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Stage 2: Inflammation > Varicella Zoster > Flashcards

Varicella Zoster Flashcards

1
Q

Describe the VZV virus

A
  • dsDNA
  • Enveloped
  • Part of alpha herpesviridae family (like HSV)
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2
Q

What does primary VZV infection cause?

A

Chickenpox (varicella)

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3
Q

Where does VZV lie latent and why?

A

Dorsal root/cranial nerve ganglia - gets into nerve root from lesions in skin and travels to these areas

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4
Q

What does reactivation of VZV cause?

A

Shingles (zoster)

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5
Q

What happens during VZV reactivation?

A
  • The virus travels down sensory nerves and produces painful vesicles in the area of skin served by the infected ganglion
  • When it is travelling down the nerve it can’t be reached by T cell response
  • More likely to get reactivation with T cell deficiency
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6
Q

What is the incubation period of varicella?

A

10-21 days

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7
Q

What symptoms occur in the prodrome of the the disease?

A

Fever, pharyngitis, malaise

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8
Q

Describe the lesions in varicella

A
  • Itchy and painful
  • Appear in crops
  • Macule to papule to vesicle (blister) to pustule (yellow) to crusts
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9
Q

In what kind of patient is varicella more severe?

A

Adults and immunocompromised

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10
Q

What does more lesions indicate?

A

Higher viral load

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11
Q

How do you get the best sample?

A

Push the base of the lesion with the swab as there are more cells at the base of the lesion

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12
Q

What are possible complications of varicella?

A

1) Severe/haemorrhagic varicella
2) Pneumonia (adults)
3) Acute cerebellar ataxia (children)
4) Encephalitis
5) Secondary bacterial infection

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13
Q

When is someone with varicella no longer infectious?

A

When all the lesions have crusted over

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14
Q

When are you infectious with varicella?

A

From 48h before the rash until all lesions are crusted

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15
Q

Can you be asymptomatic with varicella?

A

Yes

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16
Q

Describe memory immunity of varicella

A
  • After naturally acquired VZV infection there is persistence of VZV IgG and IgA as well as VZV CD8 and CD4 cells
  • Adaptive T cell response is needed to prevent/control symptomatic reactivations of endogenous VZV (booster response when encounter someone with chickenpox)
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17
Q

What are the clinical features of zoster?

A
  • Pain at site may precede eruption of painful vesicles

- Unilateral + 1-2 dermatomes involved (if immuno compromised might get multi-dermatomal shingles)

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18
Q

Why does an immunocompetent individual rarely suffer at most 2 attacks decades apart during a lifetime?

A

Bc shingles itself is a boost to VZV immunity so unlikely to get it soon after another one

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19
Q

What are three complications of zoster?

A

1) Involvement of eye in 50%, ophthalmic division of trigeminal nerve, indicated by lesion on top of nose (need to see ophthalmologist)
2) Post-herpetic neuralgia - chronic pain that continues after rash has cleared (weeks-years after) in same area as rash
3) Acute retinal necrosis PORN - can spread to both eyes and cause blindness

20
Q

What does incidence of PHN increase with?

A

Age

21
Q

What groups are more likely to get zoster?

A

Old and immunocompromised

22
Q

What are the most common dermatomes involved?

A

1) Thoracic (50%)
2) Cranial (20%)
3) Trigeminal (14%)
4) Lumbosacral (16%)

23
Q

When can children develop shingles?

A
  • If they are exposed to chickenpox as a neonate due to maternal varicella infection
  • They don’t develop a proper immune reaction or memory bc it is fought off by passive maternal antibodies instead of own immune system
24
Q

What is a common presentation of shingles in children?

A

Dermatomal rash on leg

25
Q

Describe zoster in the immunocompromised host

A
  • Higher incidence
  • More severe, extensive, prolonged rash
  • Risk of disseminated infection 6-10 days after onset of localised rash - cutaneous, visceral, pneumonitis, hepatitis, meningoencephalitis
  • More likely to get acute retinal necrosis PORN
26
Q

What are the two modes of VZV transmission?

A

Horizontal and vertical

27
Q

Describe horizontal transmission of VZV

A
  • Respiratory route
  • Starts 48h before onset of rash
  • Skin lesions are infectious until crusted
28
Q

Describe the two types of vertical transmission of varicella

A

1) Congenital infection of foetus in utero by maternal infection during pregnancy
2) Perinatal infection causing neonatal varicella

29
Q

Describe congenital varicella

A
  • Maternal varicella in the first 20 weeks of gestation results in foetal defects in <2% of cases
  • Baby tends to have localised scarring, typically over joints and skin
  • Rare
  • Detailed check to see if mother is susceptible to varicella during pregnancy
  • Give Ig if susceptible to prevent this and mainly bc mortality due to chickenpox is high during pregnancy
30
Q

Describe neonatal varicella

A
  • Maternal varicella occurring within 7 days before/after delivery is associated with high mortality of the newborn
  • Severe infection bc doesn’t have ability to fight it off as mother doesn’t have antibodies yet and immune system not developed
31
Q

How do you determine VZV susceptibility?

A
  • History of chicken pox or shingles

- VZV IgG status

32
Q

What are some possible treatments used as post exposure prophylaxis?

A
  • Aciclovir
  • Varivax vaccine (live - can’t use in pregnant or IC) - within 72h of exposure
  • VZV IgG (VZIG) - for those at risk of severe infection after significant exposure, within 7 days, prevents or ameliorates varicella, don’t give v often
33
Q

How is HSV/VZV diagnosed in skin lesions during primary or reactivated infection?

A
  • Electron microscopy
  • Immunofluorescence
  • Tissue culture
  • NAAT (PCR)
34
Q

When is antiviral therapy for VZV used?

A

1) Varicella in adults and IC

2) Treatment of zoster

35
Q

What does ophthalmic zoster require?

A

A mandatory ophthalmological assessment

36
Q

What is used to treat uncomplicated childhood varicella?

A

Nothing

37
Q

What are the first line antiviral agents for VZV (same as for HSV)?

A
  • Aciclovir (PO/IV)
  • Valaciclovir (PO)
  • Famciclovir (PO)
38
Q

Which is the preferential antiviral agent to use for VZV and why?

A

Valaciclovir bc better absorption and can use lower doses

39
Q

What do antiviral agents do?

A

Get rid of skin lesions and symptoms but the virus is still there

40
Q

What is the difference between using antiviral agents for VZV vs HSV?

A

VZV is less susceptible so higher doses are required

41
Q

For who may the Oka varicella vaccine be recommended for in the UK?

A

Susceptible healthcare workers and susceptible household contacts of immunocompromised individuals (live attenuated)

42
Q

For who is the zoster vaccine routinely offered?

A

70 and 79 year olds

43
Q

Describe the zoster vaccine

A
  • 14 x more potent than varicella vaccine
  • Can’t give to someone who hasn’t had varicella
  • Augments VZV specific T cell immunity
  • Decreases incidence of zoster and PHN
  • One dose
  • Live
44
Q

Describe the Oka varicella vaccine

A
  • Live attenuated
  • Blood test after may be negative bc sensitive to wild type antibodies against VZV and vaccine not so good at producing antibodies, more the T cell response
  • 2 dose schedule
  • May still develop chickenpox
  • Protects against severe infection
  • Minor vaccine associated rash
  • Can be used in IC?
45
Q

Describe varicella in pregnancy

A
  • More common in women born in tropical regions bc about 50% non-immune
  • Significant risk of varicella pneumonia - up to 20%, case fatality rate is high

Stage 2: Inflammation (39 decks)

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