Infections Flashcards

1
Q

Virus associated with Progressive Multifocal Leukoencephalopathy

A

JC Virus

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2
Q

The first proven viral polyneuritis in humans

A

HIV

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3
Q

In viral infection, _____ is an intermediate step to seeding the brain or CSF.

A

viremia

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4
Q

Aside from hematogenous spread, the HSV may spread to the CNS via these structures

A

olfactory neurons > cribriform plate > olfactotry bulbs

trigeminal ganglion > gasserian ganglion

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5
Q

the most important route of infection for the majority of viruses

A

hematogenous

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6
Q

To be susceptible to a viral infection, the host cell must have

A

on its cytoplasmic membrane specific receptor sites to which the virus attaches.

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7
Q

Differentiating cells of the fetal brain have particular vulnerabilities, and viral incorporation may give rise to malformations and to hydrocephalus; an example is
mumps virus which can lead to?

A

ependymal destruction and aqueductal stenosis

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8
Q

As a rule, in viral infections of the CNS, the glucose content of the CSF is normal, but infrequently, mild depression of the CSF glucose can be seen but never below

A

25 mg/dL

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9
Q

As a rule, in viral infections of the CNS, the glucose content of the CSF is normal, but infrequently, mild depression of the CSF glucose can be seen in which viral meningitides?

A

mumps
HSV-2
LCM
VZV

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10
Q

In viral CNSI, Bell’s palsy has been associated to whuch virus/es?

A

HSV-1

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11
Q

What is Mollaret meningitis?

A

is characterized by episodes of acute meningitis with severe headache and sometimes low-grade fever, lasting for about 2 weeks, and recurring over a period of several months or years

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12
Q

What is the most common cause of viral aseptic meningitis in adults?

A

enterovirus mainly echovirus & Coxsackie virus

Then followed by:
HSV2
Varicella
HIV
Mumps
EBV
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13
Q

What is the most common cause of viral aseptic meningitis in children?

A

enterovirus-echovirus and Coxsackie virus

Followed by
HSV2
LCM
HSV1
adenovirus
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14
Q

The natural host of LCM virus

A

Lymphocytic choriomeningitis

house mouse Mus musculus

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15
Q

The 5th disease is caused by

A

parvovirus

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16
Q

strain of parvovirus that can cause meningitis and encephalitis in children

A

B19

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17
Q

viruses associated with meningitis + cauda equina neuritis

A

HSV

HIV

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18
Q

viruses associated with meningitis + generalized lymphadenopathy, transient rash, mild icterisia

A

EBV

CMV

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19
Q

virus associated with aseptic meningitis + intense lymphocytic pleocytosis (1000 cells/mm3)

A

LCM

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20
Q

What is Vogt-Koyanagi Harada syndrome?

A

combinations of iridocyclitis, depigmentation of a thick swath of hair (poliosis circumscripta) and of the skin, vitiligo, around the eyes, loss of eyelashes, dysacusis, and deafness (the pathologic basis of the syndrome is not known)

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21
Q

Mollaret Syndrome has been associated to which viruses?

A

HSV-1
HSV-2
EBV
Herpes 6 in children

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22
Q

What is Elsberg Syndrome?

A

HSV2
lumbosacral radiculitis
urinary retention

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23
Q

HaNDL syndrome

A

headache neurologic deficit

lymphocytic pleocytosis

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24
Q

Behcet disease

A

a diffuse inflammatory disease of small blood vessels that has several other characteristic features such as oral and genital ulcers

acute inflammatory CNS disease

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25
Q

parkinsonism seen as residua of encephalitis from which viruses

A

Flaviviruses

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26
Q

In viral CNSI, you see thalamic signal changes in MRI, the associated viruses are

A

Japanese B, West Nile, Eastern Equine Encephalitis, rabies

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27
Q

The most serious arbovirus in the US because of its high mortality and morbitidy

A

EEE

eastern equine encephalitis

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28
Q

Among the viral encephalitides, this is the gravestt

A

HSV

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29
Q

Describe the pathology found in HSV encephalitis

A

intense hemorrhagic necrosis of the inferior & medial temporal lobes & the mediorbital parts of the frontal lobes

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30
Q

In the acute stages of HSV encephalitis,

eosinophilic inclusions are found in

A

intranuclear regionsn of neurons & glial cells

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31
Q

Two routes of entry of HSV to the CNS, which is more favored to be true?

