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Microbiology Part 2 > Lec 33 CMV EBC other Herpes > Flashcards

Lec 33 CMV EBC other Herpes Flashcards

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1
Q

What are 3 drugs used to treat CMV?

A
  • ganciclovir
  • valganciclovir
  • cidofovir
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2
Q

What are the common characteristics of herpes viruses?

A
  • large
  • enveloped
  • double strand DNA
  • ubiquitous [except HHV 8]
  • chronic/latent infection follows acute
  • reactivations common
  • mostly transmitted by close contact during asymptomatic reactivation and shedding [except varicella]
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3
Q

What is the one herpes virus that is not ubiquitous?

A

HHV8

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4
Q

Who is at higher risk for getting herpes viruses?

A
  • immunocompromised particularly with CMI deficiency
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5
Q

What are clinical symptoms of EBV?

A

causes mononucleosis syndrome

  • fever
  • pharyngitis
  • lymphadenopathy
  • hepatosplenomegaly + mild hepatitis
  • rash
  • atypical lymphocytes
  • rarely also: upper airway obstruction, splenic rupture
  • resolves in 2-3 wks –> fatigue/malaise may last longer
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6
Q

What causes mononucleosis syndrome?

A

EBV

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7
Q

What is pathogenesis of mono syndrome?

A
  • resolves in 2-3 wks –> fatigue/malaise may last longer
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8
Q

Who gets mono?

A
  • early childhood usually asymptomatic
  • adolescence/early adult hood
  • 70% of US population infected by age 30
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9
Q

What happens if you give amoxicillin to pt with EBV?

A

can trigger a non-allergic rash

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10
Q

What is pathogenesis of EBV?

A

acute

  • get EBV infection from saliva of infected person
  • EBV infects resting memory B lymphocytes and establishes latency = main target
  • host mounts immune response [humoral and cell mediated]

chronic

  • EBV transforms/immortalizes B cells
  • cell mediated immunity [EBV-specific cytotoxic T] keep B cells from proliferating out of control
  • from time to time: virus can reactivate and enter lytic replication and be shed in saliva
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11
Q

What is pathogenesis of EBV in immunocompromised?

A
  • balance is lost of im

- B cells proliferate out of control –> get lympho-proliferative disorders and cancers

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12
Q

How is EBV transmitted?

A
  • through saliva from subject with acute disease or with asymptomatic reactivation
  • through organ transplantation
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13
Q

What is the receptor for EBV infection? where is it located?

A

CD21 receptor –> on B cells and epithelial cells of oral mucosa and salivary glands

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14
Q

What is immune response to EBV?

A
  • specific cytotoxic T cells control immortalized B cell proliferation
  • expansion of this T cell population causes
  • – atypical lymphocytosis
  • – hyperplasia of lymphatic organs
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15
Q

What is basis of monospot test? who is is sensitive test for?

A

sensitive for: adolescents/adults, not young children

  • basis of test = heterophile antibodies
    ==== non-specific IgM antibodies that sometimes stick to red blood cells and don’t play a role in controlling the infection
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16
Q

What antibodies initially present in EBV infection? later? after months of time?

A

initially: high IgM and IgG against viral capsid antigen
later: antibodies against early antigen appear, IgG persists, IgM decreases

fast forward: IgG persists, IgM goes away, EBNA [antibody against epstein barr nuclear antigen] starts to appear

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17
Q

What does a positive EBNA tell you?

A

patients had mono previously [months or years ago] but it is now resolved

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18
Q

What cancers associated with EBV?

A
  • African [endemic] Burkitt’s lymphoma
  • sporadic burkitt’s lymphoma [less closely associated]
  • nasopharyngeal carcinoma
  • hodgkins lymphoma
  • primary CNS lymphoma in AIDS
  • post transplant lymphoproliferative disease
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19
Q

What are two symptoms/diseases associated with EBV and HIV co-infection?

A
  • oral hairy leukoplakia [white patch on side of tongue, non-malignant]
  • CNS lymphoma
20
Q

What is chronic active EBV? what types of antibodies do you find?

A
  • begins with infectious mononucleosis but acute infection is not adequately cleared
  • high titers of EA and VCA antibodies, lack of appropriate EBNA response
  • major organ involvement, persists for months
  • high mortality
21
Q

What is treatment for EBV?

