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Term 5: Neuro > 6/24- Infections of Nervous System II > Flashcards

6/24- Infections of Nervous System II Flashcards

1
Q

General Features of Viral Infections

A

- Portal of entry: enteric, hematogenous, traumatic

- Spread: via peripheral nerve or across BBB to CNS

CSF:

  • Mononuclear cells
  • Increased protein
  • Normal glucose (what really differentiates from bacteria)
  • No organisms ID’d on gram stain or standard culture
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2
Q

Histopathology of viral encephalitis?

A
  • Lymphocyte perivascular cuffing
  • Microglial nodules
  • Gliosis
  • Necrsosis
  • Inclusions (intranuclear or cytoplasmic)
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3
Q

What is Cowdry A?

A

Larger nuclear inclusions that push chromatin to outside

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4
Q

What are some intranuclear inclusions?

A
  • Cowdry A
  • Cowdry B
  • Ground glass
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5
Q

What are some cytoplasmic inclusions?

A

Negri bodies (rhabdo/rabies!)

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6
Q

What is this?

A

Lymphocytic vascular cutting

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7
Q

What is this?

A

Microglial nodule

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8
Q

What is this? Indicates what diseases?

A

Cowdry A intranuclear inclusions

  • Chromatin pushed to rim of nucleus

Seen in:

  • CMV
  • Herpes
  • Varicella zoster
  • Measles (SSPE)
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9
Q

What is this?

A

Negri body

  • Intracytoplasmic inclusion
  • Eosinophilic
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10
Q

What disease(s) are indicated by Cowdry B bodies?

A

Poliovirus (acute)

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11
Q

What disease(s) are indicated by Ground glass inclusions?

A

JC virus (PML)

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12
Q

Herpes Simplex Encephalitis results in what? Histology? Latency?

A
  • Hemorrhagic necrosis of temporal lobes (rapidly progressing)
  • Cowdry type A intranuclear viral inclusions in neurons and glia
  • Demonstrable with immunoperoxidase stains, in situ hybridization, PCR, or culture
  • EM morphology: targetoid spheres
  • Virus latent in sensory ganglia
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13
Q

What is this?

A

Herpes simplex encephalitis

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14
Q

Characteristics of rabies?

DNA material?

Transmission?

Replication?

Symptoms?

Histology?

A
  • RNA virus
  • Contracted from bite of infected animal (bats, skunks, rarely dogs in US)
  • Has been transmitted by corneal, solid organ, and tendon transplants!
  • Virus replicates locally in skeletal muscle and muscle spindles; ascends to CNS via peripheral nerves
  • Symptom free interval weeks-months
  • Most start straight into encephalitis, but may be preceded by Guillain-Barre-like paralysis in some
  • Intracytoplasmic neuronal inclusions: Negri bodies
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15
Q

T/F; rabies is fatal

A

True-ish; once symptoms start, rabies is fatal

  • After bite but when pre-symptomatic, can administer immunoglobulin and rabies vaccination
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16
Q

Inclusions seen with arboviral encephalitis?

A

The epidemic associated arboviral encephalitides (Eastern equine, Western equine, St. Louis) DO NOT produce viral inclusion bodies and show only the non-specific histologic features

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17
Q

What is the most common form of seasonal or epidemic viral encephalitis?

A

West Nile encephalitis

  • Most people are asymptomatic, but may be dangerous to young/elderly/immunocompromised
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18
Q

What causes poliomyelitis?

A

Enterovirus

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19
Q

Symptoms seen in poliomyelitis?

A
  • Following ingestion, replicates in lymphoid tissue of intestine -> viremia
  • Spinal cord involvement: loss of anterior horn cells/motor neurons
  • Brainstem involvement: bulbar polio
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20
Q

What is this?

A

Poliomyelitis with spinal grey matter hemorrhage and edema

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21
Q

Characteristics of arboviruses? Transmission? Features? Symptoms?

A
  • Arthropod vectors
  • Often spread from birds

Other:

  • Western, Eastern, and St. Louis strains
  • Seasonal epidemics
  • Don’t produce viral inclusions
  • Fairly rapidly progressive (days)
  • Headache, delirium …. coma
  • Potentially lethal to young/old
22
Q

Characteristics of HIV (Human Immunodeficiency Virus) as it pertains to CNS?

A
  • HIV enters the CNS early in the infection
  • CNS involvement is a significant cause of mortality and morbidity
  • Up to 50% of AIDS pts will have a neurologic complication
  • > 80% have neuropathologic findings at autopsy
23
Q

What diseases/conditions are caused by HIV in relation to the CNS?

What diseases of the CNS are associated with HIV?

A

HIV encephalitis

  • Multinucleated giant cells, perivascular
  • Dementia Vacuolar myelopathy
  • Vacuolar degeneration of posterior and lateral white matter columns (looks like B12 deficiency)

Focal CNS Lesions Associated with HIV:

  • Primary CNS lymphoma (driven by EBV)
  • Progressive Multifocal Leukoencephalopathy (PML)
  • Toxoplasmosis
24
Q

What is PML? Histologic? Involves what cells?

