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CNS infections Flashcards

1
Q

Microglia

A
  • resident scavenger
  • microglial nodules seen in viral encephalitis
  • Rod-like nuclei
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2
Q

Basic definitions of:

  1. Pachymeningitis
  2. Meningitis/leptomeningitis
  3. Encephalitis
  4. Cerebritis
A
  1. Spread of infection into dura mater layers
  2. Inflammation of pia and arachnoid layers
  3. Inflammation of brain parenchyma w/ mononuclear cells –> “chronic inflammation” –> often viral agent
  4. Inflammation of brain parenchyma w/ neutrophils –> think “acute inflammation” –> often bacterial agent
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3
Q

Basic definitions of:

  1. Myelitis
  2. Poliomyelitis
  3. Ganglionitis
  4. Radiculitis
A

Inflammation of:

  1. spinal cord
  2. spinal gray matter
  3. dorsal root ganglia
  4. intradural spinal nerve roots
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4
Q

Bacterial meningitis: most common organisms

  1. worldwide
  2. infants
  3. children/adults
  4. immunocompromised/elderly
  5. HIV
A
  1. S. pneumoniae, N. meningiditis, H. influenzae
  2. Group B strep, E. coli, Listeria
  3. Step pneumo, Neisseria, H. flu
  4. Strep pneumo, Listeria
  5. Listeria, syphilis, TB
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5
Q

Bacterial meningitis: gross findings

A
  • Opacification of leptomeninges
  • cloudy or creamy exudate
  • often around vessels due to inflammatory cells
  • vascular congestion in areas w/ purulence
    *
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6
Q

Bacterial meningitis: microscopic findings

A
  • neutrophils in leptomeningeal space
  • doesn’t always spread into parenchyma b/c pia is a good barrier
  • If it spreads into parenchyma, it can cause cerebritis
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7
Q

Brain abscess: source, common organisms, imaging, symptoms

A
  • Local:
    • sinusitis, otitis, mastoiditis
  • Hematogenous
    • infectious emboli
    • e.g. from heart (endocarditis)
  • Common organisms
    • S. aureus
    • Streptococci
    • polymicrobial
  • Usually multi-focal
  • Imaging: Ring enhancing lesions w/ surrounding edema
  • Symptoms:
    • fever, focal neurologic symptoms
  • Evolution of brain abscess:
    1. vascular congestion, early necrosis, inflammation
    2. neutrophils predominant followed by other immune cells leading to liquefactive necrosis
    3. after 10 days –> neovascularization, collagen deposition –> abscess capsule isolating necrosis
    4. capsule eventually turns into cystic cavity
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8
Q

Brain abscess: evolution of process

A
  1. vascular congestion, early necrosis, inflammation
  2. neutrophils predominant followed by other immune cells leading to liquefactive necrosis
  3. after 10 days –> neovascularization, collagen deposition –> abscess capsule isolating necrosis
  4. capsule eventually turns into cystic cavity
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9
Q

Mycobacterial infections of CNS

A
  • Chronic bacterial infection
    • necrotizing granulomatous inflammation (macrophages & giant cells)
  • CSF: lymphocytosis, low glucose, elevated protein
  • Tuberculous meningitis
    • often basal aspect of brain
    • CN involvement
  • Tuberculoma of brain and spinal cord (mass forming lesions)
    • may be associated w/ TB meningitis
  • Tuberculous vertebral osteomyelitis
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10
Q

Neurosyphilis: 3 manifestations

A
  • 30% of untreated syphilis will develop CNS disease – 3° syphilis
  • increased risk in immunosuppressed ppl
  1. Meningovascular neurosyphilis:
    • basal meningitis w/ obliterative endarteritis (inflammation of artery’s inner lining)
    • peri-vascular inflammatory infiltrate w/ plasma cells and lymphocytes
  2. Paretic neurosyphilis
    • parenchymal infection, loss of neurons, microglia proliferation, gliosis (reactive changes in glial cells)
  3. Tabes dorsalis
    • myelin loss in dorsal columns
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11
Q

Neuroborreliosis: clinical syndrome (4 features)

A
  • Borrelia burgdorferi
  • Usually in untreated lyme
  • Clinical syndrome:
    1. Aseptic lymphocytic meningitis
    2. Facial nerve palsy
    3. Neuropathies/polyradiculitis
    4. Encephalopathy
  • Features of disease are often due to immune response to spirochete
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12
Q

Manifestations of CNS viral infections w/ common organisms (4)

