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113 Cards in this Set

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  • Back
membership in the family herpesviridae is based on what?
the architecture of the virion
general characteristics of the herpes viruses?
DNA, replicate in nucleus, viral DNA pol and other enzymes associated with nucleotide biosynth. enveloped
what are the alphaherpesviruses? beta? gamma?
HSV-1, HSV-2, and varicella-zoster. HCMV, HHV6, HHV7. EBV and KSHV (kaposi's)
epi of HSV 1 and 2?
both have only human hosts, are found WW, 18 to 95% areHSV1 seropositive, while HSV2 5 to 75% are seropositive. transmission is person to person via body fluid
describe HSV pathogenesis.
primary infection: entry is via abraded skin or mucous membrane, incubation from 2 to 12 days, epithelial cells are where lesion is, lesion formation can be up to 23 days after first contact, infection of local nerve endings and traveles to the nucleus/ganglia and goes latent (usually trigem ganglia for HSV1 and sacral ganglia for HSV2). convalescence stage is when the lesion disappears and there is no scar
while HSV is latent in the nerves what is it protected from ??
immune surveilance
describe the 4 stages of lesions in HSV1
early is beginning of lesions, mid is a bit larger with replicating virus, full is full pustule with replicating virus in there, late stage is when it is healing
describe the recurrent HSV infections
reactivation of virus replication, migration of virus down the nerve to site of original infection, the lesions contain infective virus and are milder with shorter duration
what are the HSV1 syndromes?
stomatits, gingivostomatitis, fever blisters/cold sores
describe HSV1 stats in children and adults.
10 to 20% are symptomatic in children, rest are asympto, adults have infrequent symptoms and onset of primary infection later in life may be associated with an HSV pharyngitis in a mononucleosis like syndrome
describe the signs and Sx's of primary orofacial HSV 1?
usually asympto, but general flu like viral symptoms can occur and obviously lesions, lymphadenopathy, anorexia, children may not want to swallow liquids, young adults may get an HSV pharyngitis in association with mono syndrome
HSV1 recurrent infection occur how often?
33% have recurrent infections, 5% one/month, 34% one/2 to 11 mos, 61% one/yr. most are asympto
facts about herpetic keratoconjunctivits?
300,000 cases/yr in US, second to trauma as cause of corneal blindness, usually limited to one eye, associated with photophobia, tearing, eyelid edema, and pathognomonic finding of branching dendritic lesions (can dye with fluorescence), healing may take up to one month, recurrent infections are common, repeated attacks are associated with scarring, corneal damage, and blindness.
describe herpes gladiatorium
infection on the body with HSV1, viruses establish infection through cuts, wrestlers and rugby players
how can you get HSV2?
STD or perinatal infection
how does HSV2 have a role in HIV?
open wounds make it much more likely to aquire an infection
risks for HSV2 in hetero men? hetero women?
1 partner is 0%, 2 to 10 is 20%, 11 to 50 is 35%, over 50 is 70%. 1 partner is <10%, 2-10 partners is 40%, 11 to 50 partners is 62%, over 50 is >80%
primary infection of HSV2 can be associated with what?
fever, dysuria, inguinal adenopathy, malaise, stiffneck headache, photophobia, primary infection of women usually results in more sever symptoms
describe primary HSV2 infections in men.
usually about 6 to 10 lesions, can be extragenital but in that general area, systemic complications are rare but can get aseptic meningitis
describe primary HSV2 infection in womene.
bilateral on the vulva, cervix can be involved, inguinal adenopathy and dysuria, can be in perineum, butt, vag anus. most severe complications include a urinary retention syndrome in 10 to 15 % of women. aseptic meningitis in as many as 25% of women
how many adults are infected with HSV2 and what are the frequencies of recurrent infections?
4 out of 9 are infected. a third of pts have over 8 to 9 recurrent infections/yr, a third have 4 to 7/yr and a third have 2-3/yr. note they are less severe than primary infection and HSV1 genital infections are less severe and less likely to recur
can you still shed HSV if there are no lesions?
describe herpetic whitlow
HSV infections of digits, common in medical/dental personnel, HSV1 or 2, 2.4 cases per 100,000 population/yr
describe the neurological complications of HSVs
encephalitis from HSV1: severe morbidity and mortality, death in untreated is 70%, only 2.5% return to normal neuro function, 40 to 50 cases/yr but do have focal encephalopathies in 1250 pts/yr in US. HSV 2 can cause neonatal encephalitis and herpes meningitis
describe the types of neonatal HSV infections.
inutero HSV2 (5%) results in worse disease, intrapartum HSV2 (75 to 80%), postnatal (HSV1)
T/F: neonatal HSV infections are usually benign. Primary infection of the mother during the late stages of pregnancy result in greater chance of transmission to the baby.
