Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Neuropath > Infectious > Flashcards

Infectious Flashcards

1
Q

what are the 3 things you can test for when doing mycobacterial molecular testing?

A

16S rRNA gene
hsp65
IS6110

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the advantages of each mycobacterial molecular test?

A

16S is highly conserved
hsp65 is less susceptible to interference from formalin
IS6110 is more sensitive cp to non-tuberculous mycobacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what ihc should you use for leprosy

A

Fite-Faraco

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Fungal wall components that you test for

A

Galactomannan
(1,3) beta-D-glucan (not in mucorales)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Instead of 18S, what are more labs using for fungal sequencing targets?

A

ITS (internal transcribed spacer)
D1/D2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what causes SSPE subacute sclerosis panencephalitis?

A

measles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the inclusions called that you can see in SSPE?

A

Cowdry type A (eosinophilic cytoplasmic or nuclear)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What can you see on EM for SSPE?

A

Nucleocapsid filaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the 3 ways measles can manifest in the CNS?

A
  1. Acute disseminated encephalomyelitis (postinfectious inflammatory)
  2. Subacute/chronic measles inclusion body encephalitis
  3. Subacute sclerosing panencephalitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 2 main diffs btwn Measles inclusion body encephalitis and SSPE?

A
  1. Inclusion body happens in months; SSPE is much more delayed (5-15 years)
  2. Inclusion body happens in immuno-impaired; SSPE happens in immunocompetent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What age group is more likely to develop SSPE if they get measles?

A

less than 18 mo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which kills you faster: inclusion body encephalitis or SSPE?

A

Inclusion body encephalitis; usu fatal in a few weeks. Some people have SSPE for YEARS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

which has more numerous identifiable inclusions: inclusion body encephalitis or SSPE?

A

inclusion body encephalitis
:)
Sometimes SSPE can have sparse ones but mostly absent if late in the game

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

4 clinical stages of SSPE

A

BMAC
1. Behavior changes
2. Myoclonus
3. Ataxia/spasticity
4. Coma/autonomic changes
(and then death)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Grossly affected areas in SSPE

A

Cerebral cortex
white matter
basal ganglia
thalamus
(so most of the brain lmao)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what neurodegenerative finding can you have in SSPE?

A

Tangles!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is a potential (rare) complication of acute herpes encephalitis?

A

Chronic granulomatous herpes simplex encephalitis (which looks exactly like you think: granulomas + lymphs/plasma cells + calcs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

which virus has a delayed complication that involves atrophy of the cerebellum + fibrinoid necrosis + small BV mineralization?

A

Rubella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

where in the brain do you find the most numerous PML lesions?

A

cerebral white matter
But they can also be in cortex and deep grey, less commonly cerebellum, brainstem/spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what causes PML?

A

JC virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the time course for PML usually

A

“relentless progression” over a few months > increasing dementia > death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what can lead to remission of PML?

A

treatment of the underlying cause of the immunosuppression (so treating AIDS)
but watch out, cause it can cause inflammatory response and exacerbate PML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what can you see in the brain after “chasing the dragon”?

A

toxic leukoencephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

4 histo findings of PML

A
  1. Bizarre astrocytes
  2. Multifocal demyelination w/ macs, very few lymphs
  3. JC virus inclusions
  4. Intranuclear polyomavirus particles (EM)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What IHC do you use for PML?

A

SV40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What type of cell are the JC virus inclusions found in?

A

Oligos (even though the astrocytes are the ones that get bizarre)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What causes HAM?

A

HTLV-1
(HTLV-1-associated myelopathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What’s the other name for HAM?

A

Tropical spastic paraparesis
(Think of ham with pineapple)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What part of the CNS does HAM/HTLV-1 affect?

A

Thoracic cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the 3 possible gross findings in HAM?

A
  1. meningeal thickening
  2. atrophy of thoracic cord
  3. lateral fascicular column degeneration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the micro findings of HAM?