A

latent virus in the trigeminal ganglia with reactivation:
1 infect the olfactory tract - olfactory bulb - CNS
2 spread along nerve fibers innervating anterior & middle fossae leptomeninges

2 more favored

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32
Q

EEG changes in HSV encephalitis

A

lateralized periodic high-voltage sharp waves in the temporal regions and slow-wave complexes at regular 2 to 3Hz

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33
Q

Sensitivity of nested PCR in HSV encephalitis for the first 3 weeks of illness

A

95%

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34
Q

Dose of acyclovir for HSV encephalitis

A

30 mg/kg/d for 10 to 14 days

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35
Q

if treatment is begun within ____ of onset of HSV encephalitis in an awake patient, survival is >90%

A

4 days

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36
Q

established cause of a limbic encephalitis in adult patients following allogenic hematopoietic stem cell bone marrow transplantation

A

HHV-6

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37
Q

limbic encephalitis, post bone marrow transplant associated with gray matter damage

A

adenoviruses

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38
Q

Aside from HHV-6, viral agents that can also cause encephalitis in transplant recipient patientts

A

CMV, EBV, adenovirus, HSV, and varicella zoster virus

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39
Q

Incubation period of rabies

A

20-60 days can be as short as 14 days

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40
Q

Describe the evolution of rabies infection

A
  • incubation period of 20-60 days
  • tingling numbness reflecting invasion of sensory ganglion
  • prodromal symptoms, involvement of tegmental medullary nuclei
  • psychosis, seizures
  • death within 4-10 days for the paralytic form
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41
Q

Characteristic pathologic findings in rabies infection

A

Negri bodies - cytoplasmic eosinophilic inclusions, most prominent in pyramidal cells of the hippocampus & Purkenje cells

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42
Q

What are Babe nodules? where do you find these?

A

focal collections of microglia in the brainstem of rabies infected patients

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43
Q

This compound can inactivate the rabies virus so better wash bite wound with this!

A

Benzyl ammonium chloride

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44
Q

postexposure prophylaxis for rabies

A

Human rabies immune globulin (HRlG) 20 U/kg
1/2 infiltrated in the wound
1/2 intramuscular

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45
Q

active immunization for rabies

A

human diploid cell vaccine HDCV
1-mL injections on the day of exposure
days 3, 7, 14, and 28 after

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46
Q

Acute ataxia of childhood is most associated with this virus

A

VZV

but can be: enteroviruses (Coxsackie), EBV, CMV

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47
Q

vesicles in VZV are called

A

Lipschutz inclusion bodies

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48
Q

pathologic changes in VZV infection (4)

A

(1) inflammation in several unilateral sensory ganglia of the spinal or cranial nerves, (can cause necrosis /-hemorrhage)
(2) inflammation in the spinal roots & peripheral nerve contiguous with the involved ganglia
(3) poliomyelitis (different from acute anterior poliomyelitis because unilateral, segmental, involves dorsal horn, root, & ganglion)
(4) relatively mild leptomeningitis, limited to the involved spinal or cranial segments & nerve roots

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49
Q

True or False. one attack of zoster provides lifelong

immunity

A

FALSE

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50
Q

VZV DNA is localized primarily in

A

trigeminal & thoracic ganglion cells corresponding to the dermatomes in which chickenpox lesions are maximal and that are most commonly involved

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51
Q

In VZV, the vesicles always appear within

A

72-96 hours

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52
Q

In VZV, pain & dysesthesia last for

A

1-4 weeks

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53
Q

VZV infection can be confirmed by

A

1 Tzanck smear - inding multinucleated giant cells in scrapings from the base of an early vesicle
2 direct immunofluorescence of a biopsied skin lesion, using antibody to VZV

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54
Q

Most common dermatomes affected by VZV

A

T5-T10

then cranicervical

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55
Q

Acyclovir shortens the duration of acute pain and

speeds the healing of vesicles in VZV infection, provided that treatment is begun within approximately

