: isolation of the pathogen from feces, CSF, blood, or nasopharyngeal swabs.
• Serological method: evaluation of rising antibody titers in paired sera.
• CSF analysis: reveals a picture of serous inflammation (lymphocytic pleocytosis, positive Pandy's reaction, moderate intracranial hypertension).
• Complete blood count: changes are nonspecific (mild leukocytosis, decreased hemoglobin, sometimes thrombocytopenia).
• Instrumental diagnostics: electroneuromyography (ENMG) makes it possible to verify pathology at the level of the anterior horn motor neurons.

Treatment, prevention, and prognosis

Patients are subject to mandatory hospitalization in an infectious diseases hospital and isolation for up to 40 days. Strict bed rest is indicated in the acute phase.

Therapy:

• Etiopathogenetic: intravenous administration of normal human immunoglobulin and interferon preparations.
• Symptomatic: detoxification, analgesia, vitamin therapy.
• Orthopedic regimen: proper positioning of the limbs to prevent contractures.
• Rehabilitation: vascular and metabolic drugs, therapeutic exercise, massage, and physiotherapy are used in the convalescent period. Sanatorium-resort treatment is permitted after 6 months.

Prevention: The basis of prevention is vaccination with a live attenuated oral vaccine, starting from 3 months of age. Children with immunodeficiencies should receive only the inactivated vaccine (e.g., Imovax Polio) to eliminate the risk of vaccine-associated paralytic poliomyelitis (VAPP). In the focus of infection, contacts are quarantined for 20 days, and terminal disinfection is carried out. To prevent VAPP in groups/collectives, personal items of vaccinated and unvaccinated children are strictly segregated.

Prognosis: the disease is not prone to relapses and progression after the acute phase, but in paralytic forms, a persistent neurological deficit develops, leading to lifelong disability.

Class and exam questions

What else to study on this topic

• Features of bulbar and mixed forms of poliomyelitis
• Interpretation of cerebrospinal fluid findings (serous inflammation) in poliomyelitis
• Principles of orthopedic positioning for the prevention of contractures
• Differential diagnosis of VAPP and wild poliovirus
• Interpretation of electroneuromyography (ENMG) in motor neuron lesions

Other topics from the section «Chapter 12. Infectious and parasitic diseases»

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