F- symptomatic and can be lethal. T
describe congenital HSV2 infections.
in utero, 1 in 200,000 deliveries, skin vesicles, scarring, eye disease, up to microceph or multiple organ involvement, 50% mortality
describe the three types of disease seen in intrapartum or postnatal HSV2 infection.
1. localized to skin, eye and mouth 34%
2. localized CNS 34% - fever, lethargy, seizures
3. disseminated disease 32% - multiple organ systems involved, mortality is 80% wo treatment and 42% with
describe lab and serological diagnoses
cell culture - isolation is most definitive method, grow in tissue culture and see CPE of syncytial (cell fusion). cytology or histo: tzanck smear, papnicolaou smear, biopsy, cowdry type A intranuclear inclusions (halo and a ring of marginated chromatin at nuclear membrane).
ELISA, PCR can be used. serology is only useful for dx of primary vs recurrent infection
what are the drugs for HSV keratitis?
nucleoside analogs: vidarabin (adenosine), idoxuridine (thymidine), trifluridine (thymidine)
what is used to treat
HSV acyclovir resistant infections.
foscarnet: pyrophosphate analogue that binds directly to pol
describe the drugs for HSV that the TK pis the drugs.
acyclovir (injectable for infants too), valacyclovir, penciclovir, famciclovir
HSV vaccines?
epi of CMV?
humans are the natural hosts, WW, in developed countries 40 to 80% are seropositive; in developing countries 80 to 100% are seropositive. Transmission is person to person, direct exposure to body fluid including oropharyngeal secretions, urine, cervical vaginal excretions, spermaatic fluids, breast milk, tears, feces, and blood
what are the major pathological routes of CMV?
#1 viral infectious cause of congenital CNS damage, opportunistic in AIDs, cause of complications in transplant patients, causes mono, maybe risk factor in CVD and cancer
describe CMV and the fetal risk factors.
0.2-2.2% of infants are congenitally infected in US (40,000/yr), primary infections of seroneg mothers place the fetus at greatest risk, intrauterine infection is less frequent than perinatal infection but is associated with the most severe CMV disease, in immune mothers infections in the baby are generally asymptomatic
describe CMV and risk factors for neonates/young children.
infection perinatally or postnatally during breastfeeding, 45 to 91% of pregnant women are CMV seropositive prior to conception, CMV excretion occurs in 9 to 29% of these women, transmsission among toddlers in day care is very high
describe CMV and the sexually active risk factors.
is an STD, shed from the cervix, ~34% of females from STD clinics, also found in semen but rate of shedding is unknown
describe CMV and the risk factors associated with immunocompromised hosts.
transplant and AIDs patients, 50% of transplant patients show signs of HCMV infection, very common in AIDS, ~100% of homosexula men with HIV1 are co infected with HCMV
describe CMV and the risk factors associated with recipients of blood products.
21-54% of patients develop sero evidence of CMV infection, patients maybe asymptomatic, develop posttransfusion CMV mononucleosis or CMV hepatitis (seropositive recipients not protected), blood is regularly screened for CMV
how many strains of CMV are there.
quite a few so re-infection is possible with a different strand
are health care workers at risk for CMV?
describe CMV symptoms in congenital infections.
most are asympto but 10 to 25% show Sx's with mortality rates of 11 to 20%; about 80% of symptomatic infants exhibit lasting neurological abnormalities; symptoms of those with cytomegalic inclusion disease include jaundice, petechiae, and hepatosplenomegaly; more severe symptoms include deafness, chronic liver damage, tooth defects, inguinal hernia, ventricular and arterial septal defects, cleft palate, microcephaly, and end stage organ disease in the worst case scenario
what CNS pathology is commonly seen in babies with CMV?
periventricular calcifications
what are the symptoms of perinatal/young children with CMV infections?
usually asymptomatoc
describe CMV pathology in immunocompetent adults. Immunocompromised adults.
mono, CVDs, cancer… AIDS, transplants, chemo pts
describe CMV mono
21% of monos, mild, self limiting, mono Sx with higher fever, rash, abnormal liver functions, CMV mon is heterophil neg but EBV is heterophil antibody pos
describe CMV and CVD
more severe atherosclerotic Sxs, onset of restenosis following ballon angioplasty, onset of transplant vascular sclerosis; HCMV antigens and nucleic acid sequences have been demonstrated in plaques and arteries
why may HCMV contribute to AIDS progression?
it can infect the same cell types as HIV, some HCMV genes are capable of increasing the expression of the LTR region of HIV.
