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OS9.2 - Neuro > Infections > Flashcards

Infections Flashcards

1
Q

Poliovirus

A
  • NE, icosahedral capsid, ssRNA+, 3 serotypes
  • causes poliomyelitis (flaccid paralysis), as well as abortive polio and aseptic meningitis
  • diagnose by sample from stool, rectum, throat, CSF; neutralization assay and specific Abs
  • vaccines: IPV (SQ) and OPV (PO)
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2
Q

Polyoma

A
  • NE, icosahedral capsid, dsDNA circular, 2 serotypes (BK/JC)
  • will see white matter lesions on MRI in JC infxn; diagnose with PCR from CSF
  • only a problem in IC’d hosts as many people have it latent in kidney, subclinical; adjust HAART/immunosuppression
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3
Q

Prion

A
  • “proteinaceous infectious particle”
  • normal cell form located on Chr 20; called PrPc (PRion Protein-cell)
  • abnormal form is a misfolded, very stable, protease-resistant form called PrPsc (scrapie - b/c it was first found as sheep disease)
  • causes transmissible spongiform encephalopathy (TSE):
    • Human types - kuru, CJD, GSS, FFI, vCJD
    • Animal types - scrapie, bovine SE, chronic wasting disease
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4
Q

Creutzfeld-Jackob disease (CJD)

A
  • clinically has rapidly progressive dementia and myoclonus; EEG complexes (sporadic form only)
  • histology: spongiform changes, no amyloid plaques

3 forms:

  • sporadic - onset ~60yo; 5-8mo survival
  • familial - AD; onset ~45-50yo; 2-4yr survival
  • iatrogenic: transmitted through dural/corneal grafts, improperly sterilized instruments, NOT blood; 1-2yr incubation
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5
Q

Gerstmann-Strausler-Scheinker disease (GSS)

A
  • clinically has gait abnormalities and ataxia, dementia is less common but may occur late
  • AD; onset ~48yo; 5yr survival
  • histologically: amyloid plaques in addition to spongiform changes
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6
Q

Fatal Familial Insomnia

A
  • clinically has sleep disturbances and ANS dysfunction; progressive insomnia to hallucinations, then dementia, mutism, and death
  • AD; onset ~49yo; 13mo survival
  • histology: much neuronal loss; rarely spongiform changes
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7
Q

Variant CJD (vCJD)

A
  • Identified as same agent that causes “mad cow” (BSE)
  • transmitted via contaminated beef and blood; also all victims have been homozygous for Met at position 129 of PrP
  • clinically there’s progressive neuropsychiatric disorder (anxiety, depression) over 6mo, mutism at death, atypical EEG without periodicity, and prion-positive tonsil punch biopsy
  • onset ~8-10yrs post-infection (average age was 29); 14mo survival
  • histologically: see spongiform changes in basal ganglia and “florid” (flower-like) plaques
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8
Q

Reactivation of BK and JC strains of Polyoma

A

BK - causes urinary tract problems, +/- hemorrhagic cystitis

JC - reactivation will cause destruction of oligodendrocytes and progressive multifocal leukoencephalopathy (PML)

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9
Q

Strep pneumoniae

A

Causes pneumococcal meningitis, as well as otitis, sinusitis, mastoiditis (ways it gets into CNS)

  • GPC; colonizes URT, attaches with pili
  • capsule prevent phagocytosis; cell wall components immunogenic; has Choline BPs (adhesins); hemolysins, H2O2, and neuraminidase/IgA protease
  • 2 vaccines
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10
Q

Neisseria meningitidis

A

Causes meningococcal meningitis and sepsis

  • VFs: antiphagocytic capsule, endotoxic LOS, phase and antigenic variation, and pili
  • strain A causes epidemics; 2 vaccines but they don’t cover strain B
  • sudden onset high fever, stiff neck/back, myalgia, weakness, N/V/HA; then delirium and petechiae
  • Penicillin (if allergic - ceftriaxone/3rd gen)
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11
Q

H. influenzae

A
  • starts as nasopharyngeal infection, peak for meningitis is 6mo of age
  • Hib is most important pathogen
  • capsule is chief VF
  • vaccine for Hib
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12
Q

Listeria monocytogenes

A
  • GPR, facultative IC
  • requires cell-mediated immunity, so IC’d people can’t fight it (transplant, pregnant, elderly, HIV)
  • propels itself between cells, avoiding detection
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13
Q

Signs/sx of bacterial meningitis

A
  1. Hx:
    - starts as URI
    - sx: HA/N/V/stiff neck, fever, photophobia, irritability, variable degree of neuro dysfunction
  2. Physical:
    +/- petechiae/purpura (dep. on org)
    - vitals: high fever, shock
    - Kernig’s (can’t extend knee), Brudzinski signs (flex neck, hips flex too)
  3. Labs:
    - LP (*get CT first): bacteria in CSF, many PMNs, high protein, low glucose
    - CBC shows sepsis–high WBC, PMNs, left shift
    - high INR (2/2 DIC)
    - blood cultures positive
    - serum procalcitonin and CRP are higher in bact. than viral meningitis