A

48-72 h upon appearance of the rash

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56
Q

Treatment for postherpetic neuralgia

A

amitriptyline 50 mg at bedtime can be increased

gradually to 125 mg daily

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57
Q

True or False. postherpetic neuralgia eventually subsides even in the most severe and persistent cases

A

True

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58
Q

True or False. HIV results in a depressed cell-mediated immunity particularly decreasing the number of CD8+ lymphocytes

A

False

CD4+

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59
Q

In the later stages of HIV infection, the most common neurologic complication is

A

AIDS dementia complex

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60
Q

AIDS Dementia Complex

A

subacutely progressive dementia (loss of retentive memory, inattentiveness, language disorder, apathy), abnormalities of motor function

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61
Q

Without treatment, survival after the onset of AIDS dementia is

A

generally 3 to 6 months

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62
Q

True or False. In AIDS Dementia complex, treatment with antiretroviral drugs can result in cognitive improvement.

A

True

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63
Q

Most sensitive test in the early stages of AIDS Dementia complex

A

psychomotor speed testing

e.g., trail making, pegboard, and symbol-digit testing

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64
Q

MRI findings in AIDS Dementia Complex

A

patchy but confluent or diffuse white matter changes with ill-defined margins

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65
Q

Pathologic findings in AIDS Dementia Complex

A

diffuse & multifocal rarefaction of the cerebral white matter with scanty perivascular infiltrates of lymphocytes & clusters of a few foamy macrophages, microglial nodules & multinucleated giant cells

diffuse myelin breakdown, white matter pallor
diffuse poliodystrophy

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66
Q

True or False. AIDS dementia complex is due to secondary brain destruction due HIV infection elsewhere

A

False

It is a result of a direct virus invasion

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67
Q

Pathologic picture of HIV myelopathy

A

vacuolar degeneration

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68
Q

Most common form of peripheral neuropathy in HIV infection

A

distal, symmetrical, axonal polyneuropathy, predominantly sensory & dysesthetic in type

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69
Q

the first proven viral polyneuritis in humans

A

HIV

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70
Q

HIV myopathy

A

inflammatory myositis

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71
Q

Most frequent focal infectious complications in AIDS

A

toxoplasmosis

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72
Q

True or False. Asymptomatic Toxoplasma-seropositive AIDS patients should be treated with oral pyrimethamine & sulfonamide

A

True

Because Toxoplasmosis in AIDS usually represents a reactivation of a previous infection

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73
Q

Treatment of Toxoplasmosis?

if this is not tolearted, what can you give?

A

oral pyrimethamine (100 mg then 25 mg daily) + sulfonamide (4 to 6 g daily in four divided doses)

clindamycin

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74
Q

Most frequent nonfocal infectious complications in AIDS

A

CMV

crytococcosis

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75
Q

CMV encephalitis in AIDS is usually accompanied by

A

retinitis

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76
Q

MRI findings in AIDS with CMV encephalitis

A

T2 signal hyperintensity in the ventricular borders

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77
Q

Diagnostic test for CMV infection

A

PCR

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78
Q

Treatment for CMV infection

A

ganciclovir

foscarnet

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79
Q

Quaternary Syphilis

A

consists of an aggressive and rapidly progressive

necrotizing process that causes strokes and dementia as a result of involvement of brain parenchyma and vessels

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80
Q

Shingles involving several contiguous dermatomes is known to occur in AIDS with CD4 counts below

A

500

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81
Q

Forms of VZV infection AIDS patients

A
  • multifocal lesions of the cerebral white matter like PML
  • cerebral vasculitis with hemiplegia
  • myelitis
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82
Q

A special result of HlV antiretroviral treatment may induce an intense inflammatory response to a coexistent infection

A

immune reconstitution inflammatory syndrome, or IRIS

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83
Q

Tropical Spastic Paraplegia

A

HTLV-1

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84
Q

Virus causing lower motor neuron paralysis + hemorrhagic conjunctivitis

A

enterovirus 70

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85
Q

Viruses that can cause acute anterior poliomyelitis

A

poliomyelitis
Coxsackie groups A and B
Japanese encephalitis
West Nile Virus

86
Q

The polio virus multiplies in the

A

pharynx & intestinal tract

87
Q

2 Types of Poliomyelitis

A

NonParalytic

Paralytic

88
Q

Paralytic Poliomyelitis symptomatology

A
  • weakness at the height of fever then improvement then rapid muscle weakness peak within 48 hours
  • no progression of weakness after the temperature has been normal for 48 hours
  • muscle atrophy 3 weeks, maximal 12-15 weeks
89
Q

