Meningitis

I do not have the Harsh Mohan textbook in the available library, so this is a concise pathology exam answer consistent with standard Harsh Mohan-style classification and terminology. The available pathology reference similarly classifies infectious meningitis as acute pyogenic, aseptic/viral, and chronic forms. Robbins & Kumar Basic Pathology, p. 833.

1. Etiology

A. Acute pyogenic (bacterial) meningitis

B. Aseptic or viral meningitis

• Enteroviruses, especially coxsackievirus and echovirus
• Mumps virus
• Herpes simplex virus
• HIV
• Arboviruses and lymphocytic choriomeningitis virus

C. Chronic meningitis

• Tuberculous meningitis: Mycobacterium tuberculosis
• Fungal meningitis: Cryptococcus neoformans, Candida, Coccidioides etc.
• Spirochetal meningitis: syphilis, Lyme disease

D. Noninfectious meningitis

• Chemical irritation, for example after rupture of an epidermoid cyst
• Carcinomatous or leukemic infiltration of meninges
• Sarcoidosis and autoimmune disease

2. Pathogenesis

1. Hematogenous spread
   Most common route. Bacteria colonize the nasopharynx or arise from another septic focus, enter blood, cross the blood-brain barrier, and multiply in CSF.
2. Direct extension from a local focus
   From otitis media, mastoiditis, sinusitis, skull osteomyelitis, dental infection, or vertebral infection.
3. Direct implantation
   Following penetrating head trauma, neurosurgery, CSF shunts, or congenital defects such as meningomyelocele.
4. Spread along nerves or transplacental transmission
   Important for certain viruses and congenital infections.

Mechanism of damage in bacterial meningitis

• Bacterial products induce release of inflammatory mediators.
• This causes endothelial injury, increased vascular permeability, and influx of neutrophils into the subarachnoid space.
• The resulting purulent exudate, cerebral edema, vasculitis, and thrombosis cause:
  • Raised intracranial pressure
  • Reduced cerebral perfusion
  • Ischemic infarction
  • Cranial nerve damage
  • Hydrocephalus due to impaired CSF absorption

3. Morphology

A. Acute pyogenic meningitis

Gross morphology

• Leptomeninges are congested, opaque, and covered by a yellow-green purulent exudate.
• Exudate is present within the subarachnoid space and sulci.
• Distribution may suggest the agent:
  • Exudate tends to be more prominent over cerebral convexities in meningococcal and pneumococcal infection.
  • It may be more basal in H. influenzae meningitis.
• Brain may be swollen due to edema.
• Ventriculitis may occur when infection extends into ventricular system.

Microscopy

• Dense neutrophilic exudate fills the subarachnoid space.
• Leptomeningeal vessels show congestion.
• Vascular inflammation may produce thrombosis, vasculitis, and infarction of underlying brain.
• The cerebral cortex may show edema and secondary inflammatory changes.

Fate and complications

• Resolution with treatment.
• Organization of exudate causes fibrosis and adhesions, called obliterative arachnoiditis.
• Obstruction to CSF flow or absorption causes communicating hydrocephalus.
• Other complications:
  • Cerebral edema and herniation
  • Ventriculitis
  • Venous thrombosis and infarction
  • Cranial nerve palsies
  • Brain abscess
  • Subdural empyema

B. Tuberculous meningitis

Gross morphology

• Thick, gelatinous or fibrinous basal exudate, particularly in the interpeduncular fossa, around optic chiasma, and base of brain.
• Small gray-white tubercles may be visible in meninges.
• Hydrocephalus is common due to fibrosis and blockage of CSF pathways.

Microscopy

• Granulomatous inflammation with:
  • Epithelioid cells
  • Langhans giant cells
  • Lymphocytes
  • Variable central caseation
• Endarteritis and thrombosis of meningeal vessels may cause cerebral infarcts.

C. Viral (aseptic) meningitis

Gross morphology

• Meninges may appear mildly congested or nearly normal.

Microscopy

• Predominantly lymphocytic and mononuclear-cell infiltrate in leptomeninges and perivascular spaces.
• Neutrophilic exudate is absent or minimal.
• When brain parenchyma is involved, features of viral encephalitis may occur, such as microglial nodules and neuronophagia.

D. Fungal meningitis

• Usually chronic and often occurs in immunocompromised individuals.
• Cryptococcus may produce gelatinous meningeal lesions and dilated perivascular spaces containing organisms.
• Inflammation may be minimal in severely immunocompromised patients.

4. Clinical features

General features

• Fever
• Severe headache
• Vomiting, often projectile
• Photophobia
• Neck stiffness
• Altered sensorium: irritability, drowsiness, confusion, or coma
• Seizures
• Focal neurological deficits in complicated cases

Signs of meningeal irritation

• Nuchal rigidity
• Positive Kernig sign
• Positive Brudzinski sign

Features in infants

• Fever or hypothermia
• Poor feeding
• Lethargy or irritability
• High-pitched cry
• Vomiting
• Seizures
• Bulging anterior fontanelle
• Neck stiffness may be absent

Features suggesting meningococcal meningitis

• Petechial or purpuric rash
• Septicemia
• Shock and disseminated intravascular coagulation in severe disease

Features of raised intracranial pressure or complications

• Persistent vomiting
• Papilledema
• Cranial nerve palsies
• Reduced consciousness
• Seizures
• Focal deficits
• Herniation in severe untreated cases

Typical CSF findings

One-line summary