Term
| what characterizes the herpes virus family? |
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Definition
| herpesviruses are *dsDNA, have the potential for *latency, *reactivation (may be asymptomatic - but virus still sheds), and *transformation. |
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Term
| what are the 2 types of herpes simplex virus (HSV)? |
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Definition
| HSV-1 and HSV-2. these are closely related and can induce cross-reactive antibodies to each other. |
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Term
| which virus are most genital and perirectal herpes outbreaks due to? |
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Definition
| HSV-2. only 10-20% of genital herpes are due to HSV-1 (more typically associated w/oral herpes). |
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Term
| what demographics have the highest seroprevalence of HSV-2? |
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Definition
| non-hispanic black women (81% of which have not recieved a dx) |
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Term
| how is the first clinical episode of HSV-2 classified? |
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Definition
| *primary infection: first infection ever w/either HSV, disease is more severe than recurrent and no antibody is present when symptoms appear. *non-primary infection: newly acquired HSV infection of either type in a pt previously exposed to the other type, symptoms are usually milder than primary infection and antibody is present when symptoms appear. |
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Term
| what characterizes a recurrent HSV symptomatic infection? |
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Definition
| disease is usually more short/mild and antibody is present when symptoms appear (preformed antibody). |
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Term
| what characterizes an asymptomatic HSV infection? |
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Definition
| serum antibody is present, but pt has no known hx of clinical outbreaks. |
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Term
| what is the general course of HSV infection? |
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Definition
| *primary* incubation of about 5 days, then symptoms - local: pain/itching/dysuria, systemic: malaise, fever, headache, and tender lymph nodes. lesions during this period go from being papules -> vesicles -> pustules -> ulcers -> crusts. then around day 15: healing, and the virus finally stops shedding (total duration - 3 wks). *reactivation* prodrome period: 12-24 hrs of initial nondescript tingling/itching. then some localized symptoms, hard to detect micro-lesions that *still shed, but nothing as severe as the primary infection (total duration 5-10 days). |
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Term
| which HSV is more likely to recur? shed asymptomatically? |
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Definition
| HSV-2 is more likely to recur AND shed asymptomatically (when most HSV-2 infections are transmitted, likely b/c microlesions are often undetectable). |
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Term
| when do most HSV reactivations occur? |
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Definition
| most reactivations occur in the 1st 3 months after the primary infection |
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Term
| how do HSV shedding/reactivation rates compare between the sexes? how many of these shedding episodes are thought to be subclinical? |
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Definition
| HSV infected women are thought to be shedding 20% of the time (can be as high as 80%) and HSV infected men are thought to be shedding 15% of the time (can be as high as 70%). 75% of these shedding episodes are thought to be subclinical (associated w/microscopic lesions). |
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Term
| what is the first clinical HSV infection treated with? f/u tx? |
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Definition
| acyclovir, famciclovir, or valacyclovir for the 1st primary infection. f/u tx: episodic tx can decrease the degree of shedding and/or continuous tx will decrease the likelihood of recurrences. |
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Term
| how does neonatal herpes occur? |
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Definition
| HSV transmission usually occurs to infants if the mother has either a primary or recurrent infection at birth - though nosocomial/nursing transmissions are also possible. if the mother has a primary infection at birth, the baby has a higher risk of severe disease (b/c mother will have preformed antibodies during recurrent infection). |
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Term
| what is the clinical presentation of neonatal herpes? |
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Definition
| lesions on the skin, eyes, and mouth. as long as dissemination doesn't occur, there is a low mortality risk. if dissemination does occur, encephalitis is a serious risk, along w/pneumonitis, hepatitis, cardiovascular involvement, and meningoencephalitis (95% will have neurological sequelae). if untreated, disseminated HSV has a 50% mortality rate. |
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Term
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Definition
| clinical dx: insensitive/nonspecific and needs to be confirmed by lab work such as virologic tests/type-specific serologic tests. |
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Term
| what is considered the gold standard for virologic testing? |
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Definition
| viral cx: the preferred test for pts w/genital ulcers or other mucocutaneous lesions (however - hard to cx healing lesions/recurrent infections) |
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Term
| what virologic test is better for detecting HSV in healing lesions? |
