L8: viral infections pt 1 (up till vzv) Flashcards
what are the 2 patterns of infections
lytic and cytopathic viruses
what is the difference between lytic and cytopathic virus
lytic causes destruction of host cells leading to ulceration wherease cytopathic is after infect host cell, the host cell is disrupted/ dysregulated
examples of lytic virus
hsv, vzv, coxsackie
examples of cytopathic virus
CMV, EBV, HHV 6,7,8
varicella zoster virus is hhv what
HHV 3
what is HHV 4 and 5
HHV 4= EBV
HHV 5= CMV
what is HHV 8
kaposi’s sarcoma herpesvirus
what is the most common cause of oral viral infections
herpes simplex virus
what signs are seen in the initial phase of HSV
systemic signs: fever, malaise, pharyngitis
oral and facial lesgions
what signs do we see in a primary oral HSV infection
- vesicular lesions -> pseudomembranous ulcers
- gingivostomatitis/ pharyngitis
- significant pain
the 2 HSV spread via what
both spread via direct contact with mucous membrane
- HSV 1 = by saliva
- HSV 2 = by sex
is HSV infectious?
yes, both the symptomatic active lesions and asymptomatic viral shedding are
HSV lie latent in ____ and recurrence is triggered by ___, _____, ___, ___
- CNS trigeminal ganglia cells
- triggered by immunodeficiency, UV light, trauma, stress
what does “prodormal signs” refer to
the period between appearance of initial symptoms and full blown rash
what are the prodromal signs of primary orofacial HSV
- 12-24 hours prior to appearance of oral lesions will have:
malaise, fever, myalgia and sore throat
also might have pharyngitis, cervical lympadenopathy
what are the other signs of primary herpetic gingivostomatitis aka orofacial HSV
painful, enlarged, erythematous gingiva
pinhead vesicles rupture -> ulcers coalescence and form crops of ulcers (sudden onset of oral lesions)
occurs on attached AND unattached oral mucosa
what differentiates a primary orofacial HSV infection from a secondary one?
primary will have sudden onset of oral lesions on both attached and unattached mucosa whereas secondary is only attached
duration of oral lesions in primary orofacial HSV is
7-10 days
how to diagnose orofacial HSV?
- Clinical hx and pattern of lesions is quite a reliable method
- viral cultures are most definitive but not always done because need time to process plus need intact vesicles since the ruptured ones are contaminated
- biopsy is more invasive
- PCR of viral DNA
- direct fluorescent assay for HSV antigen
- serology
what are the results of serology for a positive orofacial HSV case
- antibody titers will be positive 4-8 days after initial exposure
- but requires 2 tests - on presentation and 1 month later
histopatho of HSV
- ________ epithelium
- __________ cell, ballooning ________
- ________ of chromatin with nuclear clearing and ______
- intracellular _______ from ______ vesicle with _____ cell infiltrate
- _______ cells with area of ulcer (viral altered keratinocytes)
- acantholytic epithelium
- multinucleated cell, ballooning degeneration
- margination of chromatin with nuclear clearing and enlargement
- intracellular oedema from intraepithelial vesicle with inflammatory cell infiltrate
- Tzanck cells with area of ulcer (viral altered keratinocytes)
histopatho of HSV
- _____ epithelium
- _______ cell, ____________ degeneration
- margination of ______ with _______ _______ and enlargement
- ______ oedema from _________ ______ with inflammatory cell infiltrate
- Tzanck cells with area of _______ (viral altered _____)
- acantholytic epithelium
- multinucleated cell, ballooning degeneration
- margination of chromatin with nuclear clearing and enlargement
- intracellular oedema from intraepithelial vesicle with inflammatory cell infiltrate
- Tzanck cells with area of ulcer (viral altered keratinocytes)
mx of HSV in healthy px
supportive care and symptomic mx
- bland rinse or with salt water to remove necrotic debri
- topical LA
- oral analgesics
- adequate nutrition and fluid replacement
avoid self innoculation to other regions
what topical anesthetic agents can be given to HSV px
- viscous lidocaine 2%
- diphenhydramine aka difflam
what is the systemic therapy given for primary HSV infection
- anti viral agents like acyclovir (5x a day 200mg)
- ## usually not given to healthy px as it may affect abiity to develop immunity
ddx of HSV infection
identical clinical findings got:
ANUG, VZV, herpangiana, HFMD
reccurent HSV infections occur where?
