Neuroinfectious Flashcards

1
Q

In patients with HIV aseptic meningitis, alertness and cognition are deeply affected. True or False?

A

False. In patients with HIV aseptic meningitis, alertness and cognition are preserved, distinguishing it from encephalitis and meningoencephalitis.

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2
Q

What is the pathophysiology behind aseptic meningitis in HIV?

A

It is part of the seroconversion syndrome in HIV. May appear during the initial stages of HIV infection

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3
Q

What is the CSF finding of HIV aseptic meningitis?

A

The CSF of these patients usually shows a lymphocytic pleocytosis (but usually less than 25 cells/uL) and mildly increased protein level (less than 100 mg/dL), with normal glucose levels.

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4
Q

Patient presented with bell’s palsy and lymphocytic meningitis. What is the possible organism involved and vector?

A

Borrelia burgdorferi. This spirochete is transmitted by the deer tick Ixodes.

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5
Q

What is the management of Lyme disease (First Stage: Rash and Cranial Neuroapthies)?

A
First stage (Rash and cranial neuropathies)
• oral doxycycline 100mg BID x 14 days
alternate: Amoxicillin 500mg TID; Cefuroxime axetil 500mg BID
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6
Q

What are the predisposing factors in the development of mucormycosis?

A

Diabetes mellitus and diabetic ketoacidosis are major and frequent risk factors

Others:

  • malignancies
  • high-dose steroids
  • organ transplantation
  • immunosuppression
  • iron chelation therapy (with deferoxamine)
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7
Q

What is the spectrum of cognitive disorder of HIV?

A

asymptomatic neurocognitive impairment (ANI)
minor neurocognitive disorder (MND)
HIV-associated dementia (HAD)

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8
Q

What is the CD4 count in patients with HIV and HAD?

A

patients with CD4 counts below 200 cells/mm3

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9
Q

What are the main clinical manifestations of HIV-associated neurocognitive disorder?

A

Progressive cognitive decline and prominent psychomotor dysfunction are the main clinical manifestations.

These patients have significant difficulties with attention and concentration, along with fine motor dysfunction, gait incoordination, and tremors.

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10
Q

What is the neuropathologic finding in HIV-associated dementia?

A

diffuse white matter pallor, mononuclear infiltrates, multinucleated giant cells, and vacuolar changes in the brain. The main findings are in the subcortical region, and the cerebral cortex is relatively spared.

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11
Q

HIV-associated dementia may be prevented. True or False?

A

HIV-associated dementia can be prevented by adequate early treatment of HIV with highly active antiretroviral therapy (HAART), with the goals of attaining higher CD4 counts and suppressing the virus.

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12
Q

HIV-associated dementia leads to improvements in neuropsychological performance. Prognosis is generally good, likely given the early stage of HIV in which this condition develops. True or False?

A

False.

Prognosis is generally POOR likely given the LATE stage of HIV in which this condition develops

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13
Q

While you are working your 4th-of-July shift in the emergency department, a 62-year-old farmer is brought with mental status changes and generalized weakness. The patient has been having low-grade fevers, malaise and back pain, body aches, and headaches for the past 10 days; however, he did not want to come to the hospital. Over the past 5 days, he has developed bilateral hand tremors and difficulty walking. About 3 days ago, he became confused, and today, he was noticed to be unable to move his legs. On examination, he is lethargic and confused and noticed to be flaccid in his lower extremities, with areflexia. Which of the following is the most likely diagnosis?

a. Tuberculous meningitis and Pott’s disease
b. Subacute combined degeneration of the spinal cord c. Neurosyphilis with tabes dorsalis
d. West Nile encephalitis
e. HSV encephalitis

A

D. West Nile virus (WNV) encephalitis

Trasmitted by: Culex

severe neurologic presentation will have manifestations of encephalitis; however, WNV can also invade the anterior horn cells leading to flaccid weakness with arreflexia, similar to poliomyelitis

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14
Q

What is the histopathologic finding in Crytococcal meningitis?

