Herpes Flashcards Preview

Virology, Parasitology, Mycology > Herpes > Flashcards

Flashcards in Herpes Deck (72):
1

What are the structural features of Herpes virus?

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

2

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

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

3

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

All of them; HSV1 and 2 and EBV

4

Which herpes viruses are transmitted via respiratory?

VZV, HHV6, HHV7, andHHV8

5

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

HHV5

6

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

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

7

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

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

8

What are the features of oral herpes virus?

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

9

What are the clinical syndromes of HSV?

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

10

What is eczema herpeticum?

infection of an open wound

11

What is herpes keratoconjunctivitis? Features?

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

12

What is herpetic whitlow?

infection of finger

13

What is herpes gladitorium?

infection of body/trunk

14

What are the features of genital herpes?

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

15

What are the features of neonatal herpes simplex viral infection?

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

16

How are herpes simplex viral infections diagnosed?

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

17

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

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

18

What are the features of serology with herpes simplex virus?

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

19

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

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

20

How is HSV treated?

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

21

How does IDU work?

inhibit thymidilate phosphorylase and viral DNA polymerase activity

22

How does adenine arabinose work?

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

23

What anti-virals block guanosine uptake?

acyclovir, Valtrex, and famcyclovir

24

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

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

25

How does abreva work?

binds to membrane and destroys it, fatty acid alcohol

26

How is HSV spread prevented?

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

27

What are the 5 original childhood exanthems (rashes)?

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

28

Describe the characteristic rash with varicella?

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

29

What are the epidemiologic features of varicella?

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

What are the feature of zoster?

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

What are the pathogenic features of varicella?

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

What are the features of varicella virus infecting the skin?

through specific receptors dermal vesiculopustular rash, looks like small burn

33

What are the pathogenetic features of zoster?

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

34

How is varicella-zoster diagnosed?

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

How is varicella-zoster treated?

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

What role does prevention play in varicella-zoster infection?

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

How was EBV discovered?

isolated looking for agent causing Burkitts Lymphoma

38

What are the epidemiologic features of EBV?

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

39

What are the disease and viral factors of EBV?

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

40

Who is at risk for EBV infection?

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

41

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

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

What are the pathogenic features of EBV?

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

What is the most common manifestation of EBV?

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

44

What is the clinical triad of infectious mononucleosis?

sore throat, fever, lymphadenopathy often accompanied by hepatosplenomegally

45

What are the complications associated with infectious mononucleosis?

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

46

How is infectious mononucleosis diagnosed?

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

47

What are the lab tests for infectious mononucleosis?

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

48

What are the antibodies for viral antigens in infectious mononucleosis?

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

49

How is infectious mononucleosis treated?

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

50

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

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

51

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

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

52

What are the clinical features of Burkitt's Lymphoma?

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

What are the clinical features of NPC?

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

What causes hairy oral leukoplakia?

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

55

What is the epidemiology of cytomegalovirus?

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

What diseases are associated with cytomegalovirus?

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

57

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

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

58

What are the congenital defects associated with CMV?

MR, microcephally, #1 stillbirths

59

What are the features of perinatal infection with CMV?

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

60

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

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

What diseases result from CMV infection of immunocompromised host?

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

62

How is CMV diagnosed?

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

63

How is CMV treated?

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

How is CMV prevented?

condoms and abstinence

65

What are the two types of HHV6? Disease associations?

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

66

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

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

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

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

68

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

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

69

How is HHV-6 diagnosed and treated?

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

70

What are the features of HHV-7?

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

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

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

72

What are the features of HHV-8?

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