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38 Cards in this Set

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general structure of herpes viruses
enveloped
dsDNA
in terms of glycoproteins, g__ is the most important "neutralizing epitope," whereas g__ and g__ are required for infectivity of the viruses (bc it allows them to bind to tissues)
gB

gB and gD
how are herpes simplex viruses (HSV) 1 and 2 classified?
based on antibodies to gG
HSV1 occurs _______ (and it's VERY common), whereas HSV2 doesn't appear until ____ (much less common).
early in life; puberty
how is HSV transmitted? tell me about how it's reactivated...
through break in skin (intimate contact/perinatal) --> virus moves up the nerves to sensory ganglia and reside there --> latency period

viruses rest there until reactivation occurs through some stress (menstraution, fever, stres) ==> most reactivation in healthy persons brief and asymptomatic
although >90% of primary infections of herpes are asymptomatic, what are the clinical manifestations of HSV1 in the case of primary infection(4)? reactivation?
TEND TO BE ABOVE BELT
Primary:
- gingivostomatitis (gum/tongue inflammation)
- keratoconjunctivitis
- herpetic whitlow (HSV infection of finger)
- encephalitis

Reactivation: herpes labialis (cold sore)
although >90% of primary infections of herpes are asymptomatic, what are the clinical manifestations of HSV2 in the case of primary infection? reactivation?
TEND TO BE BELOW BELT
Primary:
- genital/neonatal herpes

Reactivation: genital herpes (reactivation cases are often milder)
Most common cause of corneal blindness in the US
HSV keratitis
what are the organisms that can cross the blood-placenta barrier?
TORCHES

TO: TOxoplasmosis
R: Rubella
C: cytomegalovirus
HE: HErpes, HIV
S: syphilis
What is most common cause of viral encephalitis in the US?
HSV-1
painful grouped vesicles on an erythematous base is typical finding of what virus?
HSV 1/2
Dx and prevention of herpes simplex virus
Dx:
- Tzanck smear for MULTINUCLEATED GIANT CELLS (TSANCK HEAVENS I DO NOT HAVE HERPES!!)
- culture
-serology

Prevention: NO VACCINE AVAILABLE!!

- c section for infected mother
why do patients get hallucinations with herpes simplex virus?
virus targets temporal lobe -- but don't worry, it's TREATABLE!!
VZV stands for _________.
Varicella (chickenpox) zoster (shingles) virus. Most kids get varicella, but afterwards, the virus remains latent until later in late adulthood, can reactivate as zoster (usually with stressors or immunocompromised situations)
how is VZV transmitted? how long is the incubation period
respiratory transmission and incubates for 2 weeks, infects T cells and then followed by viremia (hematogenous spread to skin and sensory ganglia (site of lantency))
For VZV, what are the clinical presentations for primary (varicella) vs. recurrent infections (zoster)?
primary:
- fever, malaise/headache, characteristic rash that starts on face/trunk and goes all over body (chicken pox)
- severity inc with age (immunocompromed can develop pneumonia, encephalitis, hepatiis, nephritis as complication)

Recurrent infection:
- zoster (shingles) reactivate and follow distinct dermatomal distribution
- trigeminal reactivation may cause blindness
can you get perinatal infection of VZV?
yes, if mom gets sick right before pregnancy -- these perinatal infections may lead to congential abnormalities
Dx of VZV
Prevention of VZV
Tx of VZV
Dx: same as HSV, remember??

prevention: live attenuated vaccine for children/adults wiht no history of chickenpox
- high dose zoster vaccine for elderly

Tx: acyclovir, famciclovir, valacyclovir
the highest infection rate of cytomegalovirus (CMV) is in CHILDHOOD/ADULTHOOD
childhood (risk factors include day care attendance, homosexuality in men, mexicans/blacks, transplant/transfusion recipients)
how can you get CMV (3 ways)?
sexual transmission
transfusions
perinatal (major cause of congenital abnormality) -- CMV most common viral cause of mental retardation
what's the important thing about reactivation of CMV?
there's NO REACTIVATION of CMV in immunoCOMPETENT hosts
incubation period of CMV
1-2 months
although most infections of CMV are asymptomatic (80%), what are the perinatal clinical manifestations? what about in older children/adults?
what about in immunocompromised pts?
perinatal:
- Mental retardation
- Microcephaly (small head)
- DIsseminated dz
- Vision/hearing loss
"Mr. M. Div."

older children/adults:
- mononucleosis (similar to EBV) ==> fever, mild hepatitis, lymphocytosis

immunocompromised: hepatitis, retinitis, colitis, encephaliits, pneumonia
Dx and prevention of CMV
Dx:
- in blood and urine: antigen detection, viral DNA detection
- serology: presence of IgM antibodies
- histopathology: cytomegalic cells with nuclear and cytoplasmci inclusions ("owls' eyes)

prevention: screening prior to transfusion or organ transplantation
- there are antivirals for high risk population(ganciclovir/foscamet)??
most childhood infections of EBV are _______, whereas in young adults they are ________.
asymptomatic; symptomatic
how is EBV transmitted?
via oropharynx (direct contact w/ secretions "the kissing dz")
- also in genital secretions

EBV then infects the B cells!!
what are the symptoms of EBV mononucleosis due to?
the CD8 response against proliferating B cells infected with EBV (they become atypical lymphocytes! )
do normal hosts get reactivation of EBV?
no, they don't.
what are the clinical manifestations of EBV?
- infectious mononucleosis + fever (sore throat, lymphadenopathy, splenomegaly)
- oral hairy leukoplakia: occurs in HIV pts
name the associated tumors of EBV
nasopharyngeal carcinoma
Burkitt's lymphoma
non-Hodgkin's lymphoma
Hodgkin's dz
in terms of Dx for EBV, what does CBC show up as?
2 other ways to Dx (which one is definitive)?
lymphocytosis with atypical lymphocytes

heterophile antibodies (Monospot test)- non-specific

IgM to VCA (viral capsid antigen) -- DEFINITIVE!!
What does IgG-VCA show?
marker of infection at previous time
prevention and Tx for EBV?
prevention: avoid contact sports (prevent splenic rupture)
- steroids (to prevent complications)

Tx: NO ANTIVIRALS -- bc syptoms are due to immune response!! KNOW IT!
Most infection of HHV 6 occurs during early childhood (6 monts -2 years). what's the clinical manifestation for children vs. adults vs. immunocompromised pts?
children: roseola "sixth dz" (parvovirus causes "fifth dz")
- febrile illness for 3-5 days followed by diffuse rash as fever abates

adults: resembles infectious mono

immunocompromised pts: severe fever+rash
HHV 8 is transmitted how? what does it infect?
sexual contact
oral (saliva)
perinatal

infects endothelial cells
what tumors is HHV8 associated wiht?
Karposi's sarcoma (involves lower extremity)

primary effusion and body cavity lymphoma

multicentric castlemans' dz
Tx of HHV8
chemo, radiation, antiviral
What is a common lethal complication with Herpes B (Herpes Simiae)?
CNS involvment (in untreated pts) -- effective antiviral therapy is availbae and must be given early during course of illness