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🧠📖💯 > Infectious Pt. 2 > Flashcards

Infectious Pt. 2 Flashcards

1
Q

Which viruses (3) go through the peripheral nerves?

A

HSV
VZV
Rabies

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2
Q

Which viruses (3) go through the transplacental route?

A

Rubella
CMV
HIV

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3
Q

Which viruses (2) go through the oral-intestinal pathway?

A

Polio

Enterovirus

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4
Q

Which virus goes through the olfactory system?

A

HSV

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5
Q

Which virus goes through the sensory ganglia

A

VZV

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6
Q

Which virus goes through / hides in the kidney and bone marrow?

A

JC Virus

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7
Q

The JC virus depends on which cell-surface receptor to ingress into the cell?

A

Serotonin receptor

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8
Q

Which virus is associated with B cell lymphoma?

A

EBV

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9
Q

What are the 4 classifications of etiologic agents for acute aseptic meningitis?

A

Viral (majority)
Bacterial
Immune
Chemical irritant

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10
Q

Most common viral cause of acute aseptic meningitis?

A

Enterovirus

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11
Q

Dominant agent during local outbreaks for acute aseptic meningitis

A

Flaviviruses

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12
Q

Most frequent symptom of acute aseptic meningitis?

A

“Headache that is more severe than that a/w other febrile states”

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13
Q

What is the recognized host of Lymphocytic Choriomeningitis (LCM)?

A

Common house mouse

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14
Q

Etiologic agent: Mollaret Recurrent Meningitis

A

HSV-1

HSV-2 (most common)

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15
Q

Aseptic meningitis + bladder failure and vaginal/vulvar pain after herpes

A

Elsberg Syndrome

HSV-2, Mollaret Recurrent Meningitis

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16
Q

Most common encephalitis outside of North America?

A

Japanese B Encephalitis

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17
Q

Which area is known for having common birds (crows, jays) as arboviral encephalitis hosts?

a. West Nile
b. La Crosse
c. Powassan

A

ANS:
A. West Nile - common birds

Others:
B. La Crosse - Small Rodents

C. Powassan - Deer

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18
Q

Clinical picture of West Nile Virus?

A

Poliomyelitis
(febrile, flaccid, paralytic)
Facial paralysis

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19
Q

Which is more commonly a/w encephalitis, HSV-1 or HSV-2?

A

HSV-1

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20
Q

Which HSV presents with herpetic lesions of the oral mucosa?

A

ANS: HSV-1

HSV-1: oral mucosa
HSV-2: genital

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21
Q

How does HSV-1 differ in terms of clinical presentation vs. HSV-2?

A

HSV-1 Acute encephalitis

HSV-2 
Acute encephalitis (also in neonates)
Aseptic meningitis
Polyradiculitis
Myelitis
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22
Q

CSF picture of HSV encephalitis?

A

Increased pressure
Lymphocytic pleocytosis

**Hemorrhagic nature is INFREQUENTLY reflected in the CSF

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23
Q

Histopathologic findings in acute stages of HSV encephalitis?

A

Intranuclear eosinophilic inclusions (neurons, glial cells)

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24
Q

What are the 2 routes of infection of HSV encephalitis?

A

Route 1:
CNV ganglia -> nose, olfactory tract

Route 2:
CNV ganglia -> nerve fibers innervating leptomeninges (ant, mid fossae)

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25
Q

EEG findings of HSV encephalitis

A

1) Lateralized periodic high-voltage sharp waves in the temporal regions
2) Slow-wave complexes at regular 2-3s intervals

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26
Q

Treatment of HSV encephalitis?

A

Aciclovir IV 30mg/kg/d x 14-21 days

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27
Q

What is the main etiologic viral agent for encephalitis a/w stem cell transplant?

A

HHV-6

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28
Q

What are the common hosts for Rabies in Western Europe and in the US?

For both
A) Wild
B) Domestic

A

WILD
Racoons, skunks, foxes, bats

DOMESTIC
Dogs, cats

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29
Q

How long is rabies’ incubation period?

A

20-60 days

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30
Q

Characteristic symptom of rabies that signifies inflammatory response when the virus reaches the sensory ganglion

A

tingling/numbness at bite site

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31
Q

What are the 2 forms of rabies and which aspects of the neuraxis are involved for each?