A

histopathologic specimen demonstrates budding yeasts near blood vessels and surrounded by an inflammatory infiltrate,

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15
Q

What is the CD4 count in patients at risk of developing cryptococcal meningitis?

A

CD4 counts fall below 100 cells/uL

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16
Q

What is the treatment of cryptococcal meningitis?

A

• Intravenous administration of Amphotericin B (0.7-1.0mg/kg/day) or (3-4mg/kg/day) of liposomal amphotericin continued for 6wks

Addition of flucytosine (100mg/kg/d)

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17
Q

What is the most useful diagnostic test in cryptococcal meningitis?

A

India ink smear is not very sensitive; however, it is useful when it is positive

Cryptococcal antigen detection in the CSF is rapid, sensitive and specific, and clinically useful, since fungal culture may take several days to weeks for a positive result to be obtained.

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18
Q

What are the side effects of amphotericin and flucytosine therapy?

A

Amphotericin is associated with renal failure, hypokalemia, and hypomagnesemia; and flucytosine may cause hematologic abnormalities.

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19
Q

What is the histopathologic findings of toxoplasma?

A

Microglial nodule, in which an encysted bradyzoite can be seen surrounded by an inflammatory infiltrate.

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20
Q

What is the CD4 count in patients at risk of developing toxoplasmosis of the CNS?

A

CD4 counts fall below 100 cells/uL

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21
Q

What is the treatment of CNS toxoplasmosis?

A

• a presumptive diagnosis can be made on a clinical basis in a patient with HIV and empiric treatment is started before confirmatory testing

• oral sulfadizine (4g then 4-6g daily) + Pyrimethamine (200mg then 50-100mg OD)
• Leucovorin 15-20mg OD-  counteract the anti-folate action of pyrimethamine completed for 6wks
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22
Q

What is the prophylaxis for Toxoplasmosis and when it is given?

A

Trimethoprim-sulfamethoxazole

Given to:

  • Patients with HIV
  • CD4 counts of less than 100/uL
  • positive IgG antibodies to toxoplasma
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23
Q

What is the MRI finding of Primary CNS Lymphoma (PCNSL) in the setting of AIDS?

A

MRI shows one or more lesions usually in the periventricular and deep regions of the brain. lesions may have contrast enhancement, surrounding edema, and produce mass effect.

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24
Q

Patient was diagnosed with end-stage AIDS. Presenting with progressive course of multiple focal neurologic manifestations, with visual field deficits and visual agnosias. MRI shows multiple white matter nonenhancing lesions that tend to coalesce and predominate in the parieto-occipital regions. What is the likely diagnosis and what is the gold standard of treatment?

A

Progressive Multifocal Leukoencephalopathy

Brain Biopsy is the gold standard diagnostic test

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25
Q

What is the neuropathologic finding of Progressive Multifocal Leukoencephalopathy?

A

myelin loss, giant astrocytes, and altered oligodendrocytes, with enlarged nuclei and viral inclusions. On electronic microscopy, the viral particles give a “spaghetti and meatballs” appearance.

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26
Q

What is the clinical manifestation of HIV neuropathy?

A

predominantly sensory, axonal length-dependent symmetric polyneuropathy.
It is thought to be related to direct effects of the virus and cytokine upregulation.

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27
Q

HIV pt presented with numbness that occurs over weeks following the initiation of therapy. the The treatment is to discontinue the offending drug. What is the diagnosis?

A

Nucleoside analog-associated neuropathy

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28
Q

Patient presents with iridocyclitis + depigmentation of thick swath of hair + skin, vitiligo + loss of eyelashes, dysacusis and deafness. What is the diagnosis?

A

Vogt-Koyanagi-Harada Syndrome

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29
Q
Which of the following is the least  common pathogens of bacterial meningitis in neonates?
A. Escherichia coli, 
B. Enteric gram-negative bacilli
C. Listeria monocytogenes
D. group B streptococci
E. Neisseria mengitidis
A

E. Neisseria mengitidis

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30
Q

In patients who undergo neurosurgical intervention, which of the following is the least likely etiology of meningitis?

A. Pseudomonas aeruginosa
B. Staphylococcus aureus C. Staphylococcus coagulase negative (epidermidis)
E. Propionibacterium Acnes
F. Streptococcus pneumonia

A

F. Streptococcus pneumonia

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31
Q

What is the most commonly affected region in Pott’s Disease?

A

Thoracic spine

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32
Q

Which of the following is least likely true of mycobacterium tuberculosis spine involvement?
a. It spreads via hematogenous route to the vertebral bodies
b. Spinal disease starts at the spinous process.
c. Infectious process later spreads to the central part of the vertebral body and intervertebral disk
D. With progression of the infection there is disruption of the bone and the intervertebral spaces

A

B. Spinal disease starts at the anterior region of the vertebral bodies, not at the spinous processes.

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33
Q

What is the tropism of Mycobacterium leprae?

A

Tropism toward peripheral nerves (Schwann cell), especially in cooler areas of the body.

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34
Q

What are the 2 variants of Leprosy?

Give some differentiation

A

Lepromatous variant

  • occurs in impaired cell-mediated immunity
  • systemic symptoms;

Tuberculoid Variant

  • may occur in patients with good cellular immunity
  • skin lesions are better localized
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35
Q

What is the histopathologic finding of Leprosy?

A

demonstrating inflammatory granulomas with epithelioid and mononuclear infiltrates and acid-fast organisms.

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36
Q

What are the most commonly affected nerves in leprosy?

A
Ulnar Nerve (most common)
Greater Auricular Nerve
Radial Nerve
Common Peroneal Nerve
Sural Nerve
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37
Q

What is the appropriate treatment for Neisseria meningitides?

A

Penicillin G (Procaine and Probenicid) IV 18-24 million units per day (3-4 millions units q4) for 10-14 days

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38
Q

What is the appropriate treatment for Streptococcus pneumoniae?

A

vancomycin and ceftriaxone, and the duration of treatment is between 10 and 14 days.

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39
Q

What is the appropriate treatment for Listeria monocytogenes?

A

extremes of age (younger and older) and in immunocompromised patients, should be treated with ampicillin for more than 21 days

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40
Q

What is the appropriate treatment for Haemophilus influenzae?

A

β-lactamase negative- ampicillin

β-lactamase positive- third-generation cephalosporin

41
Q

What are the different stages of brain abscess?

A

initial cerebritis

  • first few days, then the formation of central necrosis with surrounding vasogenic edema
  • formation of a capsule The abscess eventually matures, with the development of collagenous tissue in the capsule and regression of the vasogenic edema.
42
Q

What is the treatment for brain abscess?

A

requires drainage of the abscess in combination with intravenous antibiotics
(third-generation cephalosporin (for streptococci and gram-negative bacilli), metronidazole (for anaerobes), and vancomycin (for staphylococci). The IV antibiotic regimen is continued for 6 to 8 weeks.

43
Q

What is the histopathologic finding of tuberculous meningitis?

A

demonstrates a granulomatous inflammatory response with multinucleated giant cells and caseating necrosis

44
Q

How to identify primary syphillis? What is the manifestation?

A

Primary syphilis is characterized by the development of a painless chancre at the site of entry (genital region). There is asymptomatic systemic spread of the organism, and the chancre eventually disappears.

45
Q

How to identify secondary syphillis? What is the manifestation?

A

Secondary syphilis develops approximately 2 to 12 weeks after the exposure, with manifestations of systemic dissemination, including constitutional symptoms, lymphadenopathy, and rash (classically palms and soles). Syphilitic meningitis and cranial neuropathies may occur in this second stage.

46
Q

How to identify tertiary syphillis? What is the manifestation?

A

Tertiary syphilis is characterized by cardiovascular complications (such as aortitis), gummatous complications, and neurologic complications.

47
Q

50/female wiht abdominal pain, diarrhea, and weight loss. She complains of arthritis, cutaneous hypopigmentation, adrenal insufficiency. She presented with meningitis. Gastrointestinal biopsy demonstrating periodic acid Schiff-positive macrophage inclusions. Diagnosis?

A

Whipple Disease caused by Tropheryma whippelii

48
Q

What is the treatment for Whipple Disease?

A

Intravenous ceftriaxone for 2 weeks, followed by a prolonged course of trimethoprim-sulfamethoxazole is the treatment of choice.

49
Q

What are the neuroimaging findings in CJD?

A

restricted diffusion of the cortex (cortical ribboning) and the head of the caudate
bilateral signal hyperintensity in both thalami (pulvinar sign and in in the anterior portions of the putamen (Caudate and anterior putamen hyperintensity –> “hockey-stick sign”)

50
Q

What is the main risk factor in developing tertiary syphilis?

A

occurs if syphilis in its primary stages is untreated and the spirochete invades the CNS

51
Q

Nontreponemal tests: Venereal Disease Research Laboratory (VDRL) test and the Rapid Plasma Reagin test are specific but not sensitive. True or False?

A

FALSE. These tests are more sensitive but less specific than treponemal tests.

52
Q

What is the treatment for Neurosyphilis?

A

First choice is penicillin G 4 million units every 4 hours for 14 days.

Antibiotic therapy may clear the infection; however, it may not reverse already established neurologic manifestations of tertiary syphilis.

53
Q

What are the affected areas of HSV Encephalitis?

A

orbitofrontal and temporal regions

54
Q

What is the treatment of HSV Encephalitis?

A

intravenous acyclovir 10 mg/kg every 8 hours (30mg/kg/day) should be started as soon as possible and continued for a minimum of 14-21days

55
Q

What are the 4 major neurologic syndromes of measles?

A
  • Acute encephalitis.
  • Postviral encephalomyelitis.
  • Measles inclusion body encephalitis, which occurs in patients with cell-mediated immunodeficiency, 1 to 6 months after measles exposure. It is characterized by a rapidly progressive dementing process with seizures, myoclonus, mental status changes, and coma.
  • SSPE, which is caused by defective measles virus maturation in neural cells.
56
Q

What is the EEG finding of SSPE?

A

periodic slow-wave complexes at regular intervals and a background of depressed activity.

57
Q

What is the imaging finding (MRI) of SSPE?

A

hyperintensity in the gray and subcortical white matter more in the posterior regions

58
Q

What is the histopathologic finding of Aspergillosis?

A

hyphae are detected in blood vessels, with the findings of necrosis, hemorrhage, and inflammation.

Gomori methenamine silver stain demonstrating septate hyphae that branch at acute angles

59
Q

What causes neuroscysticercosis? What is treatment of choice?

A

Pork tapeworm (Taenia solium)

The treatment of choice is albendazole.

60
Q

What is most commonly affected region by herpes zoster?

A

mid-thoracic region

61
Q

What VZV variant, at which the patient experiences the sensory symptoms without the rash

A

Zoster sine herpete

62
Q

Which is involved in Herpes Zoster Ophthalmicus?

A

ophthalmic division of the trigeminal nerve

63
Q

Which is involved in Ramsay-Hunt Syndrome? What is the presentation?

A

geniculate ganglion involvement.

Characterized by facial palsy combined with herpetic rash in the external auditory meatus, sometimes with vertigo, tinnitus, and deafness

64
Q

Which vessels are commonly affected in VZV Vasculopathy?

A

VZV vasculopathy is a multifocal disease and affects small and large intracranial vessels.

65
Q

What is commonly involved in mycotic aneurysm?

A

exact mechanism of formation of mycotic aneurysms is not well known,

but it is likely that they form secondary to septic emboli involving distal vessels, affecting their vasa vasorum, with destruction and weakening of the arterial wall and subsequent aneurysmal dilatation

66
Q

What is the neuropathologic findings in rabies?

A

characteristic cytoplasmic eosinophilic inclusions known as Negri bodies, which are found mainly in Purkinje cells and pyramidal cells of the hippocampus

67
Q

After an animal bite, how is vaccine rabies given?

A

After exposure, 2 vaccines given:

  1. HDCV (human diploid cell vaccine) on days 0, 3, 7, 15 and 28.
  2. human rabies immunoglobulin (20 IU/kg) as soon as possible, at least half of the dose around the wound and the rest intramuscularly.
68
Q

Buzzwords

Erythema chronicum migrans
Bilateral Facial palsies

A

Lyme Disease

69
Q

Buzzwords

AIDS and MRI showing ring-enhancing mass with edema

A

CNS Toxoplasmosis and CNS Lymphoma

70
Q

Buzzwords

AIDS with mass lesions and positive EBV in PCR

A

Primary CNS Lymphoma

71
Q

Buzzwords

AIDS with multiple nonenhancing lesions in the parieto-occipital lobe.
Pathology: Myelin loss with giant astrocytes and altered oligodendrocytes with enlarged nuclei and viral inclusions.
Spaghetti and meatballs on electron microscopy

A

Progressive multifocal leukoencephalopathy

72
Q

Buzzwords

Hypopigmented lesions an enlarged peripheral nerves

A

Mycobacterium leprae

73
Q

What is the management of Lyme disease (Central or Peripheral Nervous System Implications)?

A

If with central or peripheral Nervous System implications:
• Ceftriaxone 2g IV x 4 weeks
• Allergic to IV drugs: Tetracycline 500mg QID x 30 days
cefotaxime 2g IV q8; Penicillin G 18-20 million units per day in divided doses Q4

74
Q

This is the simplest method of demonstrating the presence of subdural effusion.

A. Asymmetric Pupils
B. Transillumination of Skull
C. Tachycardia
D. Hemiparesis

A

B. Transillumination of the Skull

75
Q

Bacterial Meningitis presents with seizure. What is the possible organism?

A. Haemophilus influenzae
B. Streptococcus pnenumoniae
C. Meningococcal meningitis
D. Pseudomonas aeruginosa

A

A. Haemophilus influenzae

76
Q

The alcoholic patient presented with bacterial meningitis. What is the possible organism?

A. Haemophilus influenzae
B. Streptococcus pnenumoniae
C. Meningococcal meningitis
D. Pseudomonas aeruginosa

A

B. Streptococcus pnenumoniae

77
Q

Which of the following does not belong?

A. Anthrax meningitis
B. Pneumococcal meningitis
C. Amebic Meningoencephalitis
D. Ebola Virus Encephalitis

A

B. Pneumococcal meningitis

Explanation:
All may present with substantial hemorrhage or substantial numbers of RBC in CSF.

78
Q

Which of the following does indicates CSF rhinorrhea?

A. Low glucose, low protein, present B2-transferrin
B. High glucose, low protein, present B2-transferrin
C. High glucose, high protein, present B2-transferrin
D. Low glucose, high protein, present B2-transferrin

A

B. High glucose, low protein, present B2-transferrin

79
Q

Which is not true of prophylaxis for bacterial meningitis?

A. Single dose Rifampin 600mg may be given
B. Single dose Ciprofloxacin 200mg may be given
C. Daily oral dose of Rifampin 600mg BID x 2 days
D. If 2 weeks or more from exposure, no prophylaxis needed.

A

A. Single dose Rifampin 600mg may be given

80
Q

In tabes dorsalis, which is not correct explanation for each symptomatology?

A. Hypotonia, Areflexia & Ataxia are due to destruction of proprioceptive fibers in the sensory roots
B. Hypotonia and insensitivity of the bladder are caused by deafferentation at L12-S1 level
C. Impotence and obstipation is due to deafferentation at S2-S3 levels
D. Lightning pains and visceral crises are due to incomplete posterior root lesions at different levels
E. Charcot joints due to partial loss of A and C fibers

A

B. Hypotonia and insensitivity of the bladder are caused by deafferentation at L12-S1 level
(S2 and S3 level)

81
Q

What is the most common sporadic cause of encephalitis?

A. Arbovirus
B. Enterovirus
C. Herpes Simplex Virus
D. HHV-6

A

C. Herpes Simplex Virus

82
Q

This virus is related with Parkinsonian Syndrome as a neurologic sequelae.

A. Flavivirus
B. Enterovirus
C. Herpes Simplex Virus
D. HHV-6

A

A. Flavivirus

83
Q

Which of the following is not true with the histopathologic finding of Arbovirus Encephalitis?

