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Micro - Herpes Viruses (i) (HSV1+2 (broad spectrum of manifestations…
Micro - Herpes Viruses (i)
Basic Features
enveloped DNA viruses
make DNAP
essential for their rep
inhibited by antivirals (e.g. acyclovir)
LATENCY
after primary infection, viruses stays in body indefinitely in an inactive state
HSV1+2 + VZV persist in N cells
EBV + CMV persist in B + T lymphocytes
can reactivate, often precipitated by stress, immunosuppression, other infections
HSV1+2 + VZV all form vesicular painful fluid-filled blister-like lesions on skin + mucous membranes -> ulcerate + become crusted
HSV1+2
infect muco-epithelial cells
cause disease @ site (cell lysis)
latent in trigeminal ganglion
1 more common (even for genital)
historically 1 was oral + 2 was genital...
but now either can cause both
broad spectrum of manifestations
some v minor + some v serious
oropharyngeal infection
primary
cold sores (common vesicular lesions on lips/face)
mostly mild/assymptomatic, lips only
fever, malaise, myalgia, painful local lymphadenopathy
sometimes vesicular lesions widely distributed (palate, pharynx, gingival, buccal mucosa, tongue)
lesions become crusted in late infection
recurrences
due to UV/sunlight/stress/trauma
usually milder + localised to corners of mouth
cut infections
herpetic whitlow (vesicular lesion on finger)
occupational risk ! easily transmitted from healthcare workers to neonates/immunocompromised patients
can be acquired due to autoinoculation
herpes gladiatorum (aka scrum pox)
transmitted by skin-skin contact
common in contact sports (rugby, wrestling)
affects skin around ear
genital herpes
if in child due to autoinoculation or sexual abuse
vesicular lesions on penis/labia/vagina/cervix
possibly urethra involved
can become rectal
keratitis
inflamm of cornea
can scar permanently + lead to visual loss
usually unilat
recurs in 30%
Dx: slit lamp exam
eczema herpeticum (severe)
encephalitis
poor outcomes + high mortality
fever. mailaise, headache, confusion, behaviour changes, seizures, coma
causes haemorrhage, necrosis, oedema of typically the fronto-temporal lobe
Dx: MRI
Tx: IV acyclovir
viraemia + disseminated disease (esp in immunosuppressed)
2 also causes recurrent benign lymphocytic meningitis
Neonatal HSV
aka skin eye mouth (SEM) disease
notifiable
90% acquired via birth canal
if mam had primary genital herpes during delivery there's a 50% transmission risk - can be asymptomatic :cry:
greatest risk of mam acquired primary infection in 3rd trimester
shedding @ birth
C-section indicated
can also be contracted through close contact with sometime with active HSV (e.g. herpetic whitlow)
high risk of dissemination + CNS involvement
because neonates have poor cell-mediated responses
risk of death, disability + neurological sequelae
if primary infection in mam occured before she became pregnant theres a low transmission risk as baby should have anti-HSV maternal Igs
Lab Dx
not required for minor infections - Dx on clinical features
gold standard = PCR on vesicular fluid
can differentiate between 1 + 2
or on CSF of encephalitis/meningitis suspected
Serology
no IgM, IgG only
can differentiate between 1 + 2
main role = to determine between active + acute infection in the maternal setting
IgG +ve = recurrent (just give prophylaxis to neonate)
IgG -ve = primary (C-section)
if neonate
surface swabs for culture (really fast, result in 2 days)
blood + CSF for PCR