Tabulate differences in CSF examination in Pyogenic, Tuberculous*, Viral Meningitis; CSF findings in Meningitis 2. Meningioma** - gross, microscopic features ( 3. Acute (purulent) Leptomeningitis - morphology, CSF findings 1. Pyogenic Meningitis - aetiology, indication of CSF examination, CSF findings in Pyogenic and Tuberculous Meningitis (answer in detail covering imp points as welll in exaam point of view 2mbbs pathology refer harsh moham add diagrams as well cover required points for muhs exam Add histo pathology diagram and gross as well FOR EXAM drawing point of view

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CNS Infections & Meningioma - Pathology Notes (2nd MBBS / MUHS Exam)

Source: Robbins & Cotran Pathologic Basis of Disease | Robbins & Kumar Basic Pathology | Bradley & Daroff's Neurology

PART 1: MENINGITIS - CLASSIFICATION & OVERVIEW

Meningitis = inflammation of the leptomeninges (pia + arachnoid) and CSF within the subarachnoid space, usually infectious.

Three broad types:

Type	Etiology	Course
Acute Pyogenic (Bacterial)	Bacteria	Acute, fulminant
Aseptic (Viral)	Viruses (enteroviruses 80%)	Subacute, self-limited
Chronic	TB, fungi, spirochetes	Weeks-months

PART 2: ACUTE PYOGENIC (BACTERIAL / PURULENT) MENINGITIS

2A. Aetiology (Age-based - Exam Favourite)

Age Group	Common Organisms
Neonates (<1 month)	Escherichia coli, Group B Streptococci
Infants / Children	Haemophilus influenzae (now rare with vaccination)
Adolescents / Young Adults	Neisseria meningitidis (meningococcus)
Older Adults (>60)	Streptococcus pneumoniae, Listeria monocytogenes
Immunosuppressed	Klebsiella, anaerobic organisms, fungi

Exam tip: The most common organism overall = S. pneumoniae. Meningococcal meningitis clusters in young adults and raises public health concerns. Vaccination against H. influenzae has markedly reduced its incidence.

2B. Indications for CSF Examination (Lumbar Puncture)

Suspected meningitis (bacterial, viral, TB, fungal)
Subarachnoid haemorrhage (xanthochromia)
Encephalitis
Unexplained altered consciousness with fever
Neurosyphilis, cryptococcal infection
Intracranial pressure assessment
Intrathecal drug administration

Contraindications to LP: Raised ICP with papilloedema (risk of herniation), bleeding disorders, infection at LP site.

2C. Clinical Features

Systemic signs: fever, rigors, malaise
Meningeal irritation: severe headache, photophobia, neck stiffness (nuchal rigidity)
Kernig's sign (+), Brudzinski's sign (+)
Clouding of consciousness, irritability
Elevated CSF pressure on LP (cloudy/frankly purulent fluid)

PART 3: MORPHOLOGY OF ACUTE PURULENT LEPTOMENINGITIS

3A. Gross Features

Meningeal vessels are congested/engorged and stand out prominently
Exudate within the leptomeninges over the brain surface - cloudy to frankly purulent
Distribution varies with organism:
- H. influenzae - basal distribution
- S. pneumoniae - over cerebral convexities near the sagittal sinus
Tracts of pus follow blood vessels on brain surface
In fulminant cases: ventriculitis (extension to ventricles)
Complications: leptomeningeal fibrosis → hydrocephalus; pneumococcal: chronic adhesive arachnoiditis (due to capsular polysaccharide)

Gross photo - Pyogenic meningitis:

Pyogenic meningitis - gross. Thick suppurative exudate covers brain surface and thickens leptomeninges. Note engorged meningeal vessels.

Gross appearance: Thick suppurative exudate covering the brain surface, thickening the leptomeninges. Meningeal vessels are engorged and prominent.

