Acute Anterior Poliomyelitis (Heine-Medin Disease)
The disease is caused by an enterovirus (RNA virus). Transmission typically occurs via the fecal-oral route, after which the pathogen replicates in lymphoid tissue. In about 1% of cases, the virus invades the CNS, binding to motor neuron receptors in the anterior horns of the spinal cord. Viral RNA blocks normal cellular protein synthesis, leading to neuronal death.
Macroscopically, the meninges are hyperemic, the spinal cord tissue is edematous, and the normal "butterfly" outline of the gray matter becomes blurred. Microscopically, neuronophagic nodules (clusters of polymorphonuclear leukocytes and microglia) form around dying cells, which are subsequently replaced by glial scars.
In the residual stage, small cysts develop at the sites of destroyed tissue. Due to the irreversible loss of motor neurons, nerve root atrophy and secondary neurogenic atrophy of skeletal muscles develop, leading to severe disability.
Neuroinfections: Herpes and Rabies
Herpes simplex virus type 1 (Herpes simplex virus type 1) invades the nervous system via retrograde axonal transport. It causes acute necrotizing encephalitis, predominantly affecting the temporal lobes and orbitofrontal gyri. Specific intranuclear viral Cowdry type A inclusion bodies form within neurons. The mortality rate of such encephalitis reaches 80%.
The varicella-zoster virus (Varicella-zoster virus) can persist in a latent phase within sensory spinal ganglia. Upon reactivation, it causes ganglionic neuronal necrosis and spreads along nerve fibers, provoking intradermal neuritis with vesicular eruptions (papulovesicular rash).
Rabies is a zoonotic infection transmitted through the bite of an infected animal. The rhabdovirus spreads along perineural spaces. The brain develops edema and severe encephalitis. A pathognomonic sign of rabies is Negri bodies—eosinophilic cytoplasmic inclusions most commonly localized in hippocampal neurons.
Tick-Borne Encephalitis
An acute natural focal disease caused by an RNA-containing flavivirus. The primary reservoirs and vectors are ixodid ticks (Ixodes persulcatus, Ixodes ricinus).
Routes of transmission:
- Transmissible — via a tick bite (incubation period 7–14 days, depending on feeding duration).
- Alimentary — via unpasteurized milk from infected goats or cows (often causes biphasic meningoencephalitis).
Clinically, the disease begins with sudden chills, fever, and facial and conjunctival hyperemia. In the severe poliomyelitic form, flaccid paralysis of the neck and upper extremity muscles develops (the characteristic "dropped head" sign). Morphologically, the acute stage reveals hemorrhages, edema, and neuronophagia, whereas chronic progression (typical of the Siberian viral subtype) shows demyelination and fibrillary gliosis.
Slow Infections, Prion Diseases, and HIV
In addition to acute infections, there are processes with a prolonged latent period:
- Persistent viral infections. These include subacute sclerosing panencephalitis (caused by the measles virus, accompanied by white matter hardening) and progressive multifocal leukoencephalopathy (caused by a polyomavirus in profound immunosuppression, leading to widespread demyelination).
- Prion diseases. Fatal neurodegenerative pathologies (e.g., Creutzfeldt-Jakob disease). They are characterized by spongiform degeneration of tissue, neuronal loss, amyloid plaques, and a total absence of inflammation.
- HIV-associated neurological disease. The human immunodeficiency virus directly causes aseptic meningitis or vacuolar myelopathy, and paves the way for opportunistic CNS infections (toxoplasmosis, cytomegalovirus, cryptococcosis).
Demyelinating Diseases
A distinct group of nervous system pathologies united by a specific pathogenesis: selective destruction of the myelin (Schwann cell/oligodendrocyte) sheath of nerve fibers in the CNS, while the axon (axis cylinder) remains relatively spared.