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90 Cards in this Set
- Front
- Back
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What percent nucleotide homology exists between HSV-1 and HSV-2?
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50%
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What percentage of U.S. adults has antibodies to HSV-1?
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80%, but half of these individuals are completely asymptomatic.
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How are HSV-1 and HSV-2 acquired?
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Direct contact with virus-containing secretions or lesions.
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Can virus be transmitted from infected individuals without visible lesions?
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YES
Asymptomatic shedding of virus can occur. |
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Where does HSV-1 and HSV-2 multiply?
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In mucosal epithelial cells.
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How can HSV-1 and HSV-2 infection present clinically?
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Most commonly as oral lesions for HSV-1 and genital lesions for HSV-2, but both viruses can infect either area.
Lesoins are usually vesicles adn painful shallow ulcers that are accompanied by fever, malaise, and myalgias. |
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How else can HSV present clinically?
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1) Gingivostomatitis (children)
2) Pharyngitis (adults) 3) Tonsillitis (adults) 4) Keratoconjunctivitis 5) Aseptic meningitis 6) Encephalitis |
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What part of the CNS does HSV preferentially infect?
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The temporal lobes by way of the trigeminal nerves
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What are the major risks for newborns of mothers infected with HSV?
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Herpes encephalitis and disseminated viral infection.
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What is the mortality rate for herpes encephalitis in children?
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70%
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What is the risk of pregnant women with genital herpes infecting their newborn during vaginal delivery?
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30-40%
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How can risk from vaginal delivery be reduced?
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Women with active HSV infection at the time of birth must undergo cesarean section to reduce exposure to HSV
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Is the risk of transmission to a newborn greater during HSV-2 primary infection or reactivation?
Why? |
Primary infection
More virus is shed during primary infection and the mother has not yet made anti-HSV antibody |
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What is the reservoir for HSV-1 and HSV-2?
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Mature neurons, commonly that trigeminal ganglia for HSV-1 and the sacral or lumbar ganglia for HSV-2.
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What can cause reactivation of a virus?
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Hormonal changes, fever, sunlight, stress, and damage to neurons.
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How does HSV-1 reactivation present?
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A clusters of vesicles on the lips, which take approximately 10 days to heal
Reactivation infections are typically less severe than primary infections. |
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How is HSV infection diagnosed?
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1) Clinical diagnosis
2) Cell culture 3) Tzanck smear 4) Serologic tests (in acute infection) 5) Polymerase chain reaction of viral DNA from spinal fluid to diagnose herpes encephalitis. |
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What is the gold standard for diagnosis?
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Cell culture
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What does the Tzanck smear show?
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Multinucleted giant cells with intranuclear inclusions.
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What is the drug of choice for treating all HSV infections?
How does it work? |
Acyclovir, a guanine analog
Is phosphorylated by viral thymidine kinase which activates it, enabling it to terminate replication of viral DNA |
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How is Acyclovir specific for viruses and not for host cells?
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Viral thymidine kinase phosphorylates acyclovir more effectively than cellular thymidine kinase, therefore there is a higher concentration of active drug in virus-infected cells.
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Does Acyclovir cure HSV?
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NO
Because it does not prevent recurrence of primary disease. |
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What are the benefits of acyclovir treatment?
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It can reduce the duration of lesions, as well as viral shedding, and if used prophylactically, it may reduce the number of recurrences
Acyclovir also reduces mortality and morbidity form herpes encephalitis. |
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What disease does primary VZV infection cause?
How does this present clinically? |
Varicella (chickenpox)
Rash that begins as pruritic macules that evolve into papules, which present simultaneously at all stages of evolution, in conjunction with a prodrome of chills, fever, malaise, headache, sore throat, and cough |
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How is VZV transmitted?
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Respiratory droplets
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How does initial infection of VZV result in disseminated disease?
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The virus initially infects respiratory mucosa, then spreads hematogenously to internal organs, an dfinally spreads to the skin.
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Can asymptomatic individuals spread the virus?
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YES
An infected individual can transmit virus before infection becomes clinically apparent |
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What is the incubation period for primary VZV infection?