3B. Microscopic Features

Neutrophils fill the subarachnoid space in severely affected areas
Neutrophils predominantly around leptomeningeal blood vessels in less severe cases
Gram stain: reveals variable numbers of bacteria
In fulminant cases: inflammatory cells infiltrate walls of leptomeningeal veins and extend into brain parenchyma (cerebritis)
Secondary vasculitis and venous thrombosis → haemorrhagic cerebral infarction
Pia rarely breached in typical bacterial meningitis

Exam drawing tip: Draw subarachnoid space filled with neutrophils (PMNs), engorged blood vessels in meninges, brain surface intact, and bacteria visible on Gram stain between cells.

3C. Waterhouse-Friderichsen Syndrome (Important Complication)

Meningitis-associated septicaemia + haemorrhagic infarction of adrenal glands
Occurs most often with meningococcal and pneumococcal meningitis
Results in adrenal insufficiency + septic shock

PART 4: CSF EXAMINATION - COMPARISON TABLE

CSF Findings in Meningitis (Most Important Exam Table)

Parameter	Normal	Pyogenic (Bacterial)	Tuberculous	Viral (Aseptic)
Appearance	Clear, colourless	Turbid / Purulent / Cloudy	Clear / Xanthochromic / Cobweb clot	Clear
Pressure	70-180 mmH₂O	Markedly elevated	Elevated (moderate)	Normal / Mildly elevated
Cell count	0-5 cells/mm³	200-20,000 cells/mm³	100-500 cells/mm³	10-500 cells/mm³
Predominant cell type	Lymphocytes	Neutrophils (PMNs)	Lymphocytes	Lymphocytes
Protein	15-45 mg/dL	Markedly elevated (100-500 mg/dL)	Elevated (100-400 mg/dL)	Mildly elevated (50-100 mg/dL)
Glucose	50-80 mg/dL (2/3 of blood glucose)	Markedly reduced (<40 mg/dL)	Reduced (moderately)	Normal
CSF:Blood glucose ratio	>0.6	<0.4 (very low)	0.4-0.5 (low)	Normal (>0.6)
Organisms on smear	Absent	Gram stain positive in ~60-80%	AFB smear (ZN stain) - positive in ~25-40%; culture gold standard	Not seen (viral, no bacteria)
Culture	Sterile	Positive for bacteria	Positive for MTB (slow, weeks)	Viral culture / PCR
Special features	-	Neutrophilic pleocytosis; may clot	Cobweb/pellicle formation (fibrin web); AFB ZN stain	Self-limited; enterovirus most common
Chloride	120-130 mEq/L	Reduced	Markedly reduced (<120 mEq/L)	Normal
Clinical course	-	Acute, fulminant; fatal if untreated	Subacute-chronic; weeks	Mild, self-limiting

Memory Aid (MUHS favourite):

Pyogenic = Pus (PMNs), Protein up, glucose Down dramatically

TB = Lymphocytes, low glucose (not as low as pyogenic), cobweb clot, AFB

Viral = Lymphocytes, normal glucose, mild protein rise

Cobweb Clot (TB - Exam Point)

In TB meningitis, when CSF is allowed to stand, a fine fibrinous "cobweb" or "pellicle" forms in the test tube - a classic finding. This is due to the high fibrin content. AFB can be found in this cobweb clot.

PART 5: MENINGIOMA

5A. Introduction

Most common intracranial extraaxial tumor (>1/3 of newly diagnosed CNS tumors)
Arises from arachnoidal (meningothelial) cap cells - hence extraaxial, dural-based
More common in females (progesterone receptor positive in >50%)
Can enlarge dramatically with pregnancy and regress after delivery
Associated with NF2 gene mutation (chromosome 22q12) in >50% of cases
Other mutations: TRAF7, KLF4, AKT1, SMO

5B. Gross Features

Well-demarcated, lobulated, firm mass attached to the dura
Compresses but does NOT invade adjacent brain / spinal cord (pushes brain aside)
Gritty consistency due to sand-like calcifications (psammoma bodies)
Often shows a dural tail sign on imaging / gross specimen
May invade bone (hyperostosis) - does NOT constitute malignancy
Meningioma en plaque = diffuse carpet-like spread along dural surface
Cut surface: grey-white, lobulated, firm to rubbery
Common locations: parasagittal (falcine), sphenoid wing, olfactory groove, parasellar, spinal canal

Exam drawing tip (gross): Draw a well-encapsulated, lobulated, firm mass attached to dura/falx with a broad dural base. The brain is pushed/compressed to one side. Mark the attachment to dura clearly.