A

Rabid form - tegmental medullary nuclei

Paralytic / Dumb form - spinal cord infection

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32
Q

Which among the 2 forms of rabies is associated with bat bites and administration of previous rabies vaccines?

a. Rabid form
b. Paralytic/dumb rabies

A

b. Paralytic/Dumb rabies

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33
Q

What are the clinical features of toxic Rabies patients?

A

Increased ICP
SIADH
DI
Dysautonomia

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34
Q

2 main histopathologic features (eponyms!) of rabies

A

Negri bodies
- cytoplasmic eosinophilic inclusions (pyramidal, purkinje cells)

Babes nodules
- focal collections of microglia

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35
Q

What are the 3 things to be done after a rabies bite?

A
  1. Clean the wound
    - Zephiran - benzyl ammonium chloride
  2. Surveillance of animal
    - 10 days
  3. Post exposure prophylaxis
    - HRIG
    - DEV
    - HDCV (D0, 3, 7, 14, 28)
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36
Q

Acute ataxia of childhood is most commonly associated with?

A

Chickenpox

37
Q

What are the DNA Viruses?

A 
Herpes Viruses (CMV, EBV, HSV, HHV)
JC Virus
38
Q

What are the RNA viruses?

A 
Rhabdoviruses
Arboviruses
Paramyxoviruses
Enteroviruses
Influenza

RAPE influenza

39
Q

Herpes Zoster can also cause poliomyelitis. How is it different from acute anterior polio?

A

Unilateral, segmental

Greater involvement of the dorsal horn, root, ganglion

40
Q

Most commonly involved areas in VZV?

A

Trigeminal, thoracic ganglion cells

41
Q

What is the “course” of VZV?

A

Vesicles -> sensory n. -> ganglion

Activation -> axon -> skin

42
Q

What are the inclusion bodies in VZV 2/2 multiplication in epidermal cells?

A

Lipschutz inclusion bodies

43
Q

When does vesicular eruption occur in VZV?

A

Within 72-96 hours (3-4 days)

44
Q

Rashes in VZV usually occur along a dermatomal level. If they occur in a generalized pattern, what is this indicative of?

A

Malignancy

45
Q

Most common dermatomal sites where you can successfully diagnose VZV via Tzanck smear?

A

T5-T10

46
Q

What can you see in CSF of patients with Zoster encephalitis?

A

VZV Membrane Antigen (VAMA)

47
Q

Treatment of Zoster is Aciclovir. Which population merits the use of IV acyclovir?

A

Immunocompromised

Disseminated (>3 dermatomes) zoster

48
Q

Topical treatment for postherpetic neuralgia

A

Capsaicin

2 ASA (crushed) + mixed w/ cold cream / chloroform 15 ml

49
Q

Criteria for AIDS

A

Either of the ff:

CD4 < 200 cells/uL
Opportunistic infection

50
Q

Most common neurologic complication in the later stages of HIV

A

HIV encephalopathy

presents as dementia

51
Q

Most sensitive tests in the early stages of HIV dementia

A

tests of psychomotor speed

52
Q

What is seen in HIV myelopathy?

A

Vacuolar degeneration

53
Q

Most common neuropathic pattern in HIV-associated peripheral neuropathy

A

Dystal, symmetric, axonal polyneuropathy

54
Q

What was the first proven viral polyneuritis in humans?

A

HIV neuropathy

55
Q

Which ARV can cause myopathy?

A

Zidovudine

2/2 effects on mitochondria

56
Q

Most common cause of focal neurologic complications among opportunistic infections of the CNS w/ HIV

A

Toxoplasmosis

57
Q

Treatment of Toxoplasmosis?

A

Pyrimethamine 200mg, then 50mg/day

Sulfadiazine 4-6 g/day x 4 doses

Alternative:
Clindamycin

58
Q

Progressive multifocal leukoencephalopathy is known to occur at what CD4 level?

A

< 50 cells/uL

59
Q

Treatment of Cytomegalovirus?

A

Ganciclovir

Foscarnet

60
Q

Etiologic agents of TB for HIV-AIDS pts?