A
  1. mixed lymphs & macs, mostly in lower thoracic
  2. hyaline thickening of BVs
  3. degeneration of lateral tracts of cord
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What does HIV look like on EM?

A

Virions have an envelope surrounding a cone-shaped core and very tiny “knobs” on their surfaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the typical gross appearance of HIV/AIDS brain?

A

mild atrophy with modest ventriculomegaly +/- gray d/c of centrum semiovale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the 3 main histo findings of “subacute encephalitis of AIDS” or “HIV leukoencephalopathy”?

A
  1. microglial nodules + vacuoles (nonspecific)
  2. Leukoencephalopathy (duh) w/ patchy demyelination + gliosis
  3. multinucleated giant cells containing HIV antigen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are the HIV antigens that you can identify in tissue with antibodies?

A

gp41
p24

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

where do the multinucleated giant cells of HIV tend to live?

A

near capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is the mechanism of CNS “neurotropism”?

A
  1. depends on chemokine receptor on cell surface
  2. some strains just like to cross the BBB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is the difference in neuro deterioration between infants/children with HIV and adults?

A

infants/children: usu direct HIV infxn
adults: opportunistic infxn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

where does vacuolar myopathy affect HIV patients?

A

spinal white matter: posterior columns and lateral corticospinal tracts, mostly thoracic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what entity does vacuolar myelopathy of AIDS mimic?

A

subacute combined degeneration of the spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what part of the brain shows abnormalities in HIV-assoc progressive encephalopathy of childhood?

A

Basal ganglia: severe atrophy and PERIVASCULAR calcs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Characteristic finding of Cryptococcus infxn (in HIV infxn)

A

Cribriform gross appearance d/t proliferation in Virchow-Robin spaces

(Crypto/cribriform)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Characteristic finding of Aspergillus fumigatus infxn (in HIV infxn)

A

hemorrhagic space-occupying lesions d/t angioinvasion (mycotic aneurysms are common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Characteristic finding in coccidioides immitis (in HIV infxn)

A

microabscesses w/ large spherules with enclosed endospores inside giant cells + endarteritis obliterans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

how can you tell CMV and VZV ventriculoencephalitis apart w/o IHC?

A

CMV will be super inflamed w/ partly necrotic ependymal and subependymal tissue
VZV will have inclusions but only slight rarefaction and minimal inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is neuro-IRIS?

A

neurologic immune reconstitution inflammatory syndrome
d/t CD8 cells going to town

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the most common causes of mass lesions in the brain in a pt with HIV?

A
  1. TOXO
  2. Primary CNS lymphoma
  3. Fungus
  4. tuberculoma
  5. PML
  6. CMV
  7. something unrelated to HIV (like a glioma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the 2 primary neoplastic complications of AIDS in the CNS?

A
  1. meningeal spread of a systemic lymphoma (common)
  2. primary CNS lymphoma (usu high-grade non-Hodgkin B-cell a/w EBV)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is Rasmussen’s encephalitis?

A

Hemispheric inflammation > seizures

Rare, in kids, lateralized brain destruction & atrophy w/ chronic encephalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the 4 main micro findings of Rasmussen’s?

A

SNTS
1. Spongy cavitation (chronic)
2. Microglial Nodules near pyknotic neurons
3. Lymphocytic vessel cuffing with T-CELLS!
4. Sharp demarcation

(in setting of severe neuron loss & astrocytic gliosis; laminar astrocytic proliferation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the clinical manifestation of Rasmussen’s encephalitis?

A

Seizures/epilepsy, usu onset btwn 2-17 yrs
epilepsia partialis continua (seizures lasting hours/days/years)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is Sturge-Weber-Dimitri syndrome?

A

Encephalotrigeminal angiomatosis

53
Q

What is the most common histo appearance of primary CNS lymphoma?

A

Angiocentric

54
Q

What are the 4 main groups of Rickettsial diseases

A
  1. spotted fevers (like RMSF, boutonneuse fever)
  2. typhus
  3. scrub typhus (actually Orientia tsutsugamushi)
  4. Q fever (Coxiella)
55
Q

the clinical manifestations of rickettsiae are a consequence of what?