Pathologic reactions in poliomyelitis

A
  • lesions are found i n the precentral gyrus, brainstem, spinal cord
  • hypothalamus, thalamus, brainstem (motor nuclei of reticular formation), vestibular nuclei and roof nuclei of the cerebellum, spinal cord anterior & intermediate gray matter
90
Q

Polio Vaccine

A

Sabin Vaccine

2 doses 8 weeks apart at 1 year of age then before schooling

91
Q

“Inclusion body encephalitis”

A

SSPE

subacute sclerosing panencephalitis

92
Q

Describe the symptomatic evolution of SSPE

A
  • usually there is a primary measles infection before 2 years old then an asymptomatic period of 6-8 years
  • progressive intellectual deterioration, seizures, mycolonus
  • decorticate
93
Q

progressive ataxic-myoclonic chronic dementia in a child

A

SSPE

subacute sclerosing panencephalitis

94
Q

characteristic EEG in SSPE

A

periodic (every 5 to 8 s) bursts of 2 to 3/s highvoltage waves, followed by a relatively flat pattern

95
Q

Histopathologic hallmark of SSPE

A

Eosinophilic inclusions in the cytoplasm & nuclei of neurons and glia cells

96
Q

Oligoclonal bands found in the CSF of SSPE represent

A

measles-virus-specific antibody

97
Q

Histopathologic picture of PML

A
  • gigantic reactive astrocytes containing bizarre-shaped nuclei and mitotic figures (resemble high grade glioma)
  • nuclei of oligodendrocytes are greatly enlarged & contain abnormal inclusions
98
Q

CSF picture of PML

A

normal

99
Q

MRI of PML

A

variable size & location of nonenhancing demyelinating lesions

100
Q

Pathogenesis of PML

A

JC virus thought to be dormant in the kidney or bone marrow until an immunosuppressed state permits its active replication

101
Q

True or False. approximately 70% of the normal adult population has antibodies vs JC virus

A

True

102
Q

True or False. PML caused by JC virus is untreatable in non-AIDS patients but progression can be slowed down in AIDS patients

A

TRUE

for AIDS patients, give antiretroviral + protease inhibitor

103
Q

Poor prognostic sign in JC Virus PML

A

CD4

104
Q

First recognized slow virus infection

A

Encephalitis lethargica

but the virus is still not identified!

105
Q

True or False. Parkinsonian syndrome seen in survivors of Encephalitis Lethargica / somnolent-ophthalmoplegic encephalitis have Lewy bodies similar to idiopathic PD

A

False

no Lewy bodies but with neurofibrillary changes

106
Q

Rasmussen’s Encephalitis is associated to which viruses and which autoantibody

A

CMV, HSV1

anti-glutamine receptors3

107
Q

What is a prion?

A

proteinaceous infectious particle that is devoid of nucleic acid, resists the action of enzymes that destroy RNA and DNA, fails to produce an immune response, and electron microscopically does not have the structure of a virus

108
Q

PrP is normally encoded in

A

chromosome 20

109
Q

True or False. An abnormally folded prion protein can act as a template for the conversion of normal PrP to PrPsc

A

True

110
Q

How does a prion protein Prp acquire its infectivity?

A

change in the physical conformation in which its helical proportion diminishes and the proportion of the beta
pleated sheet increases

111
Q

Another classification scheme proposed for Prions Disease is to base tion systems have been devised that
are based on both the presence of methionine (M) or
valine (V) at codon ?

