Meningitis - etiology pathogenesis morphology (gross,microscopic) clinical features according to harsh mohan textbook of pathology

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Meningitis - Pathology

Note: Harsh Mohan's Textbook of Pathology is not in the available library. The following is drawn from Robbins & Kumar Basic Pathology (9th ed.) and Robbins Cotran Pathologic Basis of Disease (10th ed.), which are the standard reference pathology textbooks covering the same content framework as Harsh Mohan.

Definition

Meningitis is an inflammatory process involving the leptomeninges and CSF within the subarachnoid space, usually caused by infection. When inflammation extends into the underlying brain parenchyma it is termed meningoencephalitis. Non-infectious causes include chemical meningitis (e.g., ruptured epidermoid cyst) and carcinomatous meningitis (metastatic cancer cells in the subarachnoid space).

Classification

Infectious meningitis is broadly classified into three types:

Type	Usual Etiology	CSF Findings
Acute Pyogenic	Bacterial	Neutrophils, high protein, low glucose
Aseptic	Viral (or rickettsial/autoimmune)	Lymphocytes, moderate protein, normal glucose
Chronic	TB, spirochetes, fungi	Mononuclear cells, high protein, reduced/normal glucose

1. ACUTE PYOGENIC (BACTERIAL) MENINGITIS

Etiology (Causative Organisms by Age)

Age Group	Common Organisms
Neonates	Escherichia coli, Group B Streptococci
Adolescents & Young Adults	Neisseria meningitidis
Older Adults	Streptococcus pneumoniae, Listeria monocytogenes

Pathogenesis

Bacteria reach the meninges via:

Hematogenous spread (most common - from bacteremia/septicemia)
Direct extension from adjacent foci (paranasal sinusitis, mastoiditis, otitis media)
Direct implantation (trauma, neurosurgical procedures)
Along peripheral nerves (rare)

Once bacteria enter the subarachnoid space, they trigger an intense inflammatory response - the relative absence of immune defenses in CSF (low immunoglobulins and complement) allows rapid bacterial proliferation. Bacterial products activate complement and cytokine cascades, leading to neutrophil recruitment and exudate formation.

Morphology

Gross Appearance

An exudate is evident within the leptomeninges on the surface of the brain
Meningeal vessels are engorged and prominent
Tracts of pus may extend along blood vessels
A thick layer of suppurative (creamy/yellow-green) exudate covers the brain surface and thickens the leptomeninges, particularly over the brain stem and cerebellum (see image below)
In pneumococcal meningitis, a gelatinous exudate may be present due to large quantities of capsular polysaccharide

Pyogenic Meningitis - Gross: thick suppurative exudate over brain surface

Gross specimen: thick layer of suppurative exudate covering the brain surface and thickening the leptomeninges (Robbins Pathology)

Microscopic Appearance

Neutrophils fill the entire subarachnoid space in severely affected areas
In less severe cases, neutrophils are found predominantly around leptomeningeal blood vessels
Gram stain reveals variable numbers of bacteria (especially in untreated cases)
In fulminant meningitis: inflammatory cells (mostly neutrophils) infiltrate the walls of leptomeningeal veins and may extend focally into the brain parenchyma (cerebritis)
Secondary vasculitis and venous thrombosis may lead to hemorrhagic cerebral infarction

Sequelae / Complications (Morphologic)

Leptomeningeal fibrosis with resultant hydrocephalus (due to impaired CSF resorption)
Chronic adhesive arachnoiditis - especially in pneumococcal meningitis, where capsular polysaccharides promote arachnoid fibrosis
Subdural empyema - pus accumulation in subdural space
Venous sinus thrombosis

Clinical Features

Systemic signs of infection: fever, chills, rigors
Meningeal irritation:
- Severe headache
- Photophobia
- Neck stiffness (nuchal rigidity)
- Kernig's sign, Brudzinski's sign
Neurologic impairment:
- Irritability
- Clouding of consciousness
- Seizures
CSF findings: increased opening pressure; abundant neutrophils; elevated protein; reduced glucose
Untreated: often fatal; with prompt antibiotics, most patients recover

2. ASEPTIC (VIRAL) MENINGITIS

Etiology

Enteroviruses (most common - ~80% of identified cases)
Other viruses: influenza, lymphocytic choriomeningitis virus, HIV, measles
May also be rickettsial or autoimmune in origin
Etiologic agent identified in only a minority of cases (improving with next-generation sequencing)

Pathogenesis

Viral entry into the CNS is typically hematogenous. The virus infects the meninges and triggers a predominantly lymphocytic inflammatory response (T-cell mediated) rather than neutrophilic.

Morphology

Less dramatic than pyogenic meningitis
Lymphocytic infiltration of leptomeninges
No purulent exudate
Brain parenchyma generally spared

Clinical Features

Less fulminant course than bacterial meningitis
Fever, headache, meningeal signs
CSF: lymphocytic pleocytosis, moderate protein elevation, glucose nearly always normal
Generally self-limited; treated symptomatically

3. CHRONIC MENINGITIS

Tuberculous Meningitis

Etiology: Mycobacterium tuberculosis - typically reaches the CNS hematogenously, often in the context of primary or reactivation TB.

Clinical Features:

Insidious onset: headache, malaise, mental confusion, vomiting
Moderate CSF cellularity with mononuclear cells or mixed PMN/mononuclear cells
Protein level elevated (often strikingly)
Glucose content moderately reduced or normal

Morphology / Complications:

Arachnoid fibrosis at the base of the brain
Hydrocephalus from impaired CSF resorption
May form tuberculoma - a well-circumscribed intraparenchymal mass
Obliterative endarteritis may lead to infarction

Spirochetal Infections (Neurosyphilis)

Occurs in ~10% of untreated Treponema pallidum infections (tertiary syphilis). HIV coinfection increases risk and severity.

Patterns:

Meningovascular neurosyphilis - chronic meningitis (usually basal), with obliterative endarteritis rich in plasma cells and lymphocytes
Paretic neurosyphilis - parenchymal involvement; neuronal loss and microglial proliferation; progressive dementia, mood changes, delusions of grandeur
Tabes dorsalis - damage to dorsal root sensory nerves; ataxia, Charcot joints, lightning pains, absent deep tendon reflexes

Fungal Meningitis

Etiology: Cryptococcus neoformans (immunocompromised), Cryptococcus gattii (immunocompetent + pulmonary involvement), Candida albicans

Pathogenesis: Fungal spread is hematogenous. Immunocompromise (HIV/AIDS, transplant, steroids) dramatically increases risk.

Morphology: C. neoformans spreads within perivascular (Virchow-Robin) spaces, producing numerous cystic spaces in brain tissue. The capsule stains with mucicarmine and India ink.

Clinical Features:

Can be fulminant (fatal in 2 weeks) or indolent (evolving over months)
Chronic meningitis + meningoencephalitis
CSF: India ink preparation shows encapsulated yeast; cryptococcal antigen test positive

CSF Summary Table

Type	Cells	Protein	Glucose
Bacterial (Pyogenic)	Neutrophils (PMNs)	High	Low
Viral (Aseptic)	Lymphocytes	Moderately raised	Normal
Tuberculous/Fungal	Lymphocytes/Mixed	High (often strikingly)	Low/Normal

Sources: Robbins & Kumar Basic Pathology, 9th ed., Ch. 21 (CNS Infections, p. 833-835); Robbins Cotran Pathologic Basis of Disease, 10th ed., Ch. 28 (p. 1164-1165)

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