5C. Microscopic Features (Histopathology)

Three major histological patterns:

Pattern	Features
Meningothelial (Syncytial)	Arachnoidal epithelioid cells in lobules with prominent whorls and psammoma bodies
Fibroblastic	Spindle cells in fascicular or storiform pattern; abundant collagen
Transitional	Mixed features of both above

Key Microscopic Features to Know:

Meningothelial whorls - concentric spiral arrangements of tumour cells (pathognomonic appearance)
Psammoma bodies - concentrically laminated calcifications formed from degenerated meningothelial whorls (appear as basophilic laminated concentric rings)
Cells have pale vesicular nuclei with central clearing (nuclear pseudoinclusions)
EMA (Epithelial Membrane Antigen) - positive in vast majority (key IHC marker for meningothelial differentiation)
Progesterone receptor - positive in >50%
No mitoses / very rare in Grade I (benign)

Histopathology diagram - Meningioma (Whorls & Psammoma bodies):

Meningioma histology - H&E x400. Typical meningothelial nests and whorls with focal hyalinization and concentrically laminated psammoma bodies.

H&E x400: Multiple concentric meningothelial whorls with psammoma bodies (laminated calcifications). This is the classic "storiform" pattern.

Exam drawing (microscopic): Draw 3-4 concentric whorls of cells. In the centre of some whorls, draw a pink/basophilic laminated structure (psammoma body). Cells have pale oval nuclei. Label: meningothelial cells, whorls, psammoma body.

5D. WHO Grading of Meningioma

Grade	Type	Features
Grade I	Benign	Most common; <4 mitoses/10 HPF
Grade II	Atypical	≥4 mitoses/10 HPF or 3 of 5 criteria (sheeting, hypercellularity, macronucleoli, small cells, necrosis); higher recurrence
Grade III	Anaplastic/Malignant	Frank malignancy; rare (2%); brain invasion

Special aggressive variants: Clear cell (II), Chordoid (II), Papillary (III), Rhabdoid (III).

QUICK REVISION BOX - MUHS EXAM KEY POINTS

Pyogenic Meningitis

Aetiology: age-based (E. coli/GBS in neonates → N. meningitidis in young adults → S. pneumoniae in elderly)
CSF: purulent, ↑↑pressure, neutrophils (PMNs), ↑↑protein, ↓↓glucose, Gram stain +ve
Gross: exudate over brain surface, engorged vessels
Micro: neutrophils in subarachnoid space, bacteria on Gram stain
Complication: Waterhouse-Friderichsen syndrome, hydrocephalus, cerebritis

TB Meningitis

CSF: clear/xanthochromic, cobweb clot, lymphocytes, ↑ protein, ↓ glucose and chloride, ZN stain for AFB
Base of brain predominantly affected (basal exudate)

Viral Meningitis

CSF: clear, lymphocytes, mildly ↑ protein, normal glucose (KEY differentiator)
Self-limited; enteroviruses (80%)

Meningioma

Gross: firm, lobulated, dural-attached, gritty (psammoma bodies), compresses but does not invade brain
Micro: meningothelial whorls + psammoma bodies; EMA positive; PR positive
Grade I = benign; excellent prognosis with total resection

Sources: Robbins & Cotran Pathologic Basis of Disease (10th ed.), Robbins & Kumar Basic Pathology (11th ed.), Bradley & Daroff's Neurology in Clinical Practice.

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