A

(like the rash)
due to vasculitis or endothelial involvement by inflammation

56
Q

what is the main difference in inoculation btwn Rickettsial species and Coxiella burnettii?

A

Rickettsial species transmitted via ticks or mites OR infected flea or louse feces
Coxiella infects via inhalation of aerosols (sheep/cattle/goat placenta/urine/feces/milk) (UGH)

57
Q

Micro findings of Rickettsial infxn

A

microglial nodules + Angiocentric inflammation with thrombosis and microinfarcts
WITHOUT FIBRINOID NECROSIS

58
Q

What stain can you use for Rickettsia?

A

(immunofluorescence)
Brown & Hopps modified Gram stain
they look like gram negative coccobacilli

59
Q

can you see Mycoplasma on a gram stain?

A

NOPE because they DON’T HAVE A CELL WALL (bacteria)
(otherwise this is so exceedingly rare as to be unimportant to ya girl)

60
Q

in what 2 bacterial meningitides are you more likely to see coexisting cerebral abscesses?

A
  1. citrobacter diversus
  2. proteus mirabilis
61
Q

what 2 bacteria account for over 65% of bacterial meningitis cases in “developed” countries?

A

Group B strep (strep agalactiae) (GRAM POS)

and

E coli (GRAM NEG)

62
Q

what is the method of inoculation for infants with bacterial meningitis?

A

usually oral from either:
contaminated amniotic fluid
maternal genital tract
hands (of anyone)

63
Q

A lot of these infxns are vasculocentric because they get to the brain via hematogenous spread. What is the notable histo feature of bacterial meningitis that you may see?

A

Intimal infiltration of meningeal vessels by neutrophils

64
Q

Neonates, kids, and adults most common causes of bacterial meningitis

A

Neonates: gram neg bacilli (E coli, Kleb, Citrobacter)[group B strep?]

Kids: Hib and N. meningitidis

Adults: strep pneumo

65
Q

what is the main diff btwn lumbar shunt infxn and ventricular shunt infxn?

A

Lumbar shunt infxn is usu classic meningitis, but ventricular shunt infxn is usu ventriculitis without nuchal rigidity or photophobia

66
Q

What are the inflammatory components of bacterial meningitis in the first week?

A

Early: neutrophils + necro debris

exudate extends along perivasc spaces into CNS

By the end of the first week: lymphs and macs

67
Q

what is unique about meningitis due to b. anthracis?

A

it is often hemorrhagic (the same as aspergillus if this was fungal I spose)

68
Q

what’s eisenmenger syndrome

A

cardiac VSD c/b pulmonary HTN and L to R shunt

69
Q

what is unique about Listeria monocytogenes infxn in the CNS?

A

likes the brainstem
causes purulent rhomboencephalitis w/ or w/o meningitis
Fibrinoid vascular necrosis

rhomboencephalitis is just inflam of the brainstem & cerebellum lol

70
Q

what’s the most common route of brain abscess infxn?

A

Direct spread (sinus, middle ear, dental root)

71
Q

Four stages of cerebral abscess (time course is a diff card)

A
  1. Focal suppurative encephalitis (NEUTS)
  2. # 1 with confluent central necrosis
  3. Early encapsulation (granulation tissue)
  4. Late encapsulation
72
Q

Time courses of 4 stages of cerebral abscess

A

Days 1-2: focal suppurative
Days 2-7: w/ confluent necro
Days 5-14: early encaps
After day 14: late encaps

73
Q

multiple poorly encapsulated cerebral microabscesses are a frequent feature of what?

A

septicemia d/t staph aureus

74
Q

when a capsule forms around a brain abscess, where is it thickest?

A

at the cortical aspect (rather than the ventricular aspect)

75
Q

where are empyemas most common in the CNS?

A

supratentorial

76
Q

what are most SPINAL subdural empyemas due to? even though they are VERY rare?

