Pathomorphology of Poliomyelitis
The disease is caused by three antigenic strains of the virus, with type 1 being responsible for the vast majority (85%) of diagnoses and the most severe epidemic outbreaks. Primarily, the pathogen multiplies in the pharyngeal tonsils and lymphatic follicles of the small intestine. It then reaches the lymph nodes via the lymphatic pathway, from whence it enters the blood (viremia) and disseminates throughout the body.
Involvement of the central nervous system is rare—occurring in only 1% of cases. The virus invades the RNA of the motor neuron nuclei in the spinal cord, provoking cell death. Subsequently, the infection spreads via nerve pathways to neighboring neurons and may involve the nuclei of the medulla oblongata and mesencephalon, the reticular formation, the substantia nigra, and the motor cells of the 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 sequelae).
Macroscopic appearance: The spinal cord (predominantly in the thoracic region) appears swollen. On cross-section, the classic "butterfly" pattern is obliterated, and petechial hemorrhages are visible in the anterior horn region.
Microscopic changes by stage:
- Preparalytic stage: tigroid substance disappears in the 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 areas of cell death.
- Recovery stage: cysts, small glial scars, and lymphoid infiltrates form at the sites of necrosis.
If the process extends beyond the spinal cord, the pathology is termed polyencephalomyelitis.
Varicella and Herpes Zoster
Chickenpox (Varicella) 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 absolutely identical to the causative agent of shingles. 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 manifested by 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. Upon drying, they become covered with brown crusts, leaving small ulcers after sloughing. On the mucous membranes, erosions occur with scant lymphohistiocytic infiltrates around the vessels. Similar changes may be observed in internal organs. The main complications are associated with secondary bacterial infection of the rash (most commonly Staphylococcus).
Herpes Zoster: The varicella-zoster virus can persist for years in the satellite cells of the dorsal root ganglia of the spinal cord in a latent state. Upon reactivation (usually against the background of reduced immunity), it spreads along sensory nerves to the skin. Morphologically, this manifests as radiculoneuritis. Patients experience burning and sharp pain, especially when the trigeminal nerve is affected. Complications such as encephalitis, myelitis, or interstitial pneumonia are possible, but overall the outcome is favorable.
Pathogenesis of Pertussis
Whooping cough (pertussis) 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.
The key factor in the development of the disease 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 and also to macrophage integrins. Such interaction not only ensures secure attachment of the bacterium but also allows it to penetrate inside respiratory macrophages. Subsequently, the released toxins cause severe irritation of nerve receptors, leading to characteristic paroxysms of spastic cough.
Briefly: answers to topical questions
What pathognomonic giant cells are found in the lymphoid tissue in measles?
- Warthin-Finkeldey giant multinucleated cells (Warthin-Finkeldey in the context of morphology) are a pathognomonic sign of lymphatic system involvement in measles, detected in the lymph nodes against the background of follicular hyperplasia.
What are the specific rashes on the buccal mucosa that appear before the skin rash in measles called?
- Koplik spots (Koplik-Filatovi in the context of enanthema) are a specific enanthema consisting of small whitish dots surrounded by a hyperemic halo, which appear on the mucous membranes 1–2 days before the skin rash. They have key diagnostic significance.
What fatal demyelinating CNS disease can develop years after having measles?
- Subacute sclerosing panencephalitis (panencephalitis subacuta sclerosans) is a severe progressive central nervous system disease that can develop due to reactivation of the measles virus several years after having measles and is characterized by a 100% fatality rate.
What is the term for moist gangrene of the soft tissues of the face that develops in malnourished children against the background of measles?
- Noma (noma) develops in malnourished children against the background of recently suffered acute infectious diseases, including measles, with significant suppression of defenses and immunity.
What type of inflammation develops in the larynx in measles, causing false croup?
- Serous-catarrhal inflammation of the upper respiratory tract—in measles, it manifests notably as pharyngitis and tracheitis; false croup is among the possible manifestations of measles.
What microscopic changes occur in the skin during the formation of the measles maculopapular rash?
- Skin changes—in areas of the rash in measles, microscopic findings include microvascular hyperemia, perivascular infiltration by lymphocytes and histiocytes, diapedetic hemorrhages with hemosiderin formation, as well as vacuolization and the appearance of giant epithelial cells in the epidermis.
What purulent respiratory complications are caused by secondary bacterial infection in measles?
- Purulent-necrotic bronchitis and severe pneumonia—pathological changes that develop in the respiratory system upon the addition of a secondary bacterial infection against the background of measles and qualitatively alter the morphological picture.
In which digestive system organs can inflammatory changes with giant cell formation develop in measles?
- Digestive system—inflammatory changes in measles can localize in various GI organs (including the development of stomatitis, enteritis, and colitis), however, specific microscopic data on giant cell formation in digestive organs are not detailed in the presented materials.
What tissue tropism is characteristic of the measles virus in the human body?
- Epithelium of the upper respiratory tract mucous membranes and lymphoid tissue—the main targets for the measles virus, which penetrates through the mucous membranes of the upper respiratory tract, replicates in them, affects regional lymph nodes, lymphocytes, leukocytes, monocytes, and respiratory epithelium.
To memorize the stages of poliomyelitis: "Pyknosis (preparalytic) — Necrosis (paralytic) — Cystosis (recovery)".
Class and exam questions
In which structures does the poliovirus primarily replicate?
Primary replication occurs in the pharyngeal tonsils and aggregated lymphoid follicles of the small intestine.
Where does the varicella-zoster virus persist in a latent state?
The virus persists in the satellite cells of the dorsal root ganglia of the spinal cord.
What is the main cause of death in severe poliomyelitis?
The main cause of death is paralysis of the respiratory muscles.
Which mechanism ensures the attachment of the pertussis pathogen to the epithelium?
Binding occurs via hemagglutinin, which interacts with epithelial carbohydrates and macrophage integrins.
What else to study on this topic
- Mechanisms of Bordetella pertussis toxin action on respiratory nerve receptors.
- Morphological characteristics of interstitial myocarditis as a complication of poliomyelitis.
- Development of neurotrophic atrophy of striated muscles and formation of contractures in poliomyelitis.
- Changes in internal organs during the generalized course of chickenpox.
- Pathogenesis of pulmonary atelectasis formation in autonomic center damage by the poliovirus.
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