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Virology, Parasitology, Mycology > Herpes > Flashcards

Herpes Flashcards

1
Q

What are the structural features of Herpes virus?

A

linear ds DNA, icosahedral virus particle, membrane bound (how it hides from immune system, can lyse cell if in danger, release of naked virion), lipid envelope with glycoproteins

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2
Q

What are the three types of herpes viruses? Features of each type and subfamilies belonging to each type?

A

alpha- infect many cell types, HHV1-3 aka HSV1, HSV2, and varicella-zoster (VZV); gamma- infect only one cell type, HHV4 or EBV; and Beta- infect 2-3 cell types, HHV5 (CMV), HHV6-8

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3
Q

Which herpes viruses are transmitted via close contact? Which are only transmitted this way?

A

All of them; HSV1 and 2 and EBV

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4
Q

Which herpes viruses are transmitted via respiratory?

A

VZV, HHV6, HHV7, andHHV8

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5
Q

Which is herpes virus is transmitted via transfusion, tissue transplant, close contact and congenital?

A

HHV5

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6
Q

By adulthood how many people are infected by a herpes virus? How many get the disease associated with the virus?

A

70-95%; only 15%, infection does not equal disease

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7
Q

What are the pathogenic and immune features of HSV type 1 and 2?

A

initiated by direct contact, disease dependent on site, virus-> direct cytopathology resulting in lesions, avoids antibody by cell-cell spread-> est. latency, reactivates when stimulated (stress or immunosuppression), cell mediated immunity required for resolution

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8
Q

What are the features of oral herpes virus?

A

gingivostomatitis- primary infection, 15% infected develop lesion affecting area supplied by trigeminal, clears up and virus goes latent in trigeminal

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9
Q

What are the clinical syndromes of HSV?

A

gingivostomatitis, eczema herpeticum, herpes keratoconjunctivitis, herpetic whitlow, herpes encephalitis, pharyngitis, herpes gladitorium, genital herpes, and neonatal herpesvirus

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10
Q

What is eczema herpeticum?

A

infection of an open wound

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11
Q

What is herpes keratoconjunctivitis? Features?

A

infection of eye, can lead to blindness, usually heals 1-2 wks, 10K /year go blind from this

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12
Q

What is herpetic whitlow?

A

infection of finger

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13
Q

What is herpes gladitorium?

A

infection of body/trunk

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14
Q

What are the features of genital herpes?

A

venereal, HSV2 most likely primary infection (70-90%), often asymptomatic, frequently associated with fever malaise swollen regional lymph nodes, F: legions in perineum, cervix, vaginal area, painful urination M: whole penile area, sometimes urethra, 10% of all genital infections

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15
Q

What are the features of neonatal herpes simplex viral infection?

A

frequently fatal, HSV2 majority of the time, contracted leaving the birth canal, often brain involvement and/or blindness

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16
Q

How are herpes simplex viral infections diagnosed?

A

clinical picture, cytology and histology, serology, viral isolation and identification

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17
Q

What are the features of cytology and histology of herpes simplex viruses?

A

tzanck smear, papanicolaou smear, or biopsy specimen with syncytia, cowdry type A intranuclear inclusion bodies; immunofluorescence or immunoperoxidase- Ab specific for virus can be used to directly probe tissue

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18
Q

What are the features of serology with herpes simplex virus?

A

acute vs convalescent; 4 fold increase in IgG in conjunction with switch from IgM to IgG

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19
Q

What are the methods used for herpes simplex viral isolation and identification?

A

vesicular fluid collected from a lesion and tissue culture cells infected, cells observed for CPE, can be probed for the presence of virus using monoclonal Ab

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20
Q

How is HSV treated?

A

5-iodo-2deoxyuridine (IDU), adenine arabinose, anti-virals that block guanosine uptake, methylparaben, halides, phenol, and abreva

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21
Q

How does IDU work?

A

inhibit thymidilate phosphorylase and viral DNA polymerase activity

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22
Q

How does adenine arabinose work?

A

analogue of adenosine that interferes with viral DNA synthesis as it forms ara-ATP and replaces dATP making faulty DNA

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23
Q

What anti-virals block guanosine uptake?

A

acyclovir, Valtrex, and famcyclovir

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24
Q

What products can methyl paraben be found in? halides? phenol?

A

carmex; lots of things including colgate (Cl, Fl, Br); blistex (kill anything)

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25
Q

How does abreva work?

A

binds to membrane and destroys it, fatty acid alcohol

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26
Q

How is HSV spread prevented?

A

health care professionals must carefully handle patient materials, sex contact permitted- preferably no lesions, use condoms; pregnancy- vaginal birth if no open lesion or viral shedding, C-section; no vaccine

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27
Q

What are the 5 original childhood exanthems (rashes)?