A

Staph aureus (which isn’t rare at ALL)

77
Q

where do most EPIDURAL abscesses occur in the CNS?

A

in the spinal canal

78
Q

childhood meningitis can result in empyemas/abscesses where?

A

Subdural empyema ONLY

NOT epidural abscess

79
Q

Most SPECIFIC test for prions

80
Q

what are the 3 CSF tests you can do to diagnose prions?

A

14-3-3
tau
RT-QuiC

81
Q

If you suspect prions on histology, how do you confirm?

A

IHC
and/or
western blot

82
Q

How do you identify familial prion disease?

A

Sequence PRNP gene

83
Q

gross characteristics of tuberculous meningitis

A

G, BoB, MN

  1. gelatinous subarachnoid exudate
  2. thickest in the sylvian fissures, base of brain, & spinal cord
  3. micronodular ventricular & choroid plexus appearance
84
Q

why are infarcts common in tuberculous meningitis?

A

inflammatory cells infiltrate the wall of BVs in the exudate, causing thrombosis or subintimal/intimal fibroblastic rxn (endarteritis) that can occlude the lumen

85
Q

where do the infarcts of tuberculous meningitis usually occur?

A

superficial brain parenchyma (bc the meningeal vessels within exudates are usually affected)

86
Q

what does reticulin look like in a tuberculoma/tuberculosis in the CNS?

A

no reticulin (caseous necrosis without reticulin deposition)

87
Q

what is Pott’s paraplegia

A

focal compression of the spinal cord d/t extension of tuberculous vertebral osteomyelitis into the epidural space, most often in the thoracic cord
often c/b vertebral collapse, kyphosis, infarction

88
Q

what are the 5 ways syphilis can involve the CNS?

A
  1. asymptomatic involvement (pos by serology only)
  2. syphilitic meningitis
  3. meningovascular syphilis
  4. parenchymatous neurosyphilis (tabes)
  5. gummatous neurosyphilis
89
Q

what are the 3 stages of syphilis

A
  1. primary (chancre)
  2. secondary (hematogenous)
    2.5. latent
  3. tertiary syphilis (cardiac, neuro involvement)
90
Q

when does syphilitic meningitis occur?

A

1-2 years after infxn

91
Q

when does meningovascular syphilis occur?

A

average 7 years after infxn

92
Q

what is the most susceptible vessel in meningovascular syphilis?

A

middle cerebral arterial tree

93
Q

how does gummatous necrosis of syphilis differ microscopically from caseous necrosis of tuberculosis?

A

gummatous has reticulin preservation

94
Q

what is the mechanism of tabes dorsalis?

A

chronic inflammation of the dorsal roots & ganglia with assoc degen of posterior columns

95
Q

when does tabes dorsalis occur?

A

15-20 years after infxn (w/ syphilis)

96
Q

what are the 3 clinical manifestations of tabes dorsalis?

A
  1. lightning pains or paresthesia
  2. loss of pain/proprio sensation > Charcot’s joints
  3. shuffling, broad-based gait
97
Q

what are nodules of Nageotte?

A

loss of neurons from DRG with associated proliferation of satellite cells
(they look like microglial nodules in a DRG where a ganglion cell should be)

98
Q

what do the microglia look like in syphilitic general paresis?

A

rod-shaped (can see better with silver)

99
Q

what are gummas?

A

solitary space-occupying lesions late in tertiary syphilis

100
Q

where does neurosarcoid like to thicken the leptomeninges?

A

around pituitary infundibulum and optic chiasm

101
Q

what is the most common clinical manifestation of neurosarcoidosis?

A

facial nerve palsy

102
Q

what is neuroborreliosis?

A

Lyme disease :)

103
Q

T/F: neurosarcoid can have necrotizing granulomas and involvement of vessels (fibrinoid necrosis, thrombosis).

104
Q

where does Whipple’s disease manifest in the CNS?

A

thalamus/hypothalamus
cerebellar dentate
periaqueductal

105
Q

what stains can you use to diagnose Whipple’s disease?

