Pathomorphology of Poliomyelitis
The disease is caused by three antigenic strains of the virus, with type 1 responsible for the vast majority (85%) of diagnoses and the most severe epidemics. Primarily, the pathogen replicates in the pharyngeal tonsils and lymphoid follicles of the small intestine. Then, via the lymphatic pathway, it reaches the lymph nodes, from where it enters the bloodstream (viremia) and disseminates throughout the body.
Central nervous system involvement is rare, occurring in only 1% of infected individuals. The virus invades the RNA of motor neuron nuclei in the spinal cord, triggering cell death. Subsequently, the infection spreads via nerve pathways to neighboring neurons and may involve the nuclei of the medulla oblongata and midbrain, the reticular formation, the substantia nigra, and the motor cells of the cerebral cortex. The total duration of the disease ranges from four to six weeks, progressing through preparalytic, paralytic, and recovery stages (including the stage of residual changes).
Macroscopic Appearance: 共产党 The spinal cord (predominantly in the thoracic region) appears swollen. On cross-section, the classic "butterfly" pattern is blurred, and petechial hemorrhages are visible in the anterior horns.
Microscopic Changes by Stage:
- Preparalytic stage: Nissl substance disappears from motor neurons, nuclei undergo pyknosis, and some cells die. Vascular congestion, diapedesis of erythrocytes, and marked edema of the brain tissue are observed.
- Paralytic stage: Neuronal necrosis occurs with softening of the gray matter. Inflammation and neuroglial proliferation develop around the zones of destruction.
- Recovery stage: Cysts, small glial scars, and lymphoid infiltrates form at the sites of necrosis.
If the pathological process extends beyond the spinal cord, the condition is termed polioencephalomyelitis.
Varicella and Herpes Zoster
Varicella (chickenpox) is an acute viral infection typical of preschool and early school-age children. The causative agent is a DNA virus from the herpesvirus family, which is identical to the agent of herpes zoster. Transmission occurs via airborne droplets (rarely transplacentally).
The virus exhibits a strict tropism for mucous membranes, skin, and nervous tissue. Upon reaching the respiratory epithelium, it enters the bloodstream, concentrates in the skin, and causes vasculitis, clinically manifesting as a maculopapular-vesicular rash.
Pathological Anatomy of the Skin: Ballooning degeneration develops in the cells of the stratum spinosum of the epidermis. The cells die, forming intraepidermal cavities (vesicles) accompanied by severe pruritus. As they dry, they become covered with brown crusts, upon the rejection of which small ulcers remain. On mucous membranes, erosions develop with scanty lymphohistiocytic infiltrates around blood vessels. Similar changes may be observed in internal organs. The main complications are associated with secondary bacterial superinfection of the rash (most commonly by Staphylococcus).
Herpes Zoster: Varicella-zoster virus can persist for years in the satellite cells of dorsal root ganglia of the spinal cord in a latent state. Upon reactivation (typically against the background of immunosuppression), it spreads along sensory nerves to the skin. Morphologically, this manifests as radiculoneuritis. Patients experience burning pain, particularly when the trigeminal nerve is involved. Complications such as encephalitis, myelitis, or interstitial pneumonia may occur, but the overall prognosis is favorable.
Pathogenesis of Pertussis
Pertussis (whooping cough) is caused by the Gram-negative bacterium Bordetella pertussis, which is transmitted via airborne droplets. The portal of entry is the mucous membrane of the upper respiratory tract.
A key factor in disease development is bacterial toxins. The pathogen colonizes the bronchial epithelium using a specific protein, hemagglutinin. This protein strongly binds to carbohydrate structures on the surface of epithelial cells as well as to macrophage integrins. This interaction not only ensures secure attachment of the bacterium but also allows it to invade respiratory macrophages. Subsequently, released toxins cause severe irritation of nerve receptors, leading to characteristic paroxysms of spastic cough.