A
  • Lymphocytic (Aseptic) meningitis
    • Meninges
    • Enterovirus >80% of cases
  • Acute Viral Encephalitis: (Polioencephalitis/poliomyelitis)
    • Gray matter
    • Arboviruses
  • Panencephalitis/panmyelitis
    • Gray and white matter
    • HSV (necrotizing), HIV (non-necrotizing)
  • Leukoencephalitis
    • White matter
    • JC virus Progressive Multifocal Leukoencephalopathy (PML)
    • HIV
      *
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13
Q

Lymphocytic (Aseptic) Meningitis

A
  • CSF = increased lymphocytes and mononuclear cells
  • Enterovirus = 90% of cases
  • good prognosis, self-limited, no treatment needed
  • Classic meningitis symptoms
  • Histology:
    • scant lymphocytic infiltrate into leptomeninges and virchow robin spaces
  • Other causes:
    • HSV2
    • non-infective = ibuprofen
    • syphilis, lyme disease (b/c they are spirochetes and cause chronic inflammation)
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14
Q

Acute Viral Encephalitis: pathology/histology

A
  • Perivascular inflammatory infiltrate (blue arrow)
  • Microglial nodule (red arrow)
  • Neuronophagia (black arrow)
  • Intranuclear viral inclusions (glassy inclusions)
  • Gliosis (reactive glia)
  • ** may manifest as meningoencephalitis
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15
Q

Arboviral Encephalitis

A
  • Seasonal
  • Humans = dead-end hosts
  • Inoculation by mosquito/tick then may spread to CNS
  • Variable morbidity and mortality
    • asymptomatic, flu-like,
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16
Q

HSV (Herpetic) encephalitis: presentation, tx, histology

A
  • HSV-1
  • necrosis of temporal lobes
  • bilateral or asymmetric
  • young adults
  • Present w/
    • non-specific encephalitis = headache, fever, stiff neck, drowsiness
    • focal neurologic signs = dysphasia, hemiparesis, focal seizures
    • ** Rapid progression
  • Treatment - acyclovir – often given empirically
  • Histology:
    • early: eosinophilic cytoplasm and/or inclusions in glia, neurons, endothelial cells
    • late: necrotic cells, hemorrhage , perivascular infiltrate, neuronophagia, microglial nodules, sparse nuclear inclusions
17
Q

Herpetic encephalitis: other causes (2)

A
  • CMV:
    • intrauterine infection
    • immunosuppressed patients
  • Varicella zoster (VZV) encephalitis
    • rarely in children
    • sometimes in zoster pts - older or immunosuppressed
    • can caue granulomatous arteritis
  • No predilection for temporal lobe
18
Q

Rabies: incubation & symptoms

A
  • Incubation 1-2 months (can vary)
  • non-specific prodrome
  • Furious rabies:
    • insomnia, agitation, aggressive behavior, biting, hypersalivation, hallucination, hydrophobia, dysphagia, dysarthria, nystagmus
  • Dumb rabies:
    • ascending paralysis (simulating Guillain-Barre), sensory loss, incontinence
  • coma, death within 1-2 wks
19
Q

Rabies: pathology

A
  • Negri bodies
    • round to oval eosinophilic inclusions in neuronal cytoplasm
    • in purkinje cells, hypocampal pyramidal neurons, cortical neurons, brain stem nuclei
    • contains collections of rabies virus
  • Replicates in skeletal mm @ inoculation site
  • Taken up by axons and transported to spinal cord –> brainstem –> cerebrum and cerebellum
20
Q

Poliomyelitis - Polio virus

A
  • Spinal cord gray matter motor neurons
  • Classic viral infectious pathology present: Chronic perivascular inflammation in parenchyma and meninges, Microglial nodules, Neuronophagia
  • Blood vessel congestion, possible hemorrhage
  • Paralysis
    • asymmetric
    • Palsy, atrophy of lower limbs (most often though upper limbs may be affected)
  • Poliovirus = enterovirus, fecal-oral transmission
21
Q

CNS Fungal Infection Manifestations

A
  • Diffuse encephalitis
  • Leptomeningitis
  • Space occupying lesions (granulomas/abscesses)
  • Septic infarcts (stroke-like symptoms) from fungal invasion of vessels causing thrombosis
  • Hemorrhages from mycotic aneurysm formation and rupture
  • Immunosuppressed patients
22
Q

Aspergillosis

A

Microscopic findings:

  • Infiltration of blood vessels by fungal hyphae
    • vascular thrombosis, hemorrhage, infarct
  • Variable inflammatory infiltrate
  • Silver stain – filamentous fungal forms w/ branching

Direct inoculation:

  • chronic, relatively localized infection
  • tendency to fibrosis and granuloma formation

Hematogenous dissemination

  • multiple lesions
  • follow ACA, MCA distributions affecting cortex, white matter, basal ganglia most
  • resemble hemorrhagic infarcts,
  • no fibrous capsule
23
Q

Zygomycosis (mucormycosis)

A
  • Rhinocerebral disease
    • nasal or unilateral facial swelling + hyperemia
    • may extend into orbit
    • meningeal infiltration = meningitis symptoms
    • spreading disease associated w/ seizures, aphasia, hemiplegia, coma,
  • death within days
  • common patient - uncontrolled diabetic in ketoacidosis
  • hyphae are non-septate, wider than aspergillus
24
Q

Amebic encephalitis

A
  • Meningoencephalitis
  • Cerebral swelling
  • Hemorrhagic necrosis of frontal lobes and olfactory bulbs
  • Unicellular organism, vesicular nucleus w/ prominent nucleolus
  • Associated w/ warm fresh water
    • geothermal pools
    • nasal washes w/ contaminated water
  • Infect nasal cavity and spread into CNS via cribriform plate
25
Q

Cysticercosis

A
  • cysticerci = larvae of tapeworm, Taenia solium
  • focal and generalized seizures, papilledema, headache, vomiting, ataxia, focal motor/sensory deficits, dementia,
  • ingestion of eggs in food (pork), water or fecal contamination
  • form cysts in parenchyma, meninges, ventricles
    • cysts can calcify once larvae die
  • dying organisms release substances = immunogenic –> inflammatory rxn, cysts surrounded by inflammatory cells
  • cysts are not immunogenic
26
Q

CNS infections - immunocompromised host (4)

A
  1. Cryptococcal meningitis
  2. Toxoplasmosis
  3. HIV encephalopathy
  4. Progressive multifocal encephalopathy
27
Q

Cryptococcal meningitis

A
  • Most common fungal CNS infection
  • Fulminant or indolent
  • Associated w/ pigeons
  • Minimal inflammatory reaction (immunocompromised host)
  • Collections of organisms produce gelatinous pseudocystic dilations of Virchow Robin spaces (bubbles)
  • primary infection = pulmonary then spread to CNS
  • Variable presentation
  • Organism has thick mucoid capsule
  • CSF culture OR crypto antigen assay
28
Q

Toxoplasmosis

A
  • Felines
  • immunocompentent individuals = asymptomatic
  • Often seen in HIV patients
  • Forms multiple brain absceses (ring enhancing)
29
Q

HIV encephalitis

A
  • HIV infection of microglial cells or macrophages that migrate into CNS
  • More common in untreated HIV
  • Affects subcortical white matter, basal ganglia, brainstem
  • Pathology:
    • low-grade inflammation – perivascular and parenchymal lymphocytes and microglial nodules
    • multinucleated giant cells (microglia)
  • leukoencephalopathy w/ patchy demyelination
  • variable gliosis of white matter
30
Q

Progressive Multifocal Leukoencephalopathy

A
  • JC virus (polyoma virus)
  • Tropism for oligodendroglia
    • ** Demyelinating lesions
  • Universal serologic exposure
  • Immunosuppression may reactivate latent virus
  • Symptoms:
    • focal deficits
    • often no seizures or fever
  • Progressive over a few months leading to death
  • Treatment of immunosuppression can lead to remission of PML
  • Pathology:
    • foamy macrophages, perivascular inflammation, (left image)
    • intranuclear viral inclusions (Blue arrow)
    • bizzare astrocytes w/ atypia (black arrow)
31
Q

Prion diseases

A
  • aka transmissible spongiform encephalopathies
  • fatal neurodegenerative disorders
    • neuronal loss
    • synaptic loss
    • microscopic vacuolation (spongiform change - picture)
  • Presentation:
    • rapidly progrssive dementia
    • often w/ ataxia, myoclonus, motor dysfunction, akinetic mutism
  • aggregatio of Human prion protein (PrPC) into PrPSc
  • Sporadic CJD (85%)
  • Familial CJD: Autosomal dominant
  • Variant CJD: from infected meat
  • Iatrogenic CJD: from surgical instruments or tissue implants
  • Kuru

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