A

measles, mumps, rubella, exanthema subitum (roseola infantum), and varicella-zoster

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28
Q

Describe the characteristic rash with varicella?

A

pock-type lesion, start in soft tissue area and spread over the whole body, lesions contains thousands of virions

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29
Q

What are the epidemiologic features of varicella?

A

occurs world-wide, epidemics occurred in winter and spring, transmission primarily through respiratory tract, incubation period 10-14 days at which time lesions began appearing

30
Q

What are the feature of zoster?

A

primarily adult disease, similar pock-type lesions observed with varicella, restricted to areas supplied by dorsal root ganglion of low back and back of legs, virus latent after varicella; epidemiology- worldwide, adults, immunosuppressed, reactivation of virus

31
Q

What are the pathogenic features of varicella?

A

begin in resp. (replicates here), cold-like symptoms, moves by primary viremia to liver, spleen and other organs of immune via lymphatics, replicates -> secondary viremia causing: fever, malaise, head ache, and sore throat, goes to skin (day 10-14, last 7), incubate: 10-11 days, contagious from rash appearance til crusting

32
Q

What are the features of varicella virus infecting the skin?

A

through specific receptors dermal vesiculopustular rash, looks like small burn

33
Q

What are the pathogenetic features of zoster?

A

re-activation of virus along supply of dorsal root ganglion (back of legs and buttocks)

34
Q

How is varicella-zoster diagnosed?

A

clinical picture, recognition of outbreaks most common method, cytology rare, growth in tissue culture can be done rapidly (24-48 hours), serology can be done (cheaper and easier)

35
Q

How is varicella-zoster treated?

A

predominately the symptoms: aspirin, acetaminophen, naproxen for fever and beydryl, cortisol, Metamucil baths for itching; acyclovir may shorten course but not very effective, zoster Ig if symptoms severe (immune suppressed)

36
Q

What role does prevention play in varicella-zoster infection?

A

not effective in past; stopping transmission method utilized for years, vaccine developed, concern on whether immunization would require booster, zoster vaccine for adults (10 fold the child dose, expensive)

37
Q

How was EBV discovered?

A

isolated looking for agent causing Burkitts Lymphoma

38
Q

What are the epidemiologic features of EBV?

A

transmitted through saliva (intimate oral contact, sharing items), blood transfusion or bone marrow transplant (B-cell infection)

39
Q

What are the disease and viral factors of EBV?

A

lifelong infection, recurrent disease is source of contagion, virus shed asymptomatically

40
Q

Who is at risk for EBV infection?

A

children- normally asymptomatic, mild symptoms; teenagers and adults- at risk for infectious mononucleosis; immunocompromised- risk for neoplastic (cancer, specifically lymphomas)

41
Q

Who is at risk of getting EBV? Geography or season?

A

susceptible roomates, households; virus worldwide, strong causative association with Burkitt’s lymphoma in areas where malaria is endemic, strong association w/ nasopharyngeal carcinoma where euphorbaccea plants grow

42
Q

What are the pathogenic features of EBV?

A

mechanism: infects epithelial cells of oropharynx, spreads through lymphatics, infects B-cells, T-cells begin to kill and limit B-cell outgrowth= virus latent in B cells, Tcell response contributes to symptoms of infectious mononucleosis-> swelling of liver, lymph nodes and spleen, immune shut down, may be reactivated

43
Q

What is the most common manifestation of EBV?

A

infectious mononucleosis, most people seroconvert with no apparent disease, 80-90% of all individuals infected with EBV but only 15% develop IM

44
Q

What is the clinical triad of infectious mononucleosis?

A

sore throat, fever, lymphadenopathy often accompanied by hepatosplenomegally

45
Q

What are the complications associated with infectious mononucleosis?

A

potential rupture of spleen or liver (no contact rule), rash can appear if given erythromycin (physician thought B infection)

46
Q

How is infectious mononucleosis diagnosed?

A

primarily based on clinical symptoms; lab tests, Ab to viral Ag

47
Q

What are the lab tests for infectious mononucleosis?

A

hematologic findings (atypical lymphocytes aka Downey cells- T cells), heterophile Ab an IgM that recognizes Paul-Bunnell Ag, detected by monospot test

48
Q

What are the antibodies for viral antigens in infectious mononucleosis?

A

VCA- capsid only acute, EA- early Ag variable expression, EBNA- nuclear Ag expressed late signals past infection

49
Q

How is infectious mononucleosis treated?