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Definition
| antigen detection (DFA/EIA) |
|
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Term
| how reliable is cytology (tzanck) for diagnosing HSV? |
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Definition
|
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Term
| what is the preferred virologic test for detection of HSV in spinal fluid? |
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Definition
| PCR (HSV1 is the leading cause of sporadic encephalitis ) |
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Term
| what characterizes the type-specific serologic tests used to dx HSV? |
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Definition
| antibodies will develop in a few weeks and will persist, so presences of HSV-1 and/or 2 antibodies can be detected. HSV-2: assumed genital infection. HSV-1: either oral/genital infection |
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Term
| what characterizes the epidemiology of CMV infections? |
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Definition
| CMV (betaherpes virus) has a high seroprevalance. 40-60% in upper socioeconomic groups are seropositive and ~85% in lower socioeconomic groups are seropositive. .5-2.5% of newborns are infected at birth. |
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Term
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Definition
| major mode: saliva/genital secretions. other routes: transplacental/birth canal, breast milk, blood transfusion, and organ transplantation. |
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Term
| how does CMV affect pts w/normal immunity? |
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Definition
| mostly pts w/normal immunity will become asymptomatic CMV carriers, but a mononucleosis (similar to EBV - but heterophile negative) is possible. |
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Term
| how does CMV affect babies of seronegative mothers (fetus is exposed and there is no maternal antibody to protect it)? |
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Definition
| cytomegalic inclusion disease |
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Term
| how does CMV affect immunosuppressed/AIDS pts? |
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Definition
| multisite symptomatic disease |
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|
Term
| what does cytomegalic inclusion disease refer to? |
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Definition
| cytomegalic inclusion disease = *symptomatic primary congenital infection*: either in utero (40% change of transmission to fetus) or during birth. 10-15% of infected infants are symptomatic at birth, who then have a 80-90% sequelae rate (brain damage/hearing loss) and a 36% mortality rate. conversely. asymptomatic newborns have a 5-10% sequelae rate (deafness). |
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Term
| how is cytomegalic inclusion disease diagnosed? how can in utero/at birth CMV infection be differntiated? |
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Definition
| CMV can be detected in urine w/in the 1st wk of life. if acquired at birth, shedding will start to occur 3-4 wks later and if acquired in utero, shedding will occur immediately after birth. |
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Term
| what is the implication of reactivation of CMV in the mother during pregnancy for the infant's health? |
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Definition
| the newborn will be healthy (usually asymptomatic) due to maternal antibody, but they may shed virus for a long period of time |
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Term
| what are clinical symptoms of cytomegalic inclusion disease? |
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Definition
| mostly involving the CNS/RES, symptoms consist of hearing loss, vision impairment, mental retardation, hepatosplenomegaly, and jaundice. |
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Term
| when is the risk of HSV/CMV transmission highest for a fetus/newborn? |
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Definition
| if the mother is undergoing a primary infection (recurrent infections include protective maternal antibodies) |
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Term
| what is the primary concern for CMV in newborns? |
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Definition
| congenital infection (in utero) |
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Term
| what is the primary concern for HSV/VZV in newborns? |
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Definition
| neonatal infection (most serious when mother has VZV lesions around time of birth) |
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Term
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Definition
| HPV is a naked icosahedral DNA virus which can cause latency, transformation, and reactivation (due to DNA). |
|
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Term
| what are the routes of transmission for HPV? |
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Definition
| through breaks in the skin (infects basal epithelial cells), sexual contact, and via the birth canal |
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Term
| what is one of the fasted growing sexually transmitted diseases in the US? |
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Definition
| HPV - w/highest incidence in women of the 20-24 age group |
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Term
| what % if cervical CA have HPV DNA detected w/in the tumor? |
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Definition
| 99% (50-75% of infections are thought to be via subtypes w/a higher CA risk) |
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Term
| do HIV+ pts have a higher prevalence of HPV/pre-CA lesions? |
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Definition
|
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Term
