herpes viruses Flashcards

1
Q

why are viruses dangerous to me

A

transmitted by saliva in asymptomatic and symptomatic individuals

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2
Q

herpesviridae virology

A

-family herpesviridae
enveloped
-double stranded DNA
-150kbp
-lytic infection-replicates in cytoplasm and causes cell death by bursting
-latent infection- can reactivate symptomatically or asymptoaticlaly

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3
Q

how does latency work

A

Causes tissue damage with vesicles full of fluid with active virus in them. Once the body fights of the vrisus it will move down the sensory neurons to the spinal ganglia. Hsv1 tends to be the trigeminal ganglia and hsv2 is tends to be the scaral ganglia but not strict rules. Then it wll reactive and move down the neuron to the epithelial cells and then replicate and then you get active symptoms or asymptomatic

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4
Q

primary infection

A

if you have already had hsv1 you cannot get a hsv2 infection as they follow a similar immune response

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5
Q

HSV epidemiology

A

Most primary infections before 5 years

HSV 1 UK seroprevalence up to 50-70%
HSV 2 UK seroprevelance ~10% ( more in usa 25%)

Oral - close social contact – kissing, nurseries..
Genital – sexual contact

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6
Q

what is seroprevalence

A

Seroprevalence refers to combined HSV 1 and/or 2, Newer HSV-1 data suggests lower seroprevalence. Seroprevalence varies in different countries or different groups in the same country (e.g. HSV-2 seroprevalence 25% in USA)

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7
Q

hsv primary oral herpes

A

primary infection with HSV1 OR HSV usually asymptomatic and cause cause sever gingivostomatitis - swollen lips and lesions
may require hospitalisation as dehydration or pain and child may need nasogastric feeding

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8
Q

HSV oral reactivation

A

reactivation of HSV1 or HSV2 usually asymptomatic but can cause cild sores on boarder of lips- rarely intra-oral

  • can be random and have non-specific triggers e.g. stress, fever,mesntration,cold
  • can be itching or tingling before vesicles and lasts 5-12 days
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9
Q

hsv- genital disease

A
  • HSV1 and HSV2
    reactivate is usually with HSV2
  • primary more sever than reactivation and cause discomfort
    reactivation can often be asymptomatic
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10
Q

hsv mian complications

A
  • Secondary bacterial infection (beaking down)
  • Corneal Ulcers, risk of scarring, loss of vision
  • Meningitis, self limited, usually HSV 2, can be recurrent (Mollaret’s meningitis)
  • Herpes Simplex Encephalitis, life-threatening, usually HSV 1
  • Neonatal Herpes Simplex – life threatening
  • Life threatening infection in the immunocompromised- can cause liver ailue
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11
Q

what is hsv- hepatic whitlow

A

thumb sucking/contact sports

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12
Q

HSV -ocular infection

A

dendritic ulcer and can be sight treating

Macliver drops needed

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13
Q

HSv neonatal

A

during birth process or someone who has the virus either asympomaitc or symptomatic
more risk if the mother has primary
- c-section required
- acyclovir
the baby can get a rash (dermatomes or CNSor gets multi-organ failure

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14
Q

HSv-encephalitis

A
Commonest cause of viral encephalitis
70% mortality untreated
High rate of poor neurological outcome
Temporal lobe enema
Confused and fevers but can cause phycological impairment if they survive can be missed in older patients  
mimimm of 10 days treatment iv acyclovir
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15
Q

diagnosis

A

direct viral detection
PCR
-lesion swab
cerebrospinal fluid -not common

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16
Q

treatment

A

Aciclovir
Needs activated by a viral enzyme – thymidine kinase(only active in virus cells) – so specific for infected cells
Poor oral bioavailability, 5 x per day dosing

Valaciclovir
Prodrug of aciclovir
Good oral bioavailability, but more expensive
Can get kidney issues with it

17
Q

VZV-primary infection chicken pox

A
Prodrome of fever before rash is common
Centipetal distribution- head,no arms
Macules       Papules       Vesicles       Pustules
All stages can be seen at the same time
Crops of lesions at different stages
More severe in adults
Oral vesicles can occur before those elsewhere and can be extremely painful.
range of severity
18
Q

Centripetal distrubution

A

Centripetal distrubution – vesicles start on trunk and are more numerous on trunk than limbs.

19
Q

chicken pox epidemiology

A

UK > 90% seroprevelance (naturally immune)
Outbreaks mainly in winter/spring
Attack rate for household contacts is 90%
Peak age is now <5 years
Respiratory transmission or direct contact
Incubation period 8-21 days (average 14 days)
Infectious from 2 days before rash to full crusting of vesicles
- fully crusting takes average of 5 days from rash onset

20
Q

VZV reactivation zoster shingles

A

dermatomal- never crosses dermatomes and doesn’t cross halves of bodies - in more than one dear,tome it could be immunocompromised and could be HIV

21
Q

eye shingles

A

ophthalmic zoster
affecting trinomial nerve
- ocular complications particular likely if nasocillary branch is involved
lesions on side of nose
post hepatic neuralgia- can last long tie cannot sleep

22
Q

diagnosis

A

clinical
direct viral detection
PCR-lesion swab/cerebrospinal fluid