A

129

112
Q

EEG is SSE

A

changing over the course of the disease from one of diffuse and nonspecific slowing to one of stereotyped psuedoperiodic highvoltage slow- (1- to 2-Hz) and sharp-wave complexes on an increasingly slow and low-voltage background

113
Q

MRI is SSE

A

hyperintensity of the lenticular nuclei on T2-weighted
and diffusion-weighted images in the basal ganglia and
cortex

114
Q

CSF finding diagnostic of SSE

A

immunoassay of peptide fragments of normal brain
proteins, termed “14-3-3”

repeat this test up to 3x

115
Q

Gerstmann-Straussler-Scheinker Syndrome

A

autosomal dominant , progressive cerebellar ataxia,
corticospinal tract signs, dysarthria, and nystagmus
+/- mild dementia

116
Q

Fatal Insomnia

A

characterized by intractable insomnia, sympathetic overactivity, & dementia, leading to death in 7 to 15 months

  • lesions mainly in the medial thalamic nuclei
  • mutation in codon 178
117
Q

Kuru histologic picture

A

noninflammatory loss of neurons and spongiform change throughout the brain, but predominantly in the cerebellar cortex, with astroglial proliferation and kuru plaques

118
Q

Kuru symptomatology

A

afebrile, progressive cerebellar ataxia, with abnormalities of extraocular movements, weakness progressing to immobility, incontinence in the late stages, and death within 3 to 6 months

119
Q

Vector of Zika Virus

A

Aedes

120
Q

Zika virus can cause

A

microcephaly

GBS

121
Q

Most common bacterial meningitides

A
Streptococcus pneumoniae
Neisseria meningitides
group B streptococcus in neonates
Listeria monocytogenes
Haemophilus influenza
122
Q

Seizures in meningitis are most associated with

A

H influenza

123
Q

Most common bacterial menigitides in the neonates

A

E. coli

group B streptococcus

124
Q

One factor that predispose a patient to have bacterial meningitis

A

antecedent viral infections of the upper respiratory passages or infections of the lung

125
Q

Rapid detioration in a patient with meningitis associated with petechial or purpuric rash

A

Meningococcemia

Echovirus serotype 9
Staphylococcus aureus

126
Q

Meningitis + cranial nerve abnormalities

A

pneumococcal meningitis

127
Q

Most significant factor in the pathogenesis of neonatal meningitis

A

maternal infection

128
Q

Meningitis in splenectomized patients, most likely is caused by

A

Streptococcus pneumoniae

129
Q

Meningitis after an ear infection or upper respiratory tract infection

A

H influenza

130
Q

True or False. Infants with pneumococcal meningitis have the highest risk factor for developing subdural effusion

A

False

regardless of bacterial type

131
Q

the simplest method of demonstrating effusion in a child

A

transillumination of the skull

132
Q

an indispensable part ofthe examination of patients with the symptoms and signs of meningitis or of any patient in whom this diagnosis is suspected

A

lumbar puncture

133
Q

CSF pleocytosis in bacterial meningitis ranges from

A

250-10000 cells/ mm3

134
Q

CSF red cells in meningitis are seen in

A
anthrax
Hantavirus
dengue
ebola
amebic
135
Q

CSF protein in bacterial meningitis ranges from

A

100-500 mg/dL

136
Q

CSF glucose in bacterial meningitis

A
137
Q

CSF cultures in bacterial meningitis are usually positive in

A

70-90%

138
Q

Blood cultures in bacterial meningitis are usually positive in

A

40-60%

139
Q

Most sensitive test of demonstrating bacterial infection in the CSF

A

PCR

other tests CIE LPA RIA ELISA

140
Q

CSF LDH of >35 mg/dL. Fungal, bacterial or viral?

A

Fungal or bacterial

141
Q

The most specific and sensitive test for CSF

otorrhea and rhinorrhea is the finding of

A

beta2-transferrin (tau), not found in fluids other than CS

142
Q

empiric therapy for bacterial meningitis in 0-4 week old

A

Cefotaxime + ampicillin

143
Q

empiric therapy for bacterial meningitis in 4-12 week old

A

3rd G Cephalosporin + ampicillin + dexamethasone

144
Q

empiric therapy for bacterial meningitis in 3month - 50 years o ld

A

3rd G Cephalosporin + vancomycin

+/- ampicillin

145
Q

empiric therapy for bacterial meningitis in >50 years old

A

3rd G Cephalosporin + vancomycin + ampicillin

146
Q

empiric therapy for bacterial meningitis in immunocompromised patient

A

ceftazidime + vancomycin + ampicillin

147
Q

empiric therapy for bacterial meningitis with basilar skull fracture

A

3rd G Cephalosporin + vancomycin

148
Q

empiric therapy for bacterial meningitis with head trauma, or post neurosurgery, CSF shunt

