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Repro Images + Micro > HSV 1&2 > Flashcards

HSV 1&2 Flashcards

1
Q

What is going on with the HSV when is it latent?

A

Its genome, but not progeny, exist in trigeminal and/or sacral ganglia; only gene expressed is LAT

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2
Q

What is going on with the HSV when is it reactivated?

A

It produces progeny that infect epithelial cells innervated by the latently-infected neurons

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3
Q

4 herpesviruses that are sexually transmitted

A

HSV 1, HSV 2, CMV, KSHV

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4
Q

(T/F): Acyclovir is the curative treatment of choice for HSV-1 and HSV-2 that works by terminating chain elongation.

A

False - No herpes treatments are curative! The rest of the statement is true.

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5
Q

How does HSV get into cells?

A

Direct fusion with the plasma membrane in a pH-INDEPENDENT manner

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6
Q

Immediate early genes

A

Transcription factors that switch host RNA polymerase to preferential viral gene transcription

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7
Q

Early genes

A

Proteins needed for replications

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8
Q

Late genes

A

Structural proteins

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9
Q

Two important HSV early genes

A

Thymidine kinase, DNA polymerase

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10
Q

Where does HSV replicate?

A

Nucleus of epithelial cells

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11
Q

Thymidine kinase mutants are particularly prevalent in what population?

A

AIDS patients with concurrent HSV infx

causes ACV resistance

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12
Q

Where does HSV assembly occur? Why do we care?

A

Nucleus; forms nuclear inclusion bodies (vacuoles with bugs in them) that are diagnostic

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13
Q

Describe the pathogenesis of the multinucleated giant cells seen in Tzanck smears

A

Same viral glycoproteins that allow HSV to fuse with plasma membranes are expressed on the membrane late in infection, allowing the infected cell to fuse with neighboring cells

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14
Q

What type of cells are visualized with Tzanck smears?

A

Epithelial cells; virus only produces glycoproteins when it’s replicating, and it only replicates in epithelial cells

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15
Q

Function of only HSV gene produced during latency?

A

LAT = produces RNA that silences some cellular genes to prevent apoptosis of the infected cell

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16
Q

Is HSV enveloped?

A

YES! (think: it has to fuse with plasma membrane)

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17
Q

If the HSV genome is observed to be extrachromosomal, what is happening?

A

Latency

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18
Q

HSV 1 or 2: cervicitis

A

2

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19
Q

HSV 1 or 2: encephalitis

A

1

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20
Q

HSV 1 or 2: meningitis

A

2

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21
Q

HSV 1 or 2: herpetic whitlow

A

1

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22
Q

HSV 1 or 2: keratitis

A

2

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23
Q

HSV 1 or 2: penile/vulvar vesicles

A

2

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24
Q

HSV 1 or 2: gingivostomatitis

A

1

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25
Q

HSV 1 or 2: herpes labialis

A

1

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26
Q

Who gets disseminated herpes upon reinfection?

A

Immunocompromised patients

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27
Q

Who gets disseminated herpes upon primary infection?

A

Neonates (think eczema herpeticum)

28
Q

A patients present with small penile vesicles that he has never had before. If this is a primary HSV 2 infection, when did he most likely contract the virus?

A

2 weeks ago

29
Q

Why are recurrent HSV infections shorter than primary infections?

A

Neutralizing antibodies developed after the primary infection will be present

30
Q

Primary oral HSV 1 or 2

A

Gingivostomatitis

31
Q

Recurrent oral HSV 1 or 2

A

Herpes labialis

32
Q

Manifestation of primary HSV 1 or 2 infection in females

A

Internal or external vesicles, mucopurulent cervicitis, vaginitis, rarely urethritis

33
Q

Pattern of recurrence in HSV 2 infections

A

More frequent soon after primary infection then diminish in frequency over time

34
Q

More frequent recurrence: HSV 1 or HSV 2 genital lesions

A

HSV 2

35
Q

Genital HSV prodrome

A

Flu-like sx, itching/burning in infected areas, leg/buttocks muscle aches

36
Q

Cause of HSV encephalitis in neonates

A

Primary HSV 2

37
Q

Cause of HSV encephalitis in adults

A

Recurrent HSV 1

38
Q

Sx of HSV encephalitis

A

Fever, HA, confusion, seizures

39
Q

70% mortality if untreated

A

Herpes encephalitis

40
Q

Cause of HSV meningitis

A

Primary HSV 2

41
Q

Incidence of HSV meningitis

A

10% of primary HSV 2 infections

42
Q

Sx of HSV meningitis

A

HA, stiff neck, fever, vomiting

43
Q

Mortality of HSV meningitis

A

Usually resolves in 1 week

44
Q

You were worried that your OB patient with a primary HSV 2 infection may transmit the virus during delivery despite ACV treatment (C/S was contraindicated). A couple days after delivery the mother states she is relieved that her baby didn’t get the virus as he has not developed any herpetic signs. You inform her that:

A

Neonatal herpes doesn’t present until 1-2 weeks after delivery and the infant has a 30% chance of being infected so be on the lookout for a rash

45
Q

75% morbidity/mortality

A

Severe neonatal herpes

46
Q

Manifestations of neonatal herpes

A

Zoster-form rash, encephalitis, disseminated infection leading to organ failure

47
Q

More common: adult or neonatal HSV encephalitis

A

Neonatal

48
Q

You notice your OB patient has a primary HSV infection at the time of labor. What do you do?

A

C-section!

49
Q

Rate of transmission of primary HSV infection during delivery

A

30%

50
Q

Rate of transmission of secondary HSV infection during delivery

A

2-3%

51
Q

Incidence of neonatal HSV transmitted transplacentally

A

5%

52
Q

Incidence of neonatal HSV transmitted during vaginal delivery

A

95%

53
Q

Dx of oral herpes

A

Clinical

54
Q

Dx of genital herpes

A
  1. Culture and look for cytopathic effect
  2. Fluorescent antibody screening of virus culture
  3. PCR
  4. Tzank smear
  5. Serology to detect anti-glycoprotein G Abs
55
Q

Which diagnostic tests for genital herpes can differentiate between HSV 1 and HSV 2?

A

PCR and serology

56
Q

Which diagnostic test for genital herpes only tells you the patient has had a herpes infection at some point and why?

A

Serology; you’re detecting anti-glycoprotein G Abs, so you know patient was exposed to HSV at one point but not that there is an active infection

57
Q

Dx keratitis

A

Slit lamp to look for corneal damage

can you tell apart syphilis from HSV?

58
Q

Dx HSV meningitis

A

Culture CSF to look for cytopathic effect

59
Q

Main point of diagnosing HSV meningitis

A

Rule out bacterial meningitis, which is more severe than the self-resolving aseptic (viral) meningitis

60
Q

Dx HSV encephalitis

A

PCR + Southern blot of CSF

EEG to rule it out if normal

61
Q

Tests that are no good for dx HSV encephalitis

A
  1. Culture of CSF - rarely positive

2. Antibody tests - don’t develop for 1-2 weeks and need to treat ASAP

62
Q

Dx disseminated HSV in neonate

A

Liver enzymes + other diagnostic methods mentioned

63
Q

Rules out HSV encephalitis

A

Normal EEG

64
Q

Why does ACV not attack host DNA polymerase?

A

The first phosphate must be added by viral thymidine kinase

65
Q

DOC for ACV treatment failure

A

Foscarnet because it doesn’t have to be phosphorylated

Repro Images + Micro (16 decks)

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