*Infants: fever, irritability, vomiting, crying, lethargy; if seizures or bulging fontanel it’s too late

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14
Q

Streptococcal meningitis causative agents

A
  • S. pneumo (penumococcus)
  • S. pyo (GAS)
  • S. agalacticae (GBS)
  • Viridans strep
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15
Q

Cryptococcus neoformans

A
  • includes candida, aspergillus, coccidoides, histo, blasto, zygomycetes
  • 85% of infections in HIV+ (toxo LOVES basal ganglia; will see IgM in CSF)
  • from pigeon droppings
  • look at India ink stain of CSF
  • treat with AmpB and fluytosine
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16
Q

Exserohilum rostratum

A
  • from contaminated steroid injections
  • treat with voriconazole IV >3mo; if severe/non-responder then AmpB IV
  • if asx - just observe
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17
Q

Viral vs. Bacterial meningitis

A

look to CSF:
- low glucose
- high protein
- high WBCs/NTs
If any one of the above is found, it tells you it’s bacterial etiology.
Clinically: viral is less severe–no confusion, lethargy, seizures, or neuro deficits; low back pain overshadowed by HA.

18
Q

Agents causing viral meningitis

A

80% - enterovirus (coxsackie, Echo, Entero)
10% - mumps

Recurrent aseptic meningitis - HSV-2, HIV, VZV

19
Q

Agents causing viral encephalitis

A

30% - Arbovirus (St. Louis, West Nile, La Crosse)
27% - HSV-1
23% - enterovirus

20
Q

What does viral encephalitis look like?

How to treat/prognosis?

A

Affects brain parenchyma.
- prodromal URI
- fever, HA, lethargy, disorientation/confusion (parenchyma!), seizures
- signs of inc. ICP; on LP: LC pleocytosis, few NTs, normal glucose, mildly elevated protein; no bugs found on stain
- progress to stupor/coma/death
- MRI will diagnose, PCR is definitive
Treat HSV-1 and CMV with antivirals; prognosis poor for other agents once encephalitis develops (rabies is uniformly lethal)

21
Q

HSV1 encephalitis

A
  • most commonly from reactivation/latent infection
  • temporal lobe damage - edema, necrosis
  • RBCs in CSF (necrosis)
  • 70% mortality if tx delayed (acyclovir)
22
Q

Mosquito-borne encephalitises

A

Flavas: West Nile, SLE, dengue fever, yellow fever
Alpha/Toga: EE, WE, VE
Bunya: CA, LaCrosse

23
Q

St Louis encephalitis syndrome and symptoms

A
  • HA with fever
  • aseptic meningitis
  • encephalitis
    Usually has a flu-like infection; may progress to 2ndary viremia with CNS.
24
Q

West Nile virus disease

A
  • flu-like illness with abrupt onset and mod-high fever
  • rash, lymphadenopathy, HA, sore throat, my/arthralgia, fatigue
  • acute aseptic meningitis or encephalitis
  • best dx test is IgM in CSF
25
Q

Togaviridae disease

A
  • can be asx
  • can be general febrile illness
  • can be abrupt onset of encephalitis (devastating)
  • these include WE, EE, VE, Rubella
26
Q

Rabies disease

A
  • incubation is typically 2-3mo (can be shorter/longer)
  • slow, progressive, characteristically involves CNS
  • replication in neurons first, then spreads
  • final stage virus is in high concentration in salivary glands (to bite the next victim)
  • coma and death occur 2-7d post-neuro onset
27
Q

Arenaviridae: Lymphoctytic Choriomeningitis Virus (LCMV)

A
  • replication is weird - ambisense
  • 2 phases of disease: prodrome (fever, HA, N/V, viremia), then aseptic meningitis (~10d later)
  • rarely fatal, no lasting problems
28
Q

CNS and HIV

A
  • HIV can infect CNS directly, or it can just open it up to opportunistic infections
  • acute aseptic meningitis can occur at seroconversion
  • chronic meningitis, HIV dementia, neuropathies
  • opportunistic infections: toxo (#1), crypto, TB, JC virus –> PML, CMV encephalitis
  • CNS lymphoma, metastatic Kaposi
29
Q

Rickettsial disease

A

RMSF, transmitted by ticks

  • caused by IC GNR
  • they attack vascular endothelial cells and cause systemic vasculitis; appears as distal petechial rash that then spreads proximally
  • also gets into brain parenchyma
  • tx: IV doxycycline
30
Q

How do bacteria get into the brain to cause disease like meningitis?