| what are the risk factors for genital HPV? |
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Definition
| women: younger age, multiple sex partners, and male partner sexual behavior. men: multiple sex partners and lack of circumscision |
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Term
| what is a risk factor for developing cervical CA? |
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Definition
| *persistent HPV infection |
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Term
| what does HPV replication depend on? |
|
Definition
| epithelial cell differentiation. transmission occurs through breaks in the skin down to the basal epithelial cells, where latency or transformation occurs. shedding is then dependent on differentiation of the epithelial cells (virus shed by differentiated cells) |
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Term
| how does release of productive virus present clinically? |
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Definition
| as a wart. infection is often subclinical, which when this is the case - tx is not recommended. |
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Term
| can HPV infections self-resolve? |
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Definition
| yes ~70% of HPV-infected pts become HPV DNA negative w/in 1 year and that rises to 90% in 2 yrs. |
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Term
| what characterizes a latent HPV infection? |
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Definition
| viral DNA is not integrated and tx will not clear latently infected cells |
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Term
| what characterizes a transforming HPV infection? |
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Definition
| viral DNA is integrated, basal cells replace more differentiated epithelial cells and the clinical outcome includes dysplasia/CA. during integration, some HPV early genes are inactivated (*no viral replication), but there is continued expression of HPV E6 (binds p53, targets it for degradation) and E7 (binds and inactivates Rb) genes |
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Term
| what are the HPV subtypes associated with genital warts (condylomas)? |
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Definition
| 6, 11 (same as laryngeal papillomas) |
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Term
| what are the HPV subtypes associated with cervical dysplasia/CA? |
|
Definition
|
|
Term
| what characterizes the cutaneous warts due to HPV? |
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Definition
| these are benign and may spontaneously disappear/be removed. they may recur after removal b/c of latently infected basal cells and are more common in immunosuppressed pts. |
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Term
| what characterizes the laryngeal papillomas due to HPV? |
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Definition
| these are due to HPV subtypes 6, 11 (same as genital warts) and are benign tumors growing in the respiratory tract that may cause obstruction and may need to be excised/re-excised. there is juvenile onset (children <5 infected congenitally) and adult onset ( >20 infected either from oral/genital contact or latent from birth) |
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Term
| what characterizes the genital warts due to HPV? |
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Definition
| most genital warts are associated with low risk HPV (subtypes: 6, 11) and are seen on the vagina, vulva, penis and around the penis. 70% of these infection clear w/in a yr, 90% clear w/in 2 yrs. however, HPV 16 is the high risk subtype (more likely to persist). recurrence rates after tx: 20-50% |
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|
Term
| what is the purpose of a pap smear? |
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Definition
| screening for evidence of CPE (cytopathic effects) associated w/HPV infection of certain cells. |
|
|
Term
| what are the high risk HPV subtypes? |
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Definition
| 16, 18 - associated w/the majority of invasive CA. a vaccine is available for these subtypes, however other subtypes can less commonly still cause CA. |
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Term
| can HSV-2 and chlamydia trachomatis aid in cervical CA development? |
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Definition
|
|
Term
| what are other possible outcomes for high risk HPV infected pts besides CA? |
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Definition
| low-grade/high-grade cellular abnormalities. high grade is more likely to eventually progress to CA. |
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|
Term
| what is epidermodysplasia verruciformis? |
|
Definition
| a rare defect in cell mediated immunity/NK activity due to HPV (esp subtypes 5,8) usually seen in immunocompromised pts. in pts with epidermodysplasia verruciformis, flat/reddish skin lesions on the trunk and upper extremities appear and exposure to UV light can lead to malignant transformation. |
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Term
| what are the 2 HPV vaccines? how are they produced? who are they recommended for? |
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Definition
| gardasil (immunity to HPV subtypes: 6,11,16,18) and cervarix (16, 18). both are made from non-infectious HPV-like particles (not attenuated or killed - more like a subunit vaccine). these are recommended for 11-12 yr old girls w/a catch-up vaccination at 13-26. males 9-26 can also get vaccinated. |
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Term
| should women vaccinated against high risk HPV still get pap tests performed? |
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Definition
|
|
Term
|
Definition
| *clinical dx of genital warts*, pap test (dx abnormal cells due to infection, cx (not easily available), serology (not reliable) |
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