A

PASD (macrophages contain PAS+, diastase resistant material)
Methenamine silver (stain the bacilli)
(not always seen on gram stain, can also see them on EM where they look like mini-cells within grains of rice)

106
Q

which amoeba(s) cause(s) primary amoebic meningoencephalitis (PAM)

A

Naegleria fowleri
(PAM is a Naeg)

107
Q

which amoeba(s) cause(s) granulomatous amoebic encephalitis?

A

acanthamoeba
balamuthia
Sappinia
(ABS are GAE)

108
Q

neuropath finding of malaria

A

encephalopathy with PETECHIAE IN WHITE MATTER

109
Q

what are the 4 factors that facilitate sequestration of parasitized RBCs in microvasculature of the brain in CNS malaria?

A
  1. RBC knobs & endothelial psuedopodia
  2. Ag-Ab complex deposition (plt agg, endothelial damage)
  3. cell-mediated immune response > TNF > diapedesis
  4. Endothelial adhesion molecules

(knobs, Ag-Ab, diapedesis, adhesion)

110
Q

what disease causes “slate gray brain”?

A

malaria (d/t congested WM BVs and petechial hges)

111
Q

what do the RBCs look like in CNS malaria?

A

ghost-like
(they contain malaria parasites)

112
Q

What is a Durck granuloma?

A

accumulations of microglia + astrocytes, probably d/t resorption of ring hemorrhages seen in malaria

113
Q

what is the classic (rarely seen) triad of congenital toxoplasmosis?

A
  1. hydrocephalus
  2. cerebral calcs
  3. chorioretinitis
114
Q

how does congenital toxo happen

A

mom is infected > transplacental spread
(usually late in pregnancy)

115
Q

what happens if congenital toxo happens early in pregnancy, even tho it’s rare?

A

usu more severe, with worse CNS and eye involvement

116
Q

what happens (rarely) when you treat trypanosomiasis with melarsoprol?

A

acute hemorrhagic leukoencephalopathy

117
Q

what is the histo difference between african and american trypanosomiasis (african sleeping sickness vs chagas)

A

you can see amastigote parasites within glia in Chagas, but you usually do NOT see trypanosomes in african sleeping sickness (just nonspecific meningeal inflam)

you can see microglial nodules in both

118
Q

what is the commonest parasitic CNS infxn in the world?

A

cysticercosis

119
Q

which parasitic infxn is a/w immunosuppression?

A

strongyloidiasis

120
Q

which parasitic infxn is a/w cysts in the subarachnoid space?

A

coenurosis (dog tapeworm)

121
Q

which parasitic infxn is a/w eggs & granulomas in spinal cord, roots, or brain (discrete or diffuse)

A

schistosomiasis

122
Q

which parasitic infxn is a/w larvae in leptomeninges

A

strongyloidiasis

123
Q

which parasitic infxn is a/w subarachnoid HEMORRHAGE (not cysts) and worm tracks

A

angiostrongyliasis

124
Q

which parasitic infxn is a/w dead larvae surrounded by inflammation & giant cells?

A

visceral larva migrans (toxocara)

125
Q

what are racemose cysticerci?

A

large, multiloculated grape-like clusters of cysts WITHOUT an invaginated scolex in ventricular system or basal cisterns
(neurocysticercosis)

126
Q

what is the main difference between echinococcosis and neurocysticercosis on imaging?

A

echinococcosis (hydatid) = ONE cyst

neurocysticercosis (taenia) = MANY cysts

127
Q

three layers of TAENIA/neurocysticercosis cyst

A
  1. outer Cuticular layer w/ microtrichia
  2. middle cellular
  3. inner reticular or fibrillary layer

Cu/Ce/RF
cu ce ruff teens?

128
Q

three layers of echinococcus/hydatid cyst

A
  1. outer fibrous tissue derived from host
  2. intermediate laminated chitinous or cuticular layer (***diff from OUTER cuticular layer in taenia)
  3. thin inner germinal layer w/ brood capsules

F/LC/G
high fl(c)ags

Neuropath (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions