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Infectious Disease > Virals > Flashcards

Virals Flashcards

1
Q

What is HSV I associated with?

A

Oral cold sores

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2
Q

What does HSV 2 cause?

A

Genital herpes

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3
Q

What is the herpes virus that causes Kaposi’s sarcoma?

A

HSV-8

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4
Q

True or false: EBV is a herpes virus

A

True

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5
Q

True or false: CMV is a herpes virus

A

True

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6
Q

What is the genetic makeup of herpesviridae viruses?

A

dsDNA

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7
Q

Where do herpes viruses become latent?

A

Ganglions of sensory or autonomic nerves

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8
Q

What is the route of transmission for herpes viruses?

A

Exposure to virus at the skin or mucus membranes

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9
Q

What is the mechanism of transport for herpes viruses into and out of the ganglion?

A

intra axonal transport

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10
Q

Which more commonly reactivates: HSV-1 or HSV-2?

A

HSV1

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11
Q

True or false: transmission of herpes can only occur when there is an outbreak of vesicular lesions

A

False-viral shedding periods as well

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12
Q

What is the protein that does anterograde transport out of the neuron? Retrograde?

A 
Anterograde = kinesin
Retrograde = dynein
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13
Q

True or false: HSV-1 and HSV-2 can cause lesions at any site

A

True

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14
Q

Are primary or secondary s/sx of HSV more symptomatic?

A

Primary

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15
Q

How long do primary HSV lesions usually last for?

A

10-14 days (or longer)

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16
Q

What are the prodromal ssx of HSV reactivation? How long do these recurrences last for?

A

pain, burning, tingling, and pruritus

3 days-ish

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17
Q

What are the oro-facial ssx that can present with HSV-1 infections, besides herpes labialis?

A
  • Gingivostomatitis
  • Eczema herpeticum
  • erythema multiforme
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18
Q

What are the s/sx that are associated with primary HSV-2 infections, besides the vesicular lesions of the genitalia?

A

Fever
HA
Malaise
myalgias

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19
Q

What are the s/sx of HSV proctitis?

A

Anorectal pain, discharge and tenesmus

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20
Q

Does HSV-1 or HSV-2 cause herpetic whitlow?

A

Both

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21
Q

What is Herpetic gladiatorum?

A

Herpes infection of the forearm, usually 2/2 wrestling

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22
Q

Why is herpetic eye infections an emergency?

A

Threaten sight

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23
Q

What are the strains of HSV that can cause necrotizing retinitis?

A

HSV or VZV

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24
Q

What is herpes simplex encephalitis?

A

Aseptic encephalitis caused by HSV–emergency

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25
Q

What are the CT findings of herpes encephalitis?

A

Temporal lobe enhancement

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26
Q

What is Mollaret syndrome?

A

Occasionally recurrent meningitis associated with reactivation of HSV

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27
Q

What is the survival rate of a pt who presents with HSV encephalitis with a GCS of less than 6?

A

Nearly 0%

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28
Q

Which has a worse prognosis: HSV encephalitis or meningitis?

A

Encephalitis

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29
Q

What are the s/sx of transverse myelitis caused by herpes?

A

Sacral-autonomic dysfunction

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30
Q

What cranial nerve can often be affected with HSV?

A

CN V (bell’s palsy)

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31
Q

What are the common visceral infections of HSV?

A
  • Esophagitis

- Tracheitis

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32
Q

What immunocompromised patients are particularly susceptible to HSV recurrences?

A

Hematological malignancies, especially if on CD20 inhibitors (B cell lymphomas/leukemias)

33
Q

How do you diagnose HSV infections?

A

Clinical picture + PCR or culture

34
Q

What are the drugs that are used to treat herpes infections?

A

Acyclovir
Foscarnet
Ganciclovir

35
Q

What is the MOA of acyclovir? HOw is this administered?

A

COnverted by thymidylate kinase, to then inhibit DNA polymerases

PO administration

36
Q

What is the MOA of foscarnet? HOw is this administered?

A

a structural mimic of the anion pyrophosphate that selectively inhibits the pyrophosphate binding site[citation needed on viral DNA polymerases at concentrations that do not affect human DNA polymerases.

IV administration

37
Q

What is the MOA of ganciclovir?

A

synthetic analogue of 2′-deoxy-guanosine. It is first phosphorylated to ganciclovir monophosphate by a viral kinase encoded by CMV.

This goes on to inhibit dGTP incorporation into DNA via DNA polymerases

38
Q

What is the main MOA of resistance of HSV to acyclovir?

A

Lack of thymidine kinase

39
Q

What is the major side effect of foscarnet?

A

Marrow suppression

40
Q

What are the topical agents used for HSV eye infections?

A

Idoxuridine
Trifluridine
Vidarabine

41
Q

True or false: VZV infections in adults is usually more severe than in children

A

true

42
Q

When is VZV no longer contagious?

A

When the vesicles have crusted over

43
Q

What is the characteristic of VZV lesions that is pathognomonic?

A

Vesicles are in all different stages

44
Q

What is the incubation period for VSV?

A

10-21 days

45
Q

What is the main complication of VZV infection?

A

Coinfection with staph or strep

46
Q

Can VZV cause encephalitis?

A

Yes

47
Q

What is the most common visceral involvement of VZV?

A

Pneumonia

48
Q

What is the mortality rate of VZV pneumonia that requires ventilation?

A

50%

49
Q

What are the risk factors for VZV pneumonia?

A

Smoking
Pregnant
Immunosuppression

50
Q

What is the treatment for VZV?

A

Acyclovir, but need higher doses than other HSV infections

51
Q

What is the difference of using acyclovir for VZV than for other HSV infections?

A

Need a higher dose sooner, since VZV is less susceptible to the drug

52
Q

Is it okay to give the varicella vaccine to immunocompromised patients?

A

No

53
Q

Is the VZV vaccine good for post-exposure prophylaxis?

A

Yes

54
Q

What are the spinal segments that are commonly associated with VZV reactivation?

A

T3-L3

55
Q

What is the major ophthalmic concern with VZV reactivation?

A

Herpes zoster ophthalmicus or retinal necrosis

56
Q

What is Ramsey-Hunt syndrome?

A

facial paralysis and hearing loss 2/2 VZV reactivation

57
Q

How do you diagnose zoster?

A

PCR, but tzanck smear too

58
Q

When should treatment for zoster be initiated? Why?

A

Within 72 hours–only affects the incidence of postherpetic neuralgia

59
Q

Do steroids affect the outcome of zoster?

A

Nah

60
Q

What is the most common presentation of EBV infection?

A

Subclinical viral infection–not usually mono

61
Q

How is EBV unlike other VZV infections?

A

Transforms its host cells–does not have a cytopathic effect

62
Q

True or false: asymptomatic shedding of EBV is common

A

True

63
Q

What are the classic s/sx of EBV? (4)

A

Fever
LAD
Exudative pharyngitis
Splenomegaly

64
Q

What is the incidence of a rash in EBV infected patients if they are given Ampicillin?

A

90-100%

65
Q

How long does EBV usually last?

A

3 weeks

66
Q

What virus can cause or predispose to Guillain-Barre syndrome?

A

EBV

67
Q

What is the cause of BUrkitt’s lymphoma?

A

EBV

68
Q

What are the malignancies that EBV can cause?

A
  • Lymphoproliferative disorders
  • Nasopharyngeal CA
  • T-cell lymphoma
69
Q

How do you diagnose EBV infections? (3)

A
  • Heterophile abs
  • IgG or IgM
  • PCR
70
Q

What is the treatment for EBV?

A
  • Supportive
  • Avoid contact sports
  • Acyclovir iff active infection
71
Q

How is CMV transmitted?

A

Sexual

Transplants

72
Q

What are the classic histological characteristics of CMV infections?

A

Owl-eyed cells (large cells)

73
Q

What are the s/sx of CMV mononucleosis?

A

Exudative pharyngitis and cervical LAD

74
Q

What is the most common pathogen that complicates transplants?

A

CMV

75
Q

Who is prophylaxis for CMV given to?

A

Immunocompromised hosts

76
Q

How do you diagnose CMV infections?

A

PCR

77
Q

What are the histological characteristics of CMV infections?

A

Intranuclear inclusions

78
Q

What is the treatment for CMV?

A

Ganciclovir/valganciclovir

Foscarnet

Infectious Disease (18 decks)

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