at primary site of innoculation or in the adjacent areas of surface epithelium supplied by the ganglion
prodromal symptoms of RECURRENT hsv
tingling, burning, itching, erythema
where does recurrent HSV infection affect in healthy px
the keratinized mucosa bound to bone (hard palate, attached gingiva)
describe the process of a recurrent HSV infection (like what are the signs presented)
initial lesion is multiple small raised vesicles confined to a small area -> vesicles rupture and crust
takes 7-10 days to heal
location of recurrent HSV infection in immunocompromised px?
- affects both keratinized and non keratinized mucosa
- need tx otherwise lesions will spread and worsen
- not confined to oral mucosa, can have skin lesions too
if there is a HSV infection in the immunocompromised px, he can be co infected with what?
CMV
the lesions in recurrent HSV in immunocompromised have a central zone of what
central zone of superficial necrosis with raised yellow border
90% of adults are seropositive for what virus
Varicella zoster virus
in the vzv virus, which is responsible for primary and secondary infection?
primary: varicella
secondary: herpes zoster
vzv lies latent where?
sensory nerve ganglia, dorsal root ganglia
vzv spread via what
- respiratory droplets
- direct contact with active lesions
risk factors for recurrence of VZV
- hiv infection, malignancies
- radiation
- immunosuppressive agents
- alcohol abuse
- stress, old age (because as age increase, cell mediated immunity decreases and risk increases)
systemic signs of primary vzv infection (varicella)
fever, malaise, pharyngitis, rhinitis
dermatologic findings of primary vzv infection
initial stages got what?
then stages of the lesion progress from erythema to ___ to ____ to ____
lesions continue to erupt for _____ days, old lesions can intermix with ____
contagious from ____
initial got pruritic rash (exanthem) which involved face and trunk then spreads to extremities
- stages:
erythema -> vesicle (dewdrop on rose petal) -> pustule -> crusting
lesions continue to erupt for 4-7 days, old lesions intermix with new lesions
- contagious from 2 days before rash until all lesions crust
what is described as dewdrop on rose petal?
a primary vzv infection vesicle.
this is the 2nd stage of the lesion, following erythema
oral findings of primary vzv infection
- can precede ___
- common sites are ______, palate, _____, ____-
- lesions tend to be painful or painless?
- stages of oral lesions progress from vesicles then ______
- lasts for ____ days
- can precede skin lesions
- common sites are vermillion border of lips, palate, buccal mucosa, gingiva
- painless
- vesicles rupture then form ulcers of 1-3mm (number of ulcers range from 1-30)
- lasts for 5-10 days
complications of primary VZV infection
- reyes syndrome (if aspirin is used in kids less than 12 yo)
- secondary skin infections
- encephalitis
- pneumonia
- cerebellar ataxia
- gi distrubances
- hematologic events - pancytopenia, thrombocytopenia, hemolytic anemia, sickle cell crisis
what type of hematologic events can be complications of varicella infection?
pancytopenia, thrombocytopenia, hemolytic anemia, sickle cell crisis
histopatho features of varicella infection **
- acantholysis with formation of ____
- virus laden ____ exhibits margination of ________ and multinucleation
- acantholysis with formation of Tzanck cells
- virus laden epithelial cell exhibits margination of chromatin and multinucleation
histopatho features of varicella infection **
- _______ with formation of Tzanck cells
- virus laden epithelial cell exhibits __________
- acantholysis with formation of Tzanck cells
- virus laden epithelial cell exhibits margination of chromatin and multinucleation
how to diagnose vzv?