A. Presence of perivascular cuffing by lymphocytes or mononuclear leukocytes and plasma cells
B. Brainstem is usually involved
C. Patchy infiltration of meninges
D. Widespread degeneration of single nerve cells with neuronophagia

A

B. Brainstem is usually involved

84
Q

Which of the following is the histopathologic hallmark of Viral Encephalitis?

A. Presence of perivascular cuffing by lymphocytes or mononuclear leukocytes and plasma cells
B. Brainstem is usually involved
C. Patchy infiltration of meninges
D. Widespread degeneration of single nerve cells with neuronophagia

A

C. Patchy infiltration of meninges

85
Q

Herpes Simplex Virus become latent in this region.

A. Cervical Ganglia
B. Trigeminal Ganglia
C. Geniculate Ganglia
D. Scarpa’s Ganglia

A

B. Trigeminal Ganglia

86
Q

Buzzword

Cowdry Type A

A

HSV encephalitis

87
Q

Presence of intranuclear eosinophilic inclusions in neurons is a characteristic of this viral infection.

Diagnosis and what is this eponym of this inclusion?

A

HSV Encephalitis

Cowdry Type A

88
Q

In rabies, what is the implication of tingling numbness at the site of the bite?

A. Virus reaches sensory ganglion
B. Due to involvement of tegmental area
C. Virus directly affects the anterior horn cells
D. Due to direct damage on the distal regions of peripheral nerves

A

A. Virus reaches sensory ganglion

89
Q

In rabies, what is the implication of dyaphagia, spasm of throat muscles induced by swallowing water, dysarthria?

A. Virus reaches sensory ganglion
B. Due to involvement of tegmental medullary nuclei
C. Virus directly affects the anterior horn cells
D. Due to direct damage on the distal regions of peripheral nerves

A

B. Due to involvement of tegmental medullary nuclei

90
Q

Buzzword

Eosinophilic intranuclear inclusions
Viral

A

Cowdry Type A

HSV Encephalitis

91
Q

Buzzword

Eosinophilic intracytoplasmjc inclusions
Viral

A

Negri Bodies

Rabies

92
Q

Where is the least location of Negri Bodies?

A. Purkinje cells
B. Pyramidal cells of the frontal region
C. Pyramidal cells of hippocampus
D. None of the above

A

B. Pyramidal cells of the frontal region

93
Q

What is the antiviral treatment for Herpes Simplex Virus CNS Infection?

A

Acyclovir IV 30mg/kg/day for 14-21 days

10mg/kg every 8hrs

94
Q

What is the antiviral treatment for VZV CNS Infection?

A

Intravenous Acyclovir 10-15mg/kg every 8hrs for 10-14days

95
Q

Identify antibiotics.

Which of the following inhibits transpeptidation?

A. Ampicillin
B. Ceftriaxone
C. TMP-SMX
D. Chloramphenicol

A

A. Ampicillin

96
Q

Identify antibiotics.

Antibiotics that inhibit protein synthesis. It binds to 30s ribosomal subunit.

A. Ampicillin
B. Aminoglycosides
C. TMP-SMX
D. Chloramphenicol

A

B. Aminoglycosides

97
Q

Identify antibiotics.

Antibiotics that inhibit protein synthesis. It binds to 50s ribosomal subunit.

A. Ampicillin
B. Aminoglycosides
C. TMP-SMX
D. Chloramphenicol

A

D. Chloramphenicol

98
Q

Identify antibiotics.

Inhibition of DNA gyrase (DNA Topoisomerase II) is the mechanism of action.

A. Fluoroquinolones
B. Aminoglycosides
C. TMP-SMX
D. Chloramphenicol

A

A. Fluoroquinolones

99
Q

Identify antibiotics.

Inhibits dihydrofolate reductase, preventing the production of tetrahydrofolate and dihydrofolate.

A. Fluoroquinolones
B. Aminoglycosides
C. TMP-SMX
D. Chloramphenicol

A

C. TMP-SMX