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62 Cards in this Set
- Front
- Back
what are the 2 types of HSV infection
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Type I: oral. get EARLY in life, fever blister
Type II: genital. more viscous, onset of sexual activity |
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HAV I and II are part of what viral family
whats the DNA |
alpha-herpes virus
single linear dsDNA |
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what 2 thigns are important in HSV patogenicity
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1. ability to penetrate CNS and replicate
(gets in and replicates locally but then gets into sensory ganglia and replicates there as well) 2. Ability to establish LATENCY |
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where does HSV replicate
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in the host NUCLEUS
*at site of entry adn CNS **causes DESTRUCTION |
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what happens to the host cell as HSV replicates
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it replicates in the nucleas and this DESTROYS host- ballooning, intranuclear inclusions, giant cells form
**so this destructino can happen but it can also be latent and NOT cause damage |
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does HSV always get into host and just start replicating like crazy and destroy host cells
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nope, hangs out quiet and latent
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what type of HSV is...
1. oral 2. genital 3. more likely to recurr |
oral I
genital II reoccur: II **these are guidlines, sexual practices can move these around, also there is some cross imminuty but NOT enough for resistance |
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what stain is used for HSV
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Tzank
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HSV...
1. Primary Infection 2. Recurrent Infection 3. Initial Infection |
1. Primary infection: occurs after FIRST exposure, if type I primary infection occurs early in life NO HSV AB,
2. Recurrent infection: recrudescence of an established HSV infection 3. INITIAL: pts that have AB to one type but then are first exposed to a second type |
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what is the worst for preggo mom
primary recurrent initial |
primary infection is a HUGE risk for the baby
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ok so your pt has HSV I IgG but then recently is exposed to HSV II though sexual contact. what is the type of HSV II infection
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INITIAL
**this is when you ahve one and then get the other **primary is the first time you are exposed **recrurrent is recrudescence of an establised infecion |
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what is does the primary HSV II infection look like
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painful macules/papules --> vesicles (great spreading!!!) --> pustule/ulcer
**fever, maliase, lymphadenopathy **more severe in females **lasts about 3 weeks **recall primary is the FIRST time you are exposed |
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what type of tissue does HSV LovE
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transitional epithelium
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what does an initial HSV 2 infection look like
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this happens when you have been exposed previously to HSV 1 but are then exposed to HSV for the FIRST TIME
**less severe and heals faster (<3weeks) than a PRIMARY infection |
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why is an initial HSV 2 infection less severe than a primary HSV 2 infectino
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in an initial infection you ahve been exposed to HSV 1 and so will have limited immunity
**can suppress initial infection w/acyclovir but can still be xmitted |
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in what cell type does HSV establish latency
will it remain in latency |
ganglion cells
nope, recrudesence can occur even WITH good immune system- the more severe the intial outbreak the more liekly you will have lots of recurrence |
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do HSV lesions scar
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not really, even if you have multiple outbreaks in the same ares
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what is a discordant couple
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if one has HSV and the other does not.
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can you autoinoculate HSV
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you bet
if you ahve a sore dont be touching thigns! |
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how often do HSV reinfections occutr
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1/3 get 1-2
1/3 get 4-7 1/3 get >8 **if initial infection was SEVERE its more liekly to have recurrence |
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when is HSV infection spread
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ANYTIME!!
if you have clinical sx its easier but can still xmit w/o sx |
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does humoral immunity (AB) prevent HSV reinfection
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nope
**we often see recurrence when we are stressed and immunity is decreased **transplacental AB from mom are NOT totally protective for baby |
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what other animals get HSV
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NONE, humans are hte only reservoire
there is an increase in rate of xmission |
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how is HSV spread?
when is most spreading |
from vesicular fluid, saliva and other secretions of infected ppl
**MOST ARE SPREAD WHEN ASX!!!!!! **in order to infection the virus must enter mucosa through an abraision |
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HSV I is acquired when
what about II |
I- young, early in life, from parnets
II- later, onset of sexual activity MOST PPL q/HSV II dont know they have it. scary |
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if you have an acitve HSV I infection does this make it less likely to get HIV bc you have maximal AB
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NO!!!! its EASIER to get HIV bc you have an open sore from the HSV I
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who gets HAV more M or F
married or divorced city or rural what is stongest rpedictor of getting HSV infection |
Female
more common in divorced/single more common in cities MULTIPLE sex partners |
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is neonatal HSV infection something to worry about
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OH YA!