- clinical presentation
- hx of exposure to vzv within last 3 weeks and presence of exanthem
- cytological smears
- cell culture/ immunofluorescence stains for VZV antibodies
- antibodies titers to VZV
tx of varicella infection
- supportiv care
- no antiviral therapy needed in healthy px (but may be implemented in older children with severe disease)
- in immunocompromised px, purified VZV Ig can be given to modify clinical manifestations
prevention of vzv infection can be done by
- vzv vaccine (live attenuated virus)
- but efficacy of this decreases with time and only exposure to wild type virus provides lifetime immunity
what kind of vaccine is vzv vaccine
live attenuated virus
shingles is known as what virus?
recurrent vzv infection aka herpes zoster infection
risk of reactivation of latent vzv virus increases with
-age
- hiv infection
- radiation
- tx with cytotoxic or immunosuppressive agents
- presence of malignancies
- alcohol abuse
- stress
ddx of varicella infection aka primary vzv infection?
- hsv
- drug induced stomatitis
prodromal symptoms occur in how many percent of people with shingles?
90%
10% wont have prodromal symptoms
what are the prodromal symptoms that occur in shingles?
- fever, malaise, headache
- tingling, burning, itchin
prodromal symptoms in shingles usually affect how many dermatomes?
one
what are the acute symptoms of recurrent vzv infection aka shingles?
- clusters of _____ on erythematous base which ________
- _______ occurs and resolves in healthy individuals
- coalescing _______ oral ulcerations
- clusters of fluid filled vesicles on erythematous base which ulcerates
- crusting occurs and resolves in healthy individuals
- coalescing pseudomembranous oral ulcerations
acute symptoms of recurrent vzv infection aka shingles:
- clusters of fluid filled vesicles on ________
- _____ occurs and _______ in healthy individuals
- _____ pseudomembranous ______
- clusters of fluid filled vesicles on erythematous base which ulcerates
- crusting occurs and resolves in healthy individuals
- coalescing pseudomembranous oral ulcerations
chronic symptoms of recurrent vzv infection aka shingles
- in 15 % of px
- persistent pain longer than 3 months (post herpetic neuralgia)
- increase prevalence with older age
how are the oral lesions like in shingles
- involves what type of mucosa?
- extends to where and occur in conjunction with involvement of ____
- ______ of teeth in affected quadrant
- _____ necrosis and which is secondary to damage of ______ (known as _____)
- involves both keratinized and non keratinized mucosa
- extends to midline and occurs in conjunction with involvement of overlying skin
- devitalisation of teeth in affected quadrant
- bone necrosis, damage of blood vessels aka focal ischemic necrosis
complications of shingles
- ocular involvement (common) -> can cause permanent blindless
- ramsay hunt syndrome: facial paralysis associated with herpes zoster of EAC/ face. also have hearing deficits, vertigo
- post herpetic neuralgia (common): pain persists more than 3 months after presentation of initial rash. usually in older px.
ramsay hunt syndrome is a complication of what infection
herpes zoster, aka recurrent vzv infection (shingles)
what are the characteristics of the pain in post herpetic neuralgia?
- burning, throbbing, aching, stabbing
- triggered by light stroking of area
- resolution of pain is gradual
how to treat post herpetic neuralgia
use anti viral agents long term eg famaciclovir
how to treat post herpetic neuralgia
use anti viral agents long term eg famaciclovir
dont give steroids because its not good for viral infection (systemic steroids of unclear benefit)
mx of shingles
- supportive and symptomatic relief by antipyretics and antipruritics
- antiviral meds eg acyclovir, valacyclovir, famiciclovir
- antivirals used to accelerate healing, but only effective if started within 72 hours
ddx of shingles
- hsv
- drug induced stomatitis
what are lidoderm patches and zostrix cream used for?
symptom relief for shingles aka recurrent vzv infection
targets the post herpetic neuralgia
