Purulent CNS infections: meningitis and abscess
Inflammation of the meninges is classified into leptomeningitis (involvement of the pia and arachnoid mater, most common) and pachymeningitis (inflammation of the dura mater).
Acute purulent meningitis is the most frequent manifestation of pyogenic CNS infection. Pathogens depend on age: group B streptococci and Escherichia coli predominate in the perinatal period, whereas Haemophilus influenzae, meningococci, and pneumococci are most common in adults. In meningococcal infection, the pathogen enters hematogenously, and severe septicemia can be complicated by disseminated intravascular coagulation (DIC) with acute adrenal insufficiency (Waterhouse–Friderichsen syndrome).
Pathogenesis of purulent meningitis:
- Impaired intracranial hemodynamics and increased blood-brain barrier permeability.
- Increased CSF production and development of brain edema.
- Direct toxic effect on nerve tissue.
Macroscopically, the brain in purulent meningitis is edematous with flattened gyri. The exudate is located in the subarachnoid space. In pneumococcal and meningococcal infections, it covers the basal and convex surfaces (frontal and parietal lobes) in the form of a «cap» or «hood». Over time, the exudate thickens and contains fibrin. Inadequate early treatment leads to edema, brain herniation, and death from uncal or tonsillar herniation. A late complication is the obliteration of CSF outflow pathways leading to hydrocephalus.
Brain abscess is a localized purulent inflammation of the brain parenchyma. Macroscopically, it is a cavity containing pus, most commonly located in the frontal lobes, parietal lobes, or cerebellum. Within a few weeks, a dense fibro-glial capsule forms around the lesion.
Specific infections: tuberculosis and neurosyphilis
Non-purulent infections are characterized by specific granulomatous or atrophic changes that can lead to the destruction of myelin sheaths and neuronal death.
Cerebral tuberculosis runs a subacute course and presents in two forms:
- Tuberculous meningitis: hematogenous spread from the lungs. The exudate (gelatinous, caseous) accumulates at the base of the brain. Microscopy reveals fibrinous-caseous exudate with Langhans giant cells and thrombonecrotic vasculitis. Mortality reaches 50%, with hydrocephalus being a frequent outcome.
- Tuberculoma: an encapsulated focus of caseous necrosis (more commonly in the cerebral hemispheres in adults, and in the cerebellum in children).
Neurosyphilis (caused by
- Tertiary syphilis: meningovascular form with the formation of miliary gummas (foci of necrosis with a lymphoplasmacytic rim and Langhans giant cells).
- Parenchymatous (quaternary) syphilis:
- General paresis: develops after 10–15 years. Characterized by subacute encephalitis, syphilitic capillaritis, ischemia, and progressive cortical atrophy (especially of the frontal lobes).
- Tabes dorsalis: occurs after 8–12 years. Morphologically manifested by demyelination and shrinkage of the posterior columns of the spinal cord due to Wallerian degeneration. Clinically, this causes proprioceptive deficits, lightning pains, and loss of reflexes.
Viral CNS infections
Viral infections most commonly manifest as serous meningitis or encephalitis.
Viral meningitis is mainly caused by enteroviruses. Macroscopically, meningeal edema is observed, while microscopic examination reveals lymphocytic infiltration. The course is favorable, with recovery occurring in 2–3 weeks.
Acute viral encephalitis (herpes, arboviruses, rhabdoviruses) has characteristic pathohistological features:
- Perivascular infiltrates (lymphocytes, monocytes).
- Microglial hyperplasia with nodule formation.
- Neuronophagia (engulfment of dead neurons by macrophages).
For precise diagnosis of the viral etiology of encephalitis, the detection of specific intracellular inclusions in nerve tissue is necessary. At the same time, the virus itself is extremely rarely isolated from the CSF.
To remember the forms of purulent meningitis, use the mnemonic: «Meningococci and pneumococci wear a cap, while Haemophilus influenzae hides at the base (basal surface)»
Class and exam questions
What is the difference between leptomeningitis and pachymeningitis?
Leptomeningitis is inflammation of the pia and arachnoid mater (the most common variant), whereas pachymeningitis is inflammation of the dura mater.
What is Waterhouse–Friderichsen syndrome?
It is acute adrenal insufficiency due to massive adrenal hemorrhages developing against the background of meningococcal septicemia and DIC syndrome.
Which cells are characteristic of tuberculous meningitis and syphilitic gummas?
In both cases, Langhans multinucleated giant cells are found within the inflammatory infiltrate.
Where exactly does demyelination occur in neurosyphilis?
In tabes dorsalis, demyelination and atrophy affect the posterior columns and posterior roots of the spinal cord.
What else to study on this topic
- Pathogenesis of fibro-glial capsule formation in brain abscesses
- Mechanisms of hydrocephalus development during the organization of fibrinous exudate
- Differential diagnosis of tuberculoma and cerebral gumma
- Wallerian degeneration of nerve fibers in tabes dorsalis
- Types of intracellular inclusions in various viral encephalitides
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