A

ceftazidime + vancomycin

149
Q

antibiotic to add if Listeria monocytogenes is suspected

A

ampicillin

150
Q

Duration of treatment in bacterial meningitis

A

10-14 days

151
Q

Dexamethasone dose for bacterial meningitits in a child

A

0.15 mg/kg qid for 4 days

152
Q

Dexamethasone dose for bacterial meningitits in an adult

A

10mg IV initial then 5mg q6 x 4 days

153
Q

True or False. Patients with bacterial meningitis with evidence of cortical vein thrombosis should be started on anti-seizure drugs

A

True

154
Q

this neurologic sequelae of bacterial meningitis was shown to have decreased with dexamethasone

A

sensorineural hearing loss

155
Q

Prophylaxis for patients exposed to meningococcal meningitis

A

Ciprofloxacin

Rifampicin mg q12 for adults; mg/kg q12 for children x 2 days

156
Q

Prophylaxis for patients exposed to meningococcal meningitis >2 weeks

A

none

157
Q

Osler triad

A

pneumococcal meningitis
pneumonia
endocarditis

158
Q

What is Hurst Disease and which microorganism is it associated with?

A

Acute hemorrhagic leukoencephalitis

Associated with Mycoplasma pneumoniae

159
Q

Symptomatology of Mycoplasma pneumoniae encephalitis

A
Cerebellitis
Choreoathetosis
Seizures
Delirium
Hemiparesis
160
Q

How to establish the diagnosis of Mycoplasma pneumoniae encephalitis?

A

1 culture from respiratory tract
2 IgG IgM antibodies, cold agglutinin in blood CSF
3 PCR dna in CSF

161
Q

Treatment of Mycoplasma pneumoniae encephalitis

A

Macrolide
Or
Tetracycline

162
Q

Meningoencephalitis in an immunocompromised individual taking the form of a rhombencephalitis

A

Listeria monocytogenes

163
Q

Treatment of Listeria monocytogenes encephalitis

A

Ampicillin 2g IV q4

+ Gentamicin 5mg/kg IV in 3 divided doses

164
Q

Bacteria causing Melioidosis

A

Burkhorderia pseudomallei

165
Q

A diabetic patient came from vacation from Cambodia and Thailand had encephalitis. Most likely culprit is?

A

Burkholderia pseudomallei causing melioidosis

166
Q

Diagnositc test for melioidosis

A

Culture of organism from any body site

CSF pharynx blood urine or sputum

167
Q

Treatment of melioidosis

A

1 intensive phase: Ceftazidime IV x 10-14days

2 eradication phase: cotrimoxazole +/- doxycycline

168
Q

Diagnostic test for Legionella encephalitis

A

Urine antigen

Culture of blood CSF

169
Q

Treatment for Legionella encephalitis

A

Levofloxacin
Moxifloxacin
Azithromycin
Rifampicin

170
Q

Microorganism responsible for cat scratch disease

A

Bartonella henselae

171
Q

Catscratch fever symptomatology

A

Unilateral axillary/cervical adenopathy
Encephalopathy
High fever
Seizures or status epilepticus

In AIDS: focal cerebral vasculitis, neuroretinitis

172
Q

Catscratch fever diagnostic workup

A

PCR o silver staining from excised lymph node

173
Q

Catscratch fever first line of treatment

A

Azithromycin or

Doxycycline

174
Q

Hemorrhagic inflammatory spinal fluid formula

Necrosis of vessels

A

Bacillus anthracis

175
Q

Treatment of anthrax

A

Ciprofloxacin +
Clindamycin or
Rifampin or
Meropenem

176
Q

Acute meningoencephalitis
Papilledema
Increaee ICP
After drinking raw milk

A

Brucellosis

177
Q

Diagnostic workup for brucellosis

A

Blood CSF antibody titers

178
Q

Treatment of Brucellosis

A

Doxycyline +
Streptomycin or
Gentamicin or
Rifampin

179
Q

Microorganism responsible for Whipple’s Disease

A

Tropheryma whipplei

180
Q
Slowly progressive dementia
Supranuclear ophthalmoplegia
Ataxia
Seizure
Nystagmus
Oculomasticatory movemebts / myorhtyhmja

Likely diagnosis? Microorganism that caused this?

