Pathology of CNS infections Flashcards

1
Q

Acute meningitis

A
  • Acute onset (hours), fever + nonspecific sx. Headache, altered mental status, stiff neck
  • Causes: viral, fungal, bacteria (viral usually self-limiting)
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2
Q

Acute bacterial meningitis

A
  • Overall mortality of 10-15%, with frequent and permanent complications
  • Bacteria in leptomeninges causes outpouring of PMNs into subarachnoid space
  • Very early hyperemia of leptomeningeal vessels and edema but no visible pus
  • Pus begins to accumulate in the sulci, which can cause ocular palsies and deafness
  • Eventually so much pus forms that it fills the entire subarachnoid space (pus contains dead PMNs and fibrin)
  • Arteritis and phlebitis can result in vascular thrombosis (infarcts)
  • Can lead to ischemic or hemorrhagic necrosis
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3
Q

Acute viral meningitis

A
  • Usually benign, self-limiting, resolves w/o sequelae

- Microscopically there are lymphocytes in the leptomeninges

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4
Q

Chronic meningitis

A
  • Classic meningitis sx that can evolve over weeks-months
  • Can be normal candidates plus parasites
  • Generally no sequelae
  • Most common severe is form TB and cryptococcus
  • Damage to CNs and blood vessels can lead to nerve palsies and infarcts
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5
Q

TB chronic meningitis

A
  • See abnormal enhancement of leptomeninges at base of brain in CT
  • The leptomeninges look thick and fibrotic (instead of widespread purulent exudate)
  • Can find multiple granulomas, containing giant cells and epithelioid cells
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6
Q

Cryptococcal chronic meningitis

A
  • Common in HIV and ICd pts, most common fungal infection of CNS
  • Appears as a pleomorphic budding yeast, eliciting little inflammatory response
  • Has a capsule (positive for mucin stain), under H&E shows a halo around the capsule
  • Can produce granulomas, which appears similar to TB
  • Ventricles can fill w/ gelatinous material (feels slippery)
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7
Q

Bacterial cerebritis and abscess

A
  • Most cerebrates and abscesses are bacterial, where the bacteria invade the brain parenchyma (viruses cause encephalitis)
  • Many, but not all, CNS abscesses cause focal problems
  • On CT the abscesses are ring enhancing rim around a low-density mass (also look like this: mets and GBM)
  • Almost always arise from an emboli of infected tissue (not primary abscess), usually valvular vegetations form endocarditis
  • The bacteria produce an abscess when the emboli occludes the vessel and causes ischemic necrosis
  • Center of the abscess becomes liquified and it is walled-off
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8
Q

Fungal cerebritis (aspergillus)

A
  • Predominantly affects ICd pts, causing multiple hemorrhagic and necrotic lesions (w/ acute/chronic inflammation)
  • Not as common in HIV b/c most common in those w/ neutropenia
  • H&E shows septated hyphae (stains w/ silver)
  • Has an affinity for blood vessels, destroys them causing hemorrhagic necrosis
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9
Q

Parasitic cerebritis: cysticercosis

A
  • Pork tapeworm (taenia solium), from ingesting the ova
  • Causes seizures, mass effect, obstruction of CSF
  • Elicits immune response when it dies and breaks down
  • Immune response leads to granulation tissue in surrounding parenchyma
  • Infection may be first symptomatic when parasite dies
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10
Q

Viral encephalitis

A
  • Tropism: affinity of some viruses for certain types of cells
  • Latency: reactivates if immune system is compromised
  • Viruses infecting CNS can present acutely, subacutely, or chronically
  • Can be opportunistic
  • Can infect gray or white matter, or both
  • Suggestive evidence of viral encephalitis: perivascular lymphocytes, microglial acitvation/nodules and neuronophagia (killing of infected neurons by PMNs/lymphocytes)
  • To find out which virus: cell types/brain regions affected, whether or not there is tissue necrosis and any viral inclusions
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11
Q

Opportunistic vs non-opportunistic viruses

A
  • Non: herpes (HSV), arboviruses, rabies, poli
  • Op: CMV, varicella zoster
  • Most dangerous viral encephalitis: HSV
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12
Q

HSV encephalitis

A
  • Imaging shows irregular lesions w/ edema and hemorrhage, microscopically see microglial nodules and cowdry type A viral inclusions
  • Affects both gray and white matter and demonstrates latency
  • Tropism for medial temporal and base of frontal lobes
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13
Q

Rabies encephalitis

A
  • Non-necrotizing, affects gray matter w/ some predilection for purkinje cells and medial temporal lobe including hippocampus
  • Can see neuronophagia w/ little inflammation
  • Inclusion body: Negri body
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14
Q

Polio encephalitis

A
  • When it spreads to the CNS is selectively infects motor neurons in the SC and brain stem (rarely cortex)
  • Microscopically can see inflammation/neuronophagia, and microglail nodules
  • Viral inclusions rarely seen
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15
Q

Arbovirus encephalitis

A
  • Most important cause of epidemic viral encephalitis
  • Non-specific acute viral encephalitis affecting mostly gray matter and w/o viral inclusions
  • Sx vary greatly: ranges form aseptic meningitis to necrotizing panencephalomyelitis
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16
Q

Subacute or chronic viral encephalitis

A
  • Slowly progressive neurological decline over months-years

- Includes progressive multifocal leukoencephalopathy (PML, caused by papoma/JC virus), HIV, and HTLV1

17
Q

PML

A
  • Opportunistic subacute or chronic, due to JC virus (in most people), which remains latent unless ICd
  • Infects oligodendrocytes and astrocytes but only kills the oligos
  • Multifocal areas of demyleinating (gray-white matter junction), blue->pink on luxol stain
  • Infected oligos become enlarged w/ intracellular inclusions and marginated chromatin
18
Q

HIV encephalitis

A
  • HIV infection of CNS causes HIV encephalitis (HIVE) and HIV associated dementia (HAD)
  • Invades via migration of infected monocytes and is passed on to microglial
  • Inflammatory mediators and neurotoxic viral proteins damages white matter and lead to HAD
  • Can see microglial nodules and giant cells in HIVE
19
Q

Spongiform encephalopathies

A
  • CJD due to PrPsc, either sporadic (inherited, very long incubation time) or variant (acquired, shorter incubation time)
  • Both incubation times are on the order of months-years
  • Culminates in rapidly progressing dementia and death
  • Can see vacuoles throughout brain, neuropil is swollen and punched-out (vacuoled)
  • Proliferation and hypertrophy of astrocytes (gliosis) but no inflammatory response