herpes viruses Flashcards
why are viruses dangerous to me
transmitted by saliva in asymptomatic and symptomatic individuals
herpesviridae virology
-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
how does latency work
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
primary infection
if you have already had hsv1 you cannot get a hsv2 infection as they follow a similar immune response
HSV epidemiology
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
what is seroprevalence
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)
hsv primary oral herpes
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
HSV oral reactivation
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
hsv- genital disease
- HSV1 and HSV2
reactivate is usually with HSV2 - primary more sever than reactivation and cause discomfort
reactivation can often be asymptomatic
hsv mian complications
- 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
what is hsv- hepatic whitlow
thumb sucking/contact sports
HSV -ocular infection
dendritic ulcer and can be sight treating
Macliver drops needed
HSv neonatal
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
HSv-encephalitis
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
diagnosis
direct viral detection
PCR
-lesion swab
cerebrospinal fluid -not common
treatment
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
VZV-primary infection chicken pox
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
Centripetal distrubution
Centripetal distrubution – vesicles start on trunk and are more numerous on trunk than limbs.
chicken pox epidemiology
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
VZV reactivation zoster shingles
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
eye shingles
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
diagnosis
clinical
direct viral detection
PCR-lesion swab/cerebrospinal fluid