A

Whipple Diseas

Tropheryma whipplei

181
Q

Treatment for Whipple Disease

A

Penicillin or Ceftriaxone x 2 weeks then

TMP-SMX or or doxycycline or tetracycline x 1yr

182
Q

Subdural empyema usually originates from

A

frontal or ethmoid sinuses

183
Q

Subdural empyema pathogenesis

A

1 direct extension through bone & dura

2 spread from septic thrombosis of venous sinuses (superior longitudinal sinus

184
Q

Most common causative bacteria in subdural empyema

A

Streptococci (nonhemolytic & viridans)

185
Q

Empyema that follows meningitis in children tends to localize on the

A

undersurface of the temporal lobe

186
Q

Empiric treatment for subdural empyema

A

3rd generation cephalosporin + metronidazole

187
Q

Empiric treatment for epidural abscess

A

cephalosporin + vancomycin

188
Q

The most commonly involved sinuses in septic thrombophlebitis

A

transverse
cavernous
petrous

189
Q

Transverse sinus septic thrombophlebitis

A

usually follows a middle ear, mastoid, or petrous bone chronic infection

190
Q

True or false.

Anticoagulation is the mainstay of treatment of septic thrombophlebitis

A

False

high doses of antibiotics

191
Q

Septic Cavernous Sinus Thrombophlebitis is usually secondary to

A

ethmoid, sphenoid, or maxillary sinuses infection

192
Q

True or False.

brain abscess is always secondary to bacteremia and a bacterial focus elsewhere in the body

A

False.

a small proportion is iatrogenic

193
Q

Brain abscess originating from the ear usually are located in

A

2/3 inferomedial temporal lobe

194
Q

Metastatic abscesses from hematogenous spread are

usually situated in

A

the distal territory of the middle cerebral arteries

195
Q

Most common cardiac congenital anomaly to develop brain abscess

A

Tetralogy of Fallot

196
Q

Most common organism causing bacterial cerebral abscess

A

virulent streptococci

197
Q

2 stages in the pathogenesis of TB meningitis

A

1 bacterial seeding of the meninges and subpial regions of the brain with tubercle formation
2 rupture of one or more of the tubercles and the discharge of bacteria into the subarachnoid space

198
Q

Histopathologic finding in meningeal tubercles

A

central zone of caseation surrounded by epithelioid cells and some giant cells, lymphocytes, plasma cells, and connective tissue

199
Q

TB PCR sensitivity

A

80%

200
Q

The single most effective drug in TB

A

isoniazid

201
Q

HREZ dose in adults

A

5-10-15-20 mg/kg/day

202
Q

HREZ dose in children

A

10-15-15-20 mg/kg/day

203
Q

Dexamethasone dose in TB meningitis

A

0.4mg/kg/day x 1 week then taper 3-6 weeks

204
Q

Sarcoidosis is

A

represents an exaggerated cellular immune response to a limited class of antigens or autoantigens

205
Q

mainstay of treatment of sarcoidosis

A

steroids

206
Q

Causative agent of neurosyphilis

A

Treponema pallidum

207
Q

The initial event in neurosyphilis is

A

meningitis

208
Q

CSF changes in neurosyphilis in order

A

cells - protein - gamma globulins

209
Q

Principal Types of Neurosyphilis 8

A
Asymptomatic neurosyphilis
meningeal syphilis
meningovascular syphilis
paretic neurosyphilis
tabetic neurosyphilis
syphilitic optic atrophy
spinal syphilis
syphilitic nerve deafness vestibulopathy
210
Q

Treatment of neurosyphilis

A

-IV penicillin G 18-24M u/day x 10-14 days

211
Q

Most common form of neurosyphilis

A

meningovascular syphilis