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14-16 days
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What is the reservoir for latent VZV infection?
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Multiple sensory ganglia, most commonly trigeminal and dorsal root ganglia.
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Does asymptomatic viral shedding after primary infection occur?
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NO
VZV is the only herpesvirus in which asymptomatic shedding does not usually occur |
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What is reactivated VZV?
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Herpes zoster or shingles
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How does Zoster present clinically?
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Clustered vesicular lesions in a single dermatomal pattern along with postherpetic neuralgia (pain) and abnormal sensation over the affected dermatome.
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How often does VZV reactivation occur?
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15% of individuals with varicella will develop zoster, usually later in life as immunity to VZV wanes
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What are three complications of VZV infection?
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Varicella pneumonia
Fulminant hepatic failure Varicella encephalitis |
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What is Reye syndrome?
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Encephalopathy and liver failure of unknown etiology associated with children given aspirin during VZV and influenza infection.
For this reason, aspirin should be avoided in children younger than age 18 |
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How is VZV diagnosed?
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Usually by clinical diagnosis; however, a laboratory diagnosis for atypical presentation or infections in immunocompromised patients can be performed with immunofluorescence or immunoperoxidase (24 hours), in situ DNA probe, or scraping vesicular cells and reacting with different stains
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What does cell culture demonstrate in VZV infections?
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Multinucleated giant cells with intranuclear inclusions
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What is the treatement for varicella?
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IV acyclovir is preferred for varicella, but treatment is reserved only for severe cases
Varicella Ig is also used in immunocompromised individuals |
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What is the treatment for zoster?
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Famciclovir and valacyclovir (if given early in the course of infection) can reduce acute pain and shorten duration of zoster and postherpetic neuralgia
Oral acyclovir is also effective for zoster, but has no effect on postherpatic neuralgia, which is often treated with tricyclic antidepressants or gabapentin |
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Is there a vaccine for VZV?
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Yes a live-attenuated virus is routinely given to infants
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How is CMV transmitted?
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By respiratory droplets, intrauterine infection,sexual contact, blood contact, and breast milk
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Can CMV cross the placenta?
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Yes, it is the most common cause of intrauterine viral infection and congenital abnormalities in the US
CMV is one of the TORCHES organisms |
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What percent of the adult population is CMV positive?
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More than 80%
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What is the reservoir for latent CMV?
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Unknown; possibly monocytes and macrophages
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Does asymptomatic viral shedding occur?
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YES
CMV is characterized by repeated episodes of asymptomatic viral shedding for prolonged periods |
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What group of patients is at risk for symptomatic CMV infection?
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Immunocompromised
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How does CMV present clinically in children?
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asymptomatically
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How does CMV present clinically in immunocompetent adults?
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As heterophile-negative infectious mononucleosis causing fever, myalgias, and lymphadenopathy.
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How does infectious mononucleosis with CMV differ from that caused by EBV?
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Unlike EBV, there is an absence of heterophile antibodies with CMV infection
EBV-heterophile antibody positive EMV-heterophile antibody negative |
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What are heterophile antibodies?
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IgM antibodies that agglutinate horse and sheep red blood cells
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What are clinical manifestationsof CMV infection in immunocompromised adults?
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Pneumonia, retinitis, hepatitis, encephalitis, esophagitis, enterocolitis, and gastritis
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What are clinical manifestations of CMV infection in neonates?
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Mental retardation, microcephaly, hepatosplenomegaly, seizures, deafness, and purpura
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During what stage of pregnancy does primary CMV infection result in the most severe symptoms?
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First trimester
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How is CMV diagnosed?
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Cell culture and PCR
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What does cell culture demonstrate?
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"Owl's eye" nuclear inclusion bodies in infected cells.
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How is CMV treated?
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Canciclovir, foscarnet, or cidofovir
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Is there a vaccine available for CMV?
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There is no vaccine for CMV
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Why is acyclovir ineffective against CMV infection?
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CMV lacks thymidine kinase necessary for acyclovir activation
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How are human herpesvirus (HHV)-6 and HHV-7 transmitted?