symptoms of HCMV infection in AIDS.
retinitis, gastroenteritis, meningoencephalitis, pancreatitis, cholecystits; can be sight or life threatening (40%)
treatment of HCMV and AIDS co-infection?
heart treatment??? Ganciclovir, note that HCMV induced diseases may rise as the virus acquires various drug resistance
the severity of end organ disease in transplant patients is related to what?
the severity of the immunosuppression (usually worse in bone marrow transplants)
describe the symptoms, treatment, and mortality of the most common life threatening complication of allogenic bone marrow transplant.
interstitial pneumonia from HCMV. 2 wk onset, high mortality of 84% even with antiviral therapy, fever, nonproductive cough, dyspnea, hypoxia.
what are the possible effects of HCMV infection with liver tranpslant, treatment, Dx, etc?
hepatitis from HCMV, leading cause of morbidity the first 14 wks after transplantation, fever, elevated liver enzymes, liver failure, 38% show CMV disease but 0.8% after antivirals, thus therapy is a good thing
what solid organ transplant has the lowest HCMV morbidity and what are Sx and Rx?
kidney transplant, fever, leukopenia, hepatosplenomegaly, malaise, rare hepatitis and pneumonia, responds well to anitvirals.
what clinical signs and symptoms should make you suspect HCMV infection?
newborns with microcephaly, jaundice, hepatosplenomegaly. Individuals with mono and negative heterophil antibody. Immunocompromised hosts with fever, pneumonia, etc.
how would you diagnose CMV with lab/serology?
immunofluorescence, ELISA, EM, DNA hybridization, PCR, TISSUE CULTURE IS MOST DEFINITIVE (see Owl eye inclusions that are surrounded by white clear ring), serology for CMV antibodies
treatments for HCMV?
ganciclovir, valganciclovir are used for prevention of CMV disease in transplant and AIDS. Foscarnet is for retinitis in AIDS pts. Cidofovir is a NT analog of cytosine for Rx of retinitis in AIDS pts. Formivirsen is an antisense NT for treatment of retinitis in AIDS pts. ganciclovir is drug of choice. no vaccine, controversial use of IgG for prophylaxis in transplant pts.
what diseases are produced by VZV?
primary infection of varicella (chickenpox) and secondary/recurrent infection of zoster (shingles)
epi of VZV varicella?
humans are natural hosts, WW, person to person (fluids AND aerosol - only herp virus that does this), highly contagious (secondary infections of susceptible ppl is 62 to 87%), incidence is on huge decrease since vaccine, so like 500,000/yr and lowering
describe morbidity and mortality of VZV.
usually self limiting in children, ~300K to 500K per yr go to doc bc of high fver, fatal in 2/100K children but a 15 fold increase in adults, and is 7 per 10K fatal in immunocompromised
distinguishing feature bw small pox and chicken pox?
chicken has pox marks of different shapes and sizes at one time while small pox has all at one stage
complications of varicella?
bacterial superinfection of skin lesions, CNS involvement (rare) including meningoencephalitis, peripheral neuritis, and Reye's syndrome (from asprin), additional rare complications include myocarditis, hepatitis, nephritis, orchitis, pancreatitis, arthritis, and keratitis; neonatal varicella is very rare and can be fatal; adults are more susceptible to serious complications, immunosuppressed get persistent viremia
diagnosis of varicella?
clincal presentation is enough but can isolate the virus, detect antigens in the vesicle fluids, and serology (used in retrospective studies)… all this holds true for zoster as well
treatment for varicella?
no specefic treatment for immunnocompetent children, lotion, prevent bacterial infection of scabs, can use acyclovir to reduce # of lesions, fever, itching and length of illness (1 day) but is very good in immunocompromised cases. Immune globulin if given w/i three days of infection is good, used in immunocompromised.
describe the varicella vaccine.
attenuated virus, 95 % seroconversion in healthy kids bw 12 mos and 12 yrs, recommendation is 12 to 15 mos and a booster at 4 to 6 yrs (booster bc protection wanes to ~84% in yrs 2 to 8)
benefits of the varicella vaccine?
decreased incidence of natural varicella infection, less doc visits, less hospital discharges, less deaths
problems with the varicella vaccine?
protection not absolute (can get breakthrough infection), does not protect against zoster (but to date zoster outbreaks are lower in vaccinated individuals than in those with a natural history of varicella infection)
epi of VZV zoster?
mostly in the elderly 60+, occurs in 20% of pop, 1,000,000 per year, but can be present in children. Transmission is reactivation of latent VZV
describe Sx and complications of zoster.