A

Progressive Multifocal Leukoencephalopathy (PML)

  • Papova virus (JC strain*) infection of oligodendrocytes and astrocytes
  • “Ground galss” intranuclear inclusions in oligodendrocytes (myelin loss)
  • Involvement of astrocytes as well- bizarre forms, pleomorphic enough to be mistaken for neoplastic
  • Can cause gliomas in rodents, but not seen in humans
  • Seen in AIDs/immunocompromised and MS pts treated with immunosuppressie drugs

*No connection between JC virus and CJD

25
Q

What is this?

A

Myelin loss seen in PML (Progressive Multifocal Leukoencephalopathy)

(little areas in bottom right)

  • Can be multifocal (like MS)
  • Symptoms depend on neurons de-myelinated
26
Q

What is this?

A

Intranuclear inclusions in oligo’s in PML

27
Q

What is this?

A

Pleomophic astrocyte in PML

28
Q

What is this?

A

Toxoplasmosis

  • Shaggy, ring-enhancing lesion; looks kinda like a tumor
29
Q

What is this?

A

Bradyzooite (cyst form of organism)

  • Toxoplasmosis
30
Q

Toxoplasmosis may indicate what?

A

AIDs (may be presenting system)

31
Q

What are 2ndary HIV nervous system infections (Opportunistic infections)?

A

Don’t try to memorize…

  • Cytomegalovirus
  • Varicella Zoster
  • Herpes Simplex
  • Progressive Multifocal Leukoencephalopathy
  • Candidiasis
  • Cryptococcosis
  • Toxoplasmosis
  • Amebiasis
  • Mycobacterial infection
  • Neurosyphilis
  • Bacterial infection
32
Q

What is this?

A

Taenia solium (ingested from undercooked pork or food contaminated with feces)

  • Can see scolex
33
Q

What is this?

A

Worm surface on right; GI on left

34
Q

Neurocystercercosis may cause what?

A

Seizures!!

35
Q

What is this?

A

Neurocystercercosis

36
Q

When does neurocystercercosis cause problems?

A

When the worm dies (no longer cloaked from immune system)

  • Edema
  • New onset focal neurological deficit
  • Possibly seizures
37
Q

T/F: Neurocystercercosis should always be treated

A

False; not all cases need treatment

38
Q

What causes spongiform encephalopathies?

A

Prion- transmissible agent

  • 27K-32K MW (pretty significant)
  • Transformation of alpha helix rich protein to pathologic beta sheet form (PrPc -> PrPsc– scrabie)
39
Q

T/F: Prions are killed by traditional disinfectants

A

False; must denature protein (fairly robust)

40
Q

Relative incubation period of prion diseases?

A

Extremely long (even years - decades)

41
Q

T/F: Prion diseases have antigenic/inflammatory response due to the abnormally folded protein

A

False; prion diseases have no antigenic or inflammatory responses

42
Q

What is this?

A

Spongiform change in CJD

  • Cortex, deep matter of diencephalon..
  • May see some reactive gliosis, but NO lymphocytic/PMN reaction or conventional inflammation
43
Q

What is this?

A

Extracellular collection of PrP protein- prion plaque

44
Q

What is this?

A

Immunohistochemistry showing accumulation of polymerized prion protein in CJD

45
Q

Characteristics of Creutzfeld-Jakob Disease (CJD)? Cause? Symptoms

A

May be either:

- Sporadic (85%)

- Inherited (15%)- inherited mutation of prion gene (PrNP) on chrom 20; AD

Clinical quartet:

  • Dementia (but rapidly progressing! over months)
  • Myoclonus (in part of dz, not throughout)
  • Periodic EEG (corresponding to myoclonus; massive hypersynchronous firing with jerks)
  • Rapid disease progression

WARNING: broader clinical spectrum and longer incubation increasingly being recognized

46
Q

What is iatrogenic CJD?

A

Acquired from:

  • Use of human growth hormone
  • Placement of intracerebral electrodes
  • Corneal grafts
  • Dural grafts

Ex) brain biopsy for supposed vasculitis in CJD pt with instruments used on 6 other pts without prion decontamination

47
Q

What is new variant CJD (vCJD)?

A
  • Recognized by a surveillance committee set up to monitor the BSE “mad cow” epidemic
  • Epidemiology, morphologic, and molecular data indicate that BSA is the source of

vCJD Differs from sporadic CJD:

  • Younger pts (mean 26 yo vs. 65 yo)
  • Longer duration of illness (12 mo vs. 4 mo)
  • Initial Sx: psychiatric and/or sensory dysethesias in vCJD
  • LACK periodic discharges on EEG (and no myoclonus)
48
Q

What is this?

A
  • BSE as the source of vCJD
  • VERY prominent plaques (“florid plques”) because of such high prion load
49
Q

Nuances of brain biopsy in CJD?

A
  • No frozen section!
  • Snap freeze 20 mg for Western blotting
  • Formalin fixation x 24 hrs (preserves tissue but doesn’t kill prion)
  • Immerse in 100% formic acid x 1 hr (kills prion)
  • Formalin fx x 24 hrs and process routinely
50
Q

Dr. Goodman’s Dietary Advice

A

When in Europe, Japan, and Middle East:

  • Eat no products of hoofed things (except swine)
  • Sausage, brains, and meat pies are out
  • Fish and fowl are okay

When in the US

  • So far, so good on beef
  • Theoretic risks with deer and elk

Term 5: Neuro (24 decks)

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