**can be acquired in utero bc moms AB are NOT protective or as babe passes through birth canal (a primary infection is esp worrysome) **fetal scalp monitors can be a site of viral inoculation, CI in mom w/Hx HSV 2 |
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whats the most common form of HSV infection during preggo
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recurrent infection, good bc its less severe and worrysome (primay infectino is BAD, initial is also not good)
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what are 3 pays HSV can be given to neonate
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1. in utero (rare)
2. during birth 3. post natal- from mom kissing the babe or whatever **mom having HSV AB are good bc they can help protect but BAD bc they put baby at risk for exposure |
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we know some HSV infectinos are asx (most ppl doent know they have it) is this true for neonatal infection
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nope, almost always sx, sometimes lethal
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what are some manifestations of neonatal HSV infection
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1. Encephalitis (micro/hydroencephalopathy)
2. skin disease 3. eye disease **disseminated disease has WORST prognosis |
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how is HSV dx
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tissue sample: ballooning pathology (from viral replication), Tzank smear, COWDRY A inclusions
PCR to detect HSV DNA- wont ID active/latent infection Culture > PCR test for AB is asx pts |
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does PCR ID active vs latent HSV infections, what is a better method
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nope
culture > PCR **if you sample the tissue you can have Tzank cells, coqqdry A inclusions etc |
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whats the tx for HSV
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acyclovir will suppress but...
NO Tx will elimiate latency/recurrent infection **also can still spread |
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long term tx of acyclovir for HSV is good for what
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decrease recurrence, will STILL shed virus
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how is HSV prevented in babes
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c section, major infection risk is initial or primary infection. so its in moms who are HSV - but become + at some point in preggo
vaccine in works |
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what is the deal with HPV
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initial infection is manageable but can progress to...
1. warts (6,11) 2. Cervical cancer (16,18) |
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what viral family is HPV in
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papova virus
HPV is the largest and most complex virus in this family circular dsDNA |
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we know HSV causes latent infection, what about HPV
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yep
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are HPV virus resistant
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ya! they are TOUGH!!!
resist ether, acid, heat. this means that its hard to kill it with laser surgery or coagulation procedure |
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what cells are infected with HPV
how is HPV replicated |
basal epithelium (so as the infected cell divides the daughter cell moves away from the BM and differentiates into epithelium)
**replication of HPV is not well understood. linked to host cell division. virions are made only in the differentiated cells |
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hoe does HPV get into the basal cells
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through breaks in skin
**the HPV then stim the basal cells to divide and differnetiate into epithelium. the virion is only released through differentiated epithelium NOT hte basal cells. **evades immune system |
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what causes the wart in HPV
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its viral induced division which increases numper of cells and causes thickening whoch is the wart (6/11)
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common warts
what are they called, what are they caused by |
common (cutaneous warts) are called verruca vulgaris and are caused by HPV 1-4. flat!!
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whats a plantar wart
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flat hyperkeratotic region on the feet, can be painful!!!
the common warts on teh skin are caused by HPV 1-4 and are called common (cutaneous) warts (verruca vulgaris) |
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whats condylomata acuminta
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genital warts
caused by HPV 6 or 11 **grey, fleshy color |
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cervical dysplasia is caused by what
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HPV 16,18
Precancerous lesion of cervical epithelium |
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what are respiratory papillomatosis
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juveline form of HPV <5 yp
caused by 6/11 **kid aspirated warts from the mom during birth (condylomata acuminata) |
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how does HPV 16 18 cause cervical cancer
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E6: degrades p53
E7: binds to and inactivated Rb p53 Rb **net= trigger cell cycle progression **this alone does NOT explain development into cancer, there are way more NON malignant infections |
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when we have HPV that does indeed cause cancer what can be said about the genetics
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Viral DNA is integrated into host and E6/7 are expressed. E2 is inactivated
*in NON malignant cells E2 is still expressed and so E6 and E7 are not overexpressed |
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how is HPV spread
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direct skin contact, genital contact, fomite transmission
ENDEMIC |
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what increases the transmission of plantar warts
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seen more in winter
associated with heated swimming pools and communal baths **common warts are in kids and are HPV 1-4 **ppl who handle meat, pultry, fish are lieky to get wart infections |
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HIV infection affectes HPV infection how
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more likely to get HPV if you have HIV
**the immune suppression in HIV makes it more likely to get anogenital HPV infection |
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whats the most common VD in US
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HPV
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what HPV is in the vaccine
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6 11- warts
16 18- cancer |
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how is HPV dx
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clinical findings- pap, warts
Hiso is NO good for latent infection. but for active infection will see koilocyte- large vacules |
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is recurrence of HPV common
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ya
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how is HPV prevented
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pap smear
HPV DNA test <30yo |
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molluscum contagiosum is part of what viral family
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pox virus
DNA, replication in our cytoplasm typically we fight this off so easily, bigger problem for our HIV pts |
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what is clinical manifectation of MCV infection
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Molluscum contagiosum
skin infection- multiple, small white lesions. seen in genital/anal area. not a big problem when healthy but big problem in HIV |
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whats the spread of MCV
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direct contact, usually sexual contact
**lesion goes away on own. its NOT inflammatory This disease was regarded as trivial and treated for largely cosmetic reasons until the advent of large numbers of AIDS patients |