A
  • supportive treatment
  • reduce immunosuppression in transplant recipients
  • rituximab [anti-CD20] for some EBV related malignancies
22
Q

What is rituximab? mech of action

A
  • an anti-CD20 monoclonal antibody
  • CD20 = a B cell surface receptor
  • acts by: directly causing B cell apoptosis, activating complement-dependent cytotoxicity, activating antibody-dependent cell mediated cytotoxicity
  • used to treat some EBV related malignancies
23
Q

What percentage of population of young adults has CMV?

A

70-90%

24
Q

How is CMV transmitted?

A
  • through secretions of acutely and chronically infected
  • saliva, vaginal fluid, semen, urine
  • through blood transfusion, organ transplantation, mother –> infant
25
Q

What is pathogenesis of CMV infection?

A
  • infects and remains latent in lymphocytes
  • down-regulates immune system by down-regulation MHC 1 expression
    uses UL 54 protein [ a DNA pol] and UL 97 protein [a viral kinase]
26
Q

What immune pathway is essential for maintaining control of latent CMV infection?

A

cell mediated immunity

27
Q

What is UL 54 protein?

A

CMV DNA polymerase

28
Q

What is UL 97 protein?

A

CMV viral kinase, phosphorylates Gancyclovir which is a viral polymerase inhibitor

29
Q

What syndrome associated with CMV [non-congenital] infection?

A
  • EBV negative infectious mononocleosis = milder form of EBV that is pretty asymptomatic, most patients are unaware they are infected
  • common opportunistic pathogen in transplant recipient and pts with AIDS [retinitis, pneumonia, colitis, hepatitis, esophagitis, kidney graft failure]
  • guillain barre syndrome
30
Q

What happens in congenital CMV infection?

A
  • affects 1% of newborns
  • # 1 cause of congenital hearing loss in US
  • CNS disease with calcifications
  • retinitis
  • long lasting lytic infection
31
Q

What is the biggest cause of congenital hearing loss in US?

A

congenital CMV infection

32
Q

How is CMV diagnosed? definitively?

A
  • not usually lab tested in healthy individuals
  • use PCR [in immunocompromised]
  • IgG seroconversion or IgG avidity test [for pregnant women with acute infection to test for risk of transmission to fetus]
  • urine culture [for neonatal disease]

definitively need biopsy: inclusion bodies [owl eyes] or immunohistochemistry

33
Q

How do you test whether a pregnant woman with acute CMV is likely to pass it on to fetus?

A

IgG seroconversion or IgG avidity test

34
Q

How do you diagnose congenital CMV?

A

urine culture

35
Q

What are the first line treatments for CMV?

A 
ganciclovir = nucleoside analogue
valganciclovir = better orally absorbed ganciclovir prodrug
36
Q

What is mech of ganciclovir action?

A
  • GCV phosphorylated by UL97 viral prtoein kinase
  • then phosphorylated 2x more by cell enzymes
  • GCV- tri Phosphate then inhibits DNA polymerase [UL54]
37
Q

What is mech of resistance to ganciclovir?

A

mutations in UL97 or UL54

38
Q

What are the two second line CMV treatments?

A
  • cidofovir

- foscarnet

39
Q

What is mech of action of cidifovir? how is it administered? side effects?

A
  • cidifovir = cytosine analog that inhibits viral DNA pol
  • administered IV
  • can be nephrotoxic, give with probenecid to block active tubular renal secretion
40
Q

What is mech of action of foscarnet? how is it administered? side effects?

A
  • foscarnet = non-nucleoside analog that inhibits viral DNA
  • administered IV
  • can be nephrotoxic, cause electrolyte abdnormalities
41
Q

What is disease of HHV-6? pathogenesis?

A
  • exanthema subitum [Roseola]
  • start with high fever –> then fever leaves and get rash
  • infects lymphocytes/monocytes and other tissues
  • most children infected by age 2-3
  • occurs in transplantation
42
Q

What is disease of HHV-7? pathogenesis?

A
  • causes roseola
  • infects lymphocytes
  • almost all children are infected by age 5
43
Q

What is diease associated with HHV 8?

A

karposi sarcoma

44
Q

What is roseola?

A

roseola = exanthema subitum
start with high fever for a few days then fever leaves and get rash
occurs in infants/young children

45
Q

What is karposi sarcoma?

A

get vascular tumors = HHV8 inside endothelial spindle cells

46
Q

Where is HHV8 endemic? who gets it?

A

endemic in africa, mediterranean –> spread person to person and by sexual transmission

not endemic to US –> associated with AIDS in MSM, get by sexual transmission

Microbiology Part 2 (30 decks)

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