Lec 30 Herpes and Varicella Flashcards

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1
Q

What are the common characteristics of herpes viruses – viral characteristics, transmission, who gets it?

A
  • large enveloped double strand DNA
  • ubiquitous [except HHV 8]
  • chronic/latent infection follows acute
  • reactivations common
  • most transmitted during asymptomatic shedding by close contact [except varicella]
  • important in immunocompromised especially with CMI [cell mediated immunity] deficiency
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2
Q

Mech of injury of herpes viruses?

A
  • direct cell damage [lytic phase]
  • immune reaction
  • malignant transformation
  • suppress immune system
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3
Q

What is life cycle of herpes virus?

A
  • attachment by fusion, DNA to nucleus
  • immediate early protein synthesis: proteins produced that regulate rest of viral replication, latent viruses remain in this stage
  • early protein synthesis: genome replicated by viral DNA pol
  • late prot synthesis: viral particles assemble
  • release: exocytosis or lysis
  • cell to cell spread [formation giant cells]
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4
Q

What is acyclovir?

A

herpes DNA pol inhibitor
requires phosphorylation by viral thimydine kinase, results in chain termination
acyclovir needs to be activated by herpes thymidine kinase
- resistance if pt has herpes thymidine kinase doesn’t function

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5
Q

What is pathogenesis of HSV 1 and 2?

A
  • entry via break in skin, mucosa
  • —- HSV 1 = mouth, HSV 2 = genital
  • lesions form at site of entry from lytic phase in epithelial cell
  • virus travels through sensory neurons and becomes latent in sensory ganglia
  • — geniculate [HSV 1] or dorsal root [HSV 2]
  • reactivation by triggers including: stress, immunosuppression, intercurrent illness
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6
Q

What is the Tzanck test?

A
  • diagnostic test for herpes
  • scrape lesion at mouth/genitals and look under microscope
  • look for multinucleated giant cells
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7
Q

Where does HSV1 infection occur? In who?

A

more commonly oral

in children and adults

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8
Q

Where does HSV2 infection occur? in who?

A

more commonly genital

mostly in adults

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9
Q

How are HSV1/2 transmitted?

A
  • by direct close contact

- often have have asymptomatic shedding

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10
Q

What are symptoms of HSV1/2?

A
  • most infections asymptomatic
  • crops of painful, small blisters and ulcers in skin and mucous membranes
  • can be oral, genital, in conjunctiva
  • whitlow [in finger], other body sites
  • eczema herpeticum
  • encephalitis
  • occassionally disseminates internally –> usually neonates or immunocompromised
  • can cause bells palsy
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11
Q

Can you get recurrences of HSV1/2?

A

yes but they are less severe

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12
Q

Who gets HSV encephalitis? when?

A
  • immunocompetent or immunocompromised

- year round [in contract to enterovirus mosquito-borne encephalitis]

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13
Q

What are findings of skin, eye, mouth HSV in neonate?

A
  • onset at 7-14 days

- have vesicles, conjunctivitis

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14
Q

What are findings of CNS HSV in neonate?

A
  • onset at 14-21 days

- seizures, lethargy, irritability, fever

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15
Q

What are findings of disseminated HSV in neonate?

A
  • onset at 5-10 days

- hepatitis, resp distress, shock, DIC

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16
Q

How do you diagnose HSV?

A
  • viral culture [not good for CSF]
  • DFA of skin lesion
  • PCR on CSF
  • Tzanck smear [less sensitive/specific]
17
Q

What is treatment for herpes?

A
  • oral acyclovir, valacyclovir

- for serious: IV acyclovir

18
Q

What is valcyclovir?

A

prodrug of acyclovir that is converted in body

better absorbed than acyclovir

19
Q

What are adverse events for acyclovir?

A
  • kidney disfunction [prevent with hydration]
20
Q

What is mech of resistance to acyclovir?

A

mutation in viral TK [most common
mutation in DNA pol
very rare, usually in immunocompromised

21
Q

How do you treat acyclovir resistant HSV?

A

foscarnet

22
Q

What is mech of foscarnet action? administration? side effects?

A

mech: pyrophosphate that inhibits viral DNA pol
administration: IV
side effects: nephrotoxic, hypo/hypercalcemia, hypo/hyperphosphatemia

23
Q

When do you use prophylactic valacyclovir?

A
  • in patients with frequent symptomatic recurrences [AIDS]
  • in pregnant women with recurrent HSV –> decreases shedding in genital secretions, also do C section to prevent fetal transmission
  • in transplant recipients at risk for severe disease
24
Q

What is pathogenesis of varicella?

A
  1. infection of mucosa or URI
  2. viral replication in regional lymph nodes
  3. primary viremia/incubation period
  4. viral replication in liver, spleen, other
  5. secondary viremia
  6. fever
  7. infection of skin, get vesicular rash
25
Q

In what stages of disease is varicella contagious?

A

contagious during secondary viremia, fever stage that follows, and for early part of rash [days 11-17]
== prior to onset of symptoms

26
Q

What is primary infection of varicella zoster? reactivation?

A
primary = chickenpox
reactivation = zoster [shingles]
27
Q

Where is the latency site of varicella zoster?

A

sensory/dorsal root ganglia

28
Q

How is varicella zoster spread?

A

varicella highly contagious

varicella: spread via respiratory droplets and aerosols and contact
zoster: just spread via contact

29
Q

What are complications of varicella?

A
  • bacterial superinfection
  • adults have worse disease than children
  • in immunocompromised/perinatal get: hepatitis, pneumotitis, prolonged rash, encephalitis
30
Q

What are complications of zoster?

A
  • post herpetic neuralgia [most common]
  • keratitis
  • disseminated disease in immunocompromised pts
31
Q

What is treatment for VZV?

A
  • acyclovir or valacyclovir [higher dose than HSV]

- forscarnet for resistant strains

32
Q

How do you prevent VZV?

A
  • live attenuated vaccine

- varicella zoster Ig for higher risk hosts who are exposed