A

self-limiting disease- bed rest, aspirin or acetaminophen, corticosteroid if brain involved (let virus replicate and decrease brain swelling and inflammation)

50
Q

What are the features of Epstein-barr virus induced lymphoproliferative disease?

A

immunosuppressed patients at risk, burkitt’s lymphoma (BL), and nasopharyngeal carcinoma (NPC)

51
Q

Who is at risk for Epstein-barr virus induced lymphoproliferative disease?

A

HIV, primary and secondary immunodeficiencies- x-linked lymphoproliferative syndrome, and transplant recipients

52
Q

What are the clinical features of Burkitt’s Lymphoma?

A

B cell lymphoma that is found primarily in children in endemic malaria regions of Africa, strong association of EBV with development of tumor (flakey cell)

53
Q

What are the clinical features of NPC?

A

cancer found primarily in China, along coastal regions where a lot of salted fish is consumed, areas where euphorbaccea plant is grown (antigen causes B cell proliferation- mitogen)

54
Q

What causes hairy oral leukoplakia?

A

infection of epithelial cells of the tongue with EBV, most often seen in AIDs patients

55
Q

What is the epidemiology of cytomegalovirus?

A

80-90% of adults infected, most asymptomatically seroconvert, neonates: trans placental transmission, intrauterine infections, cervical secretions, baby or child: body secretions such as breast milk, saliva, tears, urine; Adult- sexual transmission semen, blood transfusion, organ graft stupidity

56
Q

What diseases are associated with cytomegalovirus?

A

non-classical mononucleosis, most common viral congenital defects (1st trimester), perinatal infections, organ-transplant recipients, infection in immunocompromised host leading to other disease

57
Q

What are the features of non-classical mononucleosis? differential?

A

resembles classic but not as severe a sore throat, no rise in heterophile Ab; differential: EBV, CMV, toxoplasmosis, strep, acute retroviral syndrome

58
Q

What are the congenital defects associated with CMV?

A

MR, microcephally, #1 stillbirths

59
Q

What are the features of perinatal infection with CMV?

A

in US 20% of pregnant women with active disease, acquired during birth and through maternal milk, transfusion

60
Q

What are features of organ-transplant recipients leading to CMV infection?

A

on cyclosporine A extremely susceptible to virus as it can reactivate, during graft v host disease w/ strong association to this virus and pneumonitis, major cause of failure of liver and kidney transplants

61
Q

What diseases result from CMV infection of immunocompromised host?

A

respiratory, retinitis, interstitial pneumonia or encephalitis, colitis and esophagitis

62
Q

How is CMV diagnosed?

A

histology- enlarged cells, owl eye type of inclusion body; tissue culture- grown in diploid fibroblasts, culture amplification using Ab to CMV

63
Q

How is CMV treated?

A

ganciclovir- similar action as acyclovir as blocks the uptake of guanosine into growing viral DNA chain, does not terminate the chain; foscarnet: inhibits binding of pyrophosphate at viral specific DNA polymerase which is necessary for phosphorylation of nucleotides

64
Q

How is CMV prevented?

A

condoms and abstinence

65
Q

What are the two types of HHV6? Disease associations?

A

HHV6a and HHV6b; exanthema subitum (roseola infantum), Kaposi’s sarcoma, Hodgkin’s disease, multiple sclerosis

66
Q

What are the features of exanthema subitum (roseola infantum)?

A

characterized by rapid onset high fever, few days duration, followed by generalized rash for 24-48 hours most likely due to DTH reaction, disease controlled and resolved by cell-mediated immunity, virus establishes lifelong latent infection in T-cells

67
Q

How are the features of multiple sclerosis and its association with HHV-6?

A

commensal inhabitant of the brain, suggested to play a role in this disease

68
Q

What are the pathogenic features of HHV-6? Epidemiology?

A

may need helper virus HHV-7; virus worldwide, 80-90% of population infected with this virus

69
Q

How is HHV-6 diagnosed and treated?

A

immunofluorescence or molecular; supportive care (tumor-> cytotoxic aid, treat symptoms)

70
Q

What are the features of HHV-7?

A

closely related to HHV-6, disease associations (Kaposi’s sarcoma- detected in lesion, chronic fatigue syndrome, exanthema subitum- roseola infantum), pathogenesis- CD4+ T cell site of infection,

71
Q

What are the epidemiological, diagnostic, and treatment of HHV-7?

A

epidemiology- 85% of people in US infected, diagnosis- immunofluorescence and molecular, treatment- treat symptoms

72
Q

What are the features of HHV-8?

A

recently discovered- AIDs associated Kaposi’s sarcoma (KS), associated with B cells, may play a role in other proliferative diseases

Virology, Parasitology, Mycology (15 decks)

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