A

M. tuberculosis

M. avium-intracellulare

61
Q

T or F. Syphilitic meningitis and meningovascular syphilis have an increased incidence in HIV pts.

A

True

62
Q

Tropical Spastic Paraparesis is caused by?

A

HTLV-1

63
Q

Known causes of acute anterior poliomyelitis? (give 4)

A

Poliovirus (most common)

Coxsackie (A&B)
Japanese Encephalitis
West Nile Virus

64
Q

In paralytic poliomyelitis, when does weakness occur?

A

At the height of fever or as temperature falls

*Maximum severity: 48 hours

65
Q

Bulbar paralysis due to poliomyelitis is more common in which patient population?

Which part of the NS is affected?

A

Young adults

Nucleus ambiguus

66
Q

Earliest histopathologic changes in the anterior horns for polio?

A

Central chromatolysis of nerve cells

67
Q

CD4 count at which JC virus occurs

A

< 200 cells/uL

Most often < 50 cells/uL

68
Q

PML is associated with all of the following EXCEPT:

a. Lymphoma
b. Chronic myelogenous leukemia
c. HIV
d. TB
e. None of the above

A

e. None of the above

69
Q

What is usually the first presentation of PML?

a. Seizures
b. Focal deficits
c. Personality changes & intellectual impairment

A

c. Personality changes and intellectual impairment

70
Q

Characteristic EEG finding for SSPE?

A

Periodic bursts (5-8s) of 2-3s high-voltage waves followed by a relatively flat pattern

71
Q

Histopathologic hallmark of SSPE

A

Eosinophilic inclusions in cytoplasm and nuclei

72
Q

What is von Economo Disease and its clinical features?

A

Encephalitis Lethargica

Somnolence
Ophthalmoplegia
Hyperactivity
Movement Disorders

Delayed EPS (Parkinsonian syndrome in survivors)

73
Q

CJD has a higher association among the following populations EXCEPT:

a. Israelis (Libyan origin)
b. Jews
c. North African (immigrants to France)
d. Slovakia

A

b. Jews

74
Q

What is CJD’s only clear mechanism of spread?

A

Iatrogenic

75
Q

What is the primary pathogenic mechanism of CJD?

A

Conversion of PrpC -> PrPSc

Cellular prion protein (PrPC) to its misfolded pathogenic form (PrPSc) which is protease resistant.

76
Q

Which variant of CJD presents with cerebellar ataxia?

A

Brownell-Oppenheimer variant

77
Q

Which variant of CJD presents with visual disturbances?

A

Heidenhai variant

78
Q

What are the distinctive EEG changes in CJD?

A

1) Diffuse and nonspecific slowing
2) Stereotyped high-voltage slow and sharp-wave complexes (on an increasingly slow and low-voltage background)

Pseudo-periodic high-voltage sharp waves

79
Q

The most sensitive test for CJD?

a. CSF studies
b. EEG
c. MRI
d. Immunoassay

A

c. MRI

Hyperintensity of cortex, BG, lenticular nuclei

80
Q

What do immunoassay studies for CJD test for?

A

Peptide fragments of normal brain protein “14-3-3”

81
Q

T or F. Prions can be detected in the urine of CJD pts.

A

True

82
Q

Myoclonus and corresponding sharp waves in EEG of CJD patients are due to?

A

Loss of inhibitory neurons in the thalamic reticular nuclei

83
Q

Which spongiform disease is familial (AD) that presents with dysesthesias, proximal lower extremity weakness as an early feature?

A

Gerstmann-Straussler-Sheinker Syndrome

84
Q

Which part of the brain is affected in fatal insomnia?

A

Medial thalamic nuclei

85
Q

Kuru is classically found in which patient population?

A

Fore tribe, New Guinea

86
Q

What is the presentation of Kuru?

A

Ataxia, emotional lability, uncontrollable laughter

87
Q

What are found in Kuru plaques?

A

Amyloid-like material, PAS positive stellate plaques

88
Q

PRPsc has what kind of protein structure?

A

B-pleated sheet

89
Q

Pleomorphic, less clearly circumscribed eosinophilic inclusions, rabies

A

Lyssa Bodies

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