unilateral painful vesicular reuptions usually on head or upper trunk, severe systemic infections in the immunocompromised. Complications include post-herpectic neuralgia (pain form many months after recrudescence happens in about 50% of pts), and repeated attacks that can lead to motor paralysis
zoster treatment?
analgesics, prevent bac infection of scabs, steroids (controversial), usually do not need antivirals but there has been mortalities, can use acyclovir, valacyclovir, and famciclovir in the immunocompromised
zoster vaccine info.
varicella vaccine can reactivate and cause shingles, but there is a zoster vaccine that can be given to the elderly which has much more attenuated virus in it bc that is needed to stimulate elderly's immune response, it reduces burden of illness, decreased incidence of disease and post-herpetic neuralgias
HHV6 epi?
humans are natural hosts, prevalence is approaching 100% seropositive rates, transmission is person to person via direct exposure to secretions
pathology of HHV6.
roseola (exanthem subitum): common, mild febrile disease of infants, fever lasts a few days followed by a rash that resolves spontaneously, complications include invasion of CNS, high fever, vomiting, diarrhea, and hepatosplenomegaly, 10 to 45% of infant ER visits bc of febrile illness. SEVERE disease in immunocompromised: most severe in transplants, reactivation of latent virus can result in marrow suppression, pneumonitis, encephalitis, hepatitis, skin rash and fever, AIDS pts are second group at risk where active CNS infection, pneumonitis, retinitis, and disseminated infection can contribute as cause of death. some evidence of an association with MS and chronic fatigue syndrome
diagnosis and treatment of HHV6?
detect antigen via immunofluorescence or ELISA, treatment: can use ganciclovir and foscarnet but like CMV it is generally resistant to acyclovir, no vaccines
what percentage of US mothers at time of delivery have a recurrent or primary infection with HCMV?
with a primary HCMV infection, the mother has what risk of transmission to baby? Latency decreases this by how much?
40%, by 8 to 10%
most common congenital CMV infection complications?
hearing problems and learning difficulties
what is the seroconversion rate for women of childbearing age? Of childbearing age with toddlers?
1 to 2%, doubles with toddlers
almost all babies with congenitial CMV have what abnormalities?
kidney, which is why you do urine cultures to check babies for CMV
how can you distinguish between congenital and perinatal (or postnatal) HCMV infection?
if IgG is higher in baby than in the mother, if urine culture before 3 wks old is pos, then congenital infection. If IgM is in child usually, but not always indicates perinatal. Note that 50% of children can get CMV from asympto mom during birth (perinatal), 30 to 50% can get it from breast feeding
describe lauren's symptoms.
Lauren enhibited UMN abnormalities such as increased DTR, increased rigidity, persistence of cortical thumbs (hiding of thumb in grip with other fingers) she also had bilateral hip dislocations, and scoliosis she had enlarged ventricles at birth and her EEG was normal she was able to smile, follow, recognize faces, and coo at 11 weeks old her urine culture was (+) for CMV IgM
describe the characteristics of the gamma herpes viruses
characterized by latent infection of lymphocytes with associated cell proliferation, they cause disease during latency
what virus confers to cells an unlimited growth potential and if the most efficient transforming agent in vitro?
EBV epi?
ubiquitous, 50% have it by age 5, over 95% in world have it, usually asymptomatic, lifetime persistance, excreted intermittently in saliva throughout life
transmission of HBV?
lotsa asymptomatic shedders, saliva, blood transfusion, tissue transplants, sexual transmission
what does EBV do when it gets into the cell?
circularizes its genome to become plasmid like
what cells are initially infected with EBV, then spreads to what cells and causes what to happen?
primary oropharyngeal infection… goes to B lymphocytes, and viral DNA goes to nucleus and forces proliferation of the B lymphocytes, thus no infectious virions made, stays in DNA form w/I the cell, lifelong persistance within the host
manifestations of mono from EBV?
clinical triad is fevere, sore throat, and cervical lymphadenopathy/hepatosplenomegally; hematologic there will be greater than 10% lymphocytes; serologically there are transient heterophile antibodies and permanent EBV specefic antibodies
when will acyclovir work in EBV patients?
only during lytic infections which are rare and not the preffered way for this virus to replicate
describe HBV infection of B cells.
binding of CD21 receptor (usually for complement component) to viral glycoprotein, fusion/entry from HLA class II coreceptir to viral glycoproteins
what viral proteins are necessary for replication of the virus within the B lymphocyte?
only one, the EBNA 1 protein that binds the viral genomes ORF in the nucleus so it can replicate with the cell, note it is dependent on celllular enzymes so there is no role for acyclovir in this process
describe the cytotoxic T cells seen on a blood smear in EBV infection and their purpose.