A
  • virulence factors, esp. pili, can penetrate endothelial cells and cross BBB
  • once they get access to CSF, where there’s lots of food and few immune cells, they proliferate
  • immune response is intense and becomes systemic causing vasculitis, thrombophlebitis, decrease in CBF, SIADH, shock/hypotension, vicious feed forward cycle to coma/death
31
Q

Meds for meningitis

A

Steroids THEN Abx,
- treat empirically, don’t wait
- give steroids to calm the immune system
- if abx are started too late, they will lyse the bacteria, spread more antigens, and make the immune response/meningitis worse
- use: vanc, 3rd/4th gen ceph, then cover specific bugs:
• ampicillin - Listeria
• acyclovir - HSV
• doxy - rickettsia
- also supportive care: electrolytes, EVD, isolation, prophylaxis for contacts

32
Q

Causes of meningitis by demographic:

  • community
  • neonates
  • pregnancy, IC’d, elderly
  • trauma, post-surgical
A
  • community: strep pneumo, neisseria meningitidis
  • neonates: GBS, E. coli, listeria
  • pregnancy, IC’d, elderly: listeria
  • trauma, post-surgical: staph aureus, gram neg’s, pneumococcus
33
Q

How does craniopharyngioma cause meningitis?

A
  • its interior breaks down into crank-case oil
  • this leaks and irritates meninges
  • proliferation of PMNs looks a lot like meningitis, but CSF glucose is normal
34
Q

Review the case of Subacute bacterial endocarditis from the pre-study

A
  • case in the lecture of the IVDU who gets endocarditis, septic embolus to the brain which caused cerebritis/abscess, then the abscess ruptured and he go real bad
  • septic emboli also cause splinter hemorrhages in extremities, osler’s nodes, Janeway lesions (palms/soles), and Roth’s spots (retinal hemorrhage w/ central clearing)
35
Q

Clinical diagnosis of cerebral abscess

A
  • tumor headache (worse on lying down, present upon awakening) due to CSF pressure wave
  • papilledema, TVO (2/2 pressure wave, b/c post circ. is a lower pressure system), seizures, focal deficits
  • Contrast CT/MRI: ring enhancing lesion, surrounding edema
  • RF for cerebral abscess: IVDU, penetrating trauma, sepsis, sinusitis, pulm AV shunts (as in HHT, which allow emboli to get to brain w/o being filtered)
36
Q

Spinal epidural abscess

A
  • abscess produces a mass effect on the spine
  • point tenderness, severe back pain, worse on lying down 2/2 inc. venous pressure
  • fever and general malaise
  • bowel/bladder dysfunction - one this starts you have 24-28hrs to save the spinal cord
  • MCC is staphylococcus and RFs include IVDU, trauma, osteomyelitis, sepsis, GU instrumentation
  • Tx: high dose steroids, Abx (cover staph, strep, anaerobes), drainage
37
Q

Lyme disease

A
  • spirochete borriela burgdorferei transmitted by ticks
  • 2-30d: flu-like illness, erythema migrans, HA, stiff neck, nerve palsy, arthritis (large joints)
  • months: encephalopathy, radiculopathy (band-like shock sensations), cognitive impairment (verbal, lethargy)
  • Tx: IV ceftriaxone 6-8wk
38
Q

Syphilis

A
  • caused by treponema pallidum
  • 1˚ = chancre at site; 2˚ = rash (palmar/plantar, no scars), arthritis, meningitis; 3˚ = skin, osseous, CV, neuo complaints after 15-20yr
  • neurosyphilis appears as contrast-enhancing ring lesion that can present as seizure or other neuro complaint; labs include serum/CSF VDRL, FTA, RPR, CSF pleocytosis
  • tx: high dose IV penicillin
39
Q

TB meningitis

A
  • HA, fever
  • LP: positive fluorescent AB stain of CSF, very high protein, modest dec. in glucose
  • CXR reveals something - granuloma, scarring, etc.
  • TB can cause a subacute or chronic meningitis; if untx’d will cause granulomatous meningitis especially severe at brain base
  • comes from primary lung or GI infxn, then bacteremia that lodges in brain, tubercle reactivation year laters to seed meninges
  • path: meningitis, vasculitis/infarction, tuberculoma
  • Tx: Inh, Rif, Pyrazinimide; plus streptomycin or ethambutol; steroids
40
Q

Arnold-Chiari malformation

A
  • downward displacement of cerebellar tonsils through foramen magnum
  • different reasons; myelomeningocele, occipital encephalocele, cerebellar hypoplasia, or a congenital malformation of the tonsils
  • causes obstructive hydrocephalus; LP would cause herniation
41
Q

Chronic meningitis

A

low-grade fever, HA, lethargy, poor appetite, cranial neuropathy, personality change, cognitive impairement

42
Q

Zoster ophthalmicus

A
  • caused by herpes zoster affecting the ophthalmic division of CN5
  • cornea can become ulcerated
  • tx with acyclovir and steroids

OS9.2 - Neuro (10 decks)

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