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Oral secretions
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What disease do HHV-6 and HHV-7 cause?
How does this present clinically? |
Roseola infantum
High fever followed by erythematous macular rash and possibly febrile seizures. |
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How often are HHV-6 infections symptomatic?
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33-50% of infections are symptomatic
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How often are HHV-7 infections symptomatic?
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Rarely; generally asymptomatic
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Where does viral replication take place?
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Salivary glands
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What percent of the population has been exposed to HHV-6 and -7?
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90% of the population has detectable antibody by 3 years of age
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How does HHV-6 coinfection with human immunodeficiency virus (HIV) accelerate progress to terminal acquired immune deficiency syndrome (AIDS)?
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1) HHV-6 induces synthesis of CD4 on lymphocytes, allowing more cells to be infected with HIV
2) HHV-6 accelerates the rate of cell death by transactivating transcription of HIV |
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How does HHV-6 usually present in AIDS patients?
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As encephalitis
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How are HHV-6 and HHV-7 diagnosed?
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No good single diagnostic test, but PCR amplification can be used to detect DNA in cerebrospinal fluid (CSF) or serum
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How are HHV-6 and HHV-7 treated?
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Ganciclovir, cidofovir, and foscarnet
For aids patients, treatment of HIV helps treatment for HHV-6 |
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Is there a vaccine available for HHV-6 or HHV-7
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NO
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How is EBV transmitted?
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Contact with respiratory secretions and saliva
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What is the reservoir for latent EBV?
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B lymphocytes
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What is the B-cell receptor for EBV?
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The complement C3b receptor
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What do the early genes of EBV encode?
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Unlike other herpesviruses, early genes of EBV induce cell multiplication and immortalization rather than cell death.
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How does EBV present clinically?
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1) Infectious mononucleosis with fever, haryngitis, and lymphadenopathy
2) Hepatitis (rare) 3) Encephalitis (rare) |
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When is the peak incidence of EBV infectious mononucleosis?
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Between 15 and 19 years of age; because it is spread via close contact, it is often known as kissing disease
Most EBV infections occur earlier in life but in contrast to late childhood infections, early childhood infections are usually asymptomatic. |
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What is the typical incubation period for EBV?
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4-7 weeks
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How does infectious mononucleosis from EBV differ from infectious mononucleosis caused by CMV or toxoplasmosis?
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1) Burkett's lymphoma
2) Nasopharyngeal carcinoma 3) B-cell lymphomas |
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What populations have a high rate of nasopharyngeal carcinoma caused by EBV?
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Inuits (Eskimos) and people living in SE Asia and North Africa.
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What nonmalignant lesion does EBV cause in AIDS patients?
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Hairy leukoplakia of the tongue
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What percent of the population has been exposed to EBV?
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90%
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How is EBV diagnosed?
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1) Presence of heterophile antibodies
2) Detection of EBV-specific antibodies such as viral capsid antigen, early antigen, Epstein-Barr nuclear antigen (monospot test). 3) Presence of atypical lymphocytes on peripheral blood smear. |
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What are 'atypical lymphocytes'?
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Cytotoxic T lymphocytes activated by EBV infection.
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What is teh treatment for EBV infection?
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Supportive treatment only, because antiviral therapy has no effect on the course of typical EBV infection.
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Is there a vaccine for EBV?
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NO
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What is the primary mode of transmission?
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Sexual
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What does HHV-8 cause?
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Kaposi sarcoma and primary effusion lymphoma.
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What is Kaposi sarcoma?
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A vascular neoplasm consisting of nodules in the skin, mucous membranes, and visceral organs usually with an indolent course.
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What are the clinical manifestations of Kaposi sarcoma?
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Reddish-purple skin nodules, oral mucosa discolorations, lymphadenopathy, and organ failure
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What population is at increased risk for developing Kaposi sarcoma?
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Patients with HIV
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How is HHV-8 identified?
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Serologically by detection of antibody with enzyme-linked immunoabsorbent assay or immunofluorescence reaction or by PCR amplification with subsequent DNA hybridization
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