T cells are the atypical lymphocytes seen in a blood smear, not B cells. They have larger nuclei than normal and a large cytoplasm indented with RBC's. Can have up to 70% T cells in total WBCs in acute mono thus distinction between leukemia and mono may be necessary. note these T cells are not the cells infected by EBV. they target EBV late proteins (EBNAs and LMPs) which are causing the proliferation of the virus. They are also eliminating infected proliferating B cells
what are the proteins that drive EBV infected cells to proliferate?
6 EBNAs (EB nuclear antigens) and 3 LMPs (latent membrane proteins) types 1 and 2; note they are also needed for transformation in vitro
why are heterophile Ab's made in EBV infection and what do they do?
they do not react with EBV antigen bc they are a non specefic auto antibody from the B cell proliferation, they hemagglutinate sheep RBC's (the monospot test)
when do you want to use EBV specefic antibodies for diagnosis?
when leukemia is suscpected bc the monospot test may be pos in leukemia bc the heterophile antibodies are non specefic, so you want EBV specefic antibodies. Patterns of EBV Ab can be useful for acute vs chronic infection, remember EBV Abs persist for life.
what will the serum antibodies look like in an acute EBV infection?
IgM to the viral capsids and no EBNA antibodies bc they do not appear until the T cell response is active and can destroy the EBV infected B cells (this can be up to three months later). Note in chronic you have EBNA Ab's and capsid IgG
what are most of the clinical symptoms of EBV due to?
immune mediated response to lysis of infected B cells
what are the EBV mono complications?
splenic rupture due to over expansion of B cells; hematologic: neutropenia, thrombocytopenia, hemolytic anemia all due to the large number of auto Ab's produced; neurologic: enceph/meningitis (most frequent cause of death, 85% completely recover) note enceph can exist without other mono Sxs so keep EBV in mind with enceph.
age related spectrum of EBV?
children: usual asymptomatic seroconversion, can get atypical presentations of rashes, neutropenia, respiratory infection, periorbital swelling, 50% are HETEROPHILE NEG (up to 80% in less than 4) thus may need EBV specefic Ab tests. Young adults: 50% symptomatic at primary infection, 90% heterophile positive. Elderly: fever, ab pain, hepatic abnormalities are all common abnormal presentations
differentials of EBV mono?
strep pharyngitis or any pharyngitis, heterophile negative mono (CMV, toxoplasmosis, acute HIV infection can all cause mono like Sx), gonococcal pharyngitis, retropharyngeal abscess
treatment of EBV mono?
no antivirals, supportive, corticosteroids will help with in complications of impending airway obstruction, severe thrombocytopenia, hemolytic anemia
What are the EBV B cell diseases besides mono?
post transplant lymphoproliferative disorder, hodgkins lymphoma, burkitt's lymphoma (associated with chrom translocation involving chrom 8 and 14, 2 or 2
what percentage of circulating memory cytotoxic T cells are EBV specefic in life long carriers?
what viral proteins are necessary for the malignancies of EBV?
all 6 EBNAs and 3LMPs in post transplant lymphomas; EBNA1, LMP1, LMP2A in nasopharyngeal carcinoma, hodgkins, and gastric carcinoma; only EBNA1 in Burkitt's
what EBV viral proteins act like the B cell receptor/surface Ig and the CD40 receptor on B cells to stimulate infected B cells to remain in the long term memory pool?
LMP 2 acts like the B cell receptor (note it is active without antigen bound to it unlike the real B cell receptor) and LMP 1 acts like CD40
when can EBV latent infections become lytic?
when the infected memory B cell differentiates into a plasma cell and secretes virus via lysis rather than antibody, usually in oropharyngeal area
why do bone marrow transplant patients especially get EBV lympho proliferative disease that can be fatal?
there are no T cells to get rid of the EBV infected B cells so they run wild
what are cellular characteristics of Hodgkins lymphoma?
dual nuclei B cell with non fuctional surface immunoglobulins that are rescued by EBV and allowed to proliferate
how can you get nasopharyngeal carcinoma in EBV? Epi?
shedding of virus during lytic phase makes it infect epithelial cells, seen in AIDS patients. Prevalent in southern Asia and eskimos, sporadically in US and western Europe, 100% of poorly differentiated NPC contain EBV, characterized by latent infection.
where are burkitt's lymphomas coming from ?
the memory B cell pool
what percentage of gastric carcinoma is EBV associated?
describe oral hairy leukoplacia.
in immunosuppressed, non malignant hyperplastic lesion of epi cells of tongue, looks like candida, lotsa viral replication and acyclovir will work in this case, but it is non life threatening disease