CNS Infections Pathology

On this page
  1. Direct answer
  2. What you must remember
  3. One lumbar puncture, three diagnoses
  4. Where students slip
  5. Frequently asked questions
  6. Related topics

Direct answer

Cerebrospinal fluid separates the meningeal syndromes: turbid fluid with neutrophils, very low glucose and high protein in pyogenic meningitis; clear or xanthochromic fluid with lymphocytosis, high protein, low glucose and a cobweb coagulum in tuberculous meningitis; and lymphocytes with normal glucose in viral meningitis. Japanese encephalitis, transmitted by Culex mosquitoes across the rice-growing belts of Uttar Pradesh and Bihar, remains India's most important viral encephalitis, while neurocysticercosis is the commonest parasitic disease of the central nervous system and a leading cause of new-onset seizures in Indian adults. Herpes simplex encephalitis, rabies with its Negri bodies, brain abscess from contiguous spread and progressive multifocal leukoencephalopathy complete the exam set.

What you must remember

  • Pyogenic meningitis: Streptococcus pneumoniae and Neisseria meningitidis lead in adults, and meningococcaemia may add Waterhouse-Friderichsen syndrome — bilateral adrenal haemorrhage with fulminant shock; purulent exudate over the cerebral convexities; treat before culture returns in the sick patient.
  • Tuberculous meningitis: basal gelatinous exudates around the circle of Willis — hence cranial nerve palsies, hydrocephalus from basal cistern blockage, and vasculitic strokes in young Indian patients; CSF shows lymphocytosis with low glucose and a cobweb clot; steroids reduce neurological sequelae.
  • Viral meningitis: enteroviruses the usual cause; lymphocytic pleocytosis with normal glucose and modest protein rise; benign course.
  • Herpes simplex encephalitis: haemorrhagic necrotising encephalitis of the temporal lobes; fever, altered behaviour and seizures; treat empirically with aciclovir while polymerase chain reaction confirms.
  • Japanese encephalitis: Culex tritaeniorhynchus breeding in rice paddies with pigs as amplifying hosts; monsoon epidemics in Uttar Pradesh and Bihar affecting children; thalamic involvement on imaging is characteristic; vaccination is the control measure.
  • Rabies: Negri bodies in hippocampal pyramidal neurons and cerebellar Purkinje cells; furious and paralytic forms; case fatality essentially absolute once symptoms begin — India carries a substantial share of global deaths, which is why dog-bite wound care and immunisation protocols are examined in detail.
  • Brain abscess: contiguous spread — otitis media seeding temporal lobe or cerebellum, frontal sinusitis seeding frontal lobe; ring-enhancing lesion; rupture into the ventricle is catastrophic.
  • Neurocysticercosis: Taenia solium larvae in brain; single ring-enhancing lesion with perilesional oedema causing seizures in a young adult is the classic Indian presentation; albendazole with corticosteroids for degenerating cysts, with calcified healed lesions needing only antiepileptics.

One lumbar puncture, three diagnoses

Three cerebrospinal fluid reports arrive in an hour. The first is frankly turbid: 4,000 neutrophils per microlitre, glucose 15 milligrams per decilitre (blood 110), protein 300 — pyogenic meningitis; the culture will name the organism tomorrow but antibiotics go in now, because outcome tracks the hour of the first dose. The second is clear under pressure with 150 lymphocytes, glucose 25, protein 180, and a fine cobweb pellicle formed overnight on standing — tuberculous meningitis until proven otherwise, and the Ziehl-Neelsen or cartridge-based nucleic acid test on the fluid, along with chest imaging and fundoscopy for choroid tubercles, follows; antitubercular therapy plus dexamethasone begin without waiting, since the basal exudate threatens cranial nerves and the cerebral vessels.

The third is clear with 80 lymphocytes, glucose 62, protein 45 — viral meningitis, and the clinical picture decides the counsel: an enterovirus case recovers with support, whereas confusion, behaviour change or focal seizures makes herpes simplex encephalitis the working diagnosis — aciclovir starts empirically and polymerase chain reaction confirms retrospectively.

Where students slip

Computed tomography before lumbar puncture is either always demanded or always omitted by candidates; the reasoned answer is before, when there are focal signs, papilloedema, seizures or depressed consciousness — to prevent herniation from a mass lesion — and without delay otherwise in the clearly meningitic patient. Second, a partially treated pyogenic meningitis converts its profile to look lymphocytic with borderline glucose, mimicking tuberculosis; the history of prior antibiotics must be dragged out. Third, every ring-enhancing lesion in an Indian adult is treated as neurocysticercosis when the differential includes tuberculoma and toxoplasmosis — the single-versus-multiple pattern, the scolex within the cyst, and the HIV status of the patient resolve most cases.

Frequently asked questions

What CSF profile indicates tuberculous meningitis?

Lymphocytic pleocytosis with high protein, low glucose and a cobweb coagulum, with basal exudates causing cranial nerve palsies, hydrocephalus and vasculitic strokes.

Which encephalitis causes seasonal outbreaks in Uttar Pradesh and Bihar?

Japanese encephalitis — Culex tritaeniorhynchus vector, rice-paddy breeding, pigs as amplifiers, thalamic lesions and childhood predilection.

Where are Negri bodies found?

Hippocampal pyramidal neurons and cerebellar Purkinje cells in rabies; their absence does not exclude the disease, which is confirmed by immunofluorescence on brain tissue.

Which sites do brain abscesses seed from?

Otitis media to the temporal lobe or cerebellum; frontal sinusitis to the frontal lobe; haematogenous spread produces multiple lesions at grey-white junctions.

How is a single ring-enhancing lesion in an Indian adult with seizures managed?

Most often neurocysticercosis — albendazole with corticosteroids for the degenerating cyst with antiepileptic cover, with tuberculoma and toxoplasmosis excluded; calcified lesions are healed and need only seizure control.

Which virus causes progressive multifocal leukoencephalopathy?

JC virus, destroying oligodendrocytes of immunosuppressed patients and producing multifocal demyelination without inflammatory infiltrate.

Same topic for other exams

Practise this in the PrepElephant app

Question banks, previous-year questions, mock tests and revision tools — for CNS Infections Pathology and MBBS Pathology. Free to start.

Get the free app WhatsApp