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Viremia Flashcards

1
Q

What are the four major diseases that viruses that cause circulatory infections cause?

A
  1. CA
  2. Birth defects
  3. Immunosuppression
  4. Cardiac dysfunction
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2
Q

What is the state of viral infection for mono?

A

Productive, but disease due to immnopathology

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3
Q

What is the state of viral infection for oral hairy leukoplakia?

A

Productive

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4
Q

What is the state of viral infection for Burkitt’s lymphoma?

A

Latent

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5
Q

What is the state of viral infection for Hodgkin’s disease?

A

Latent

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6
Q

What is the state of viral infection for nasopharyngeal carcinoma?

A

Latent

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7
Q

What is the state of viral infection for PTLD?

A

Latent

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8
Q

What are the six diseases that the epstein Barr virus can present as?

A
  1. Mono
  2. Oral hairy leukoplakia
  3. Burkitt’s lymphoma
  4. Hodgkins lymphoma
  5. Nasopharyngeal carcinoma
  6. PTLD
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9
Q

What is the family of EPV? Enveloped? Genome?

A

Herpesviridae
Enveloped
dsDNA

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10
Q

What is the component of the complement that herpes viruses use to attach and enter into cells?

A

C3d

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11
Q

What two types of cells do EPVs replicate in?

A

B cells

Epithelial

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12
Q

What is the pathophysiology of EBV?

A

Infects B cells, causes them to reproduce and create heterophile antibodies

T cells come in to kill, but not perfect. leave memory B cells

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13
Q

What is the first test for EBV?

A

Look for heterophile antibodies

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14
Q

What cells contribute to EBV latency?

A

Memory B cells

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15
Q

What are the genes associated in EBV carcinogenesis?

A
  1. Latent membrane protein 1
  2. LMP2
  3. EBV nuclear antigen-1
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16
Q

What is LMP1? What does this protein lead to?

A

6 transmembrane domains protein with a CD40 homologue

Leads to high proliferation

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17
Q

What is LMP2?

A

Protein that increases growth of B cells

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18
Q

What is EBV nuclear antigen 1

A

Transactivation of EBV

inhibit apoptosis

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19
Q

What is the primary mode of transmission for EBV?

A

Saliva

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20
Q

What are the four major symptoms of mono?

A
  1. Fever, malaise etc
  2. Exudativepharyngitis
  3. Splenomegaly
  4. TTP lymphadenitis
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21
Q

What is the biochemical markers for mono?

A

Heterophile antibodies

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22
Q

What is the epidemiology of mono ( in the US)?

A

Young adulthood

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23
Q

What is the major complication of mono?

A

Spleen rupture

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24
Q

What is the pathogenesis of mono?

A

Immune targeting of the infected B cells

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25
Q

What is the treatment for mono?

A
  1. Supportive

2. Avoid splenic rupture

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26
Q

Ampicillin treatment of EBV causes what?

A

A diffuse, petechial rash

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27
Q

How long are symptoms present with mono?

A

About a month

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28
Q

How long do atypical lymphocytes caused by EBV last?

A

About a month

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29
Q

How long does the heterophile titer remain elevated in EBV?

A

About a month

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30
Q

When does anti-EA production start in EBV infection?

A

about 10 days, and continues to end of the month of infx

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31
Q

When does anti-VCA production start in EBV mono infection?

A

day 10 to forever (IgM to IgG)

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32
Q

When do antibodies to the EBNA start?

A

Months later

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33
Q

How do you diagnose mono?

A

Mono spot test looking for heterophile antibodies agglutination to sheep or horse RBC

Antibodies to EBV

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34
Q

What are downey cells? What are the three characteristics of these cells?

A

Atypical T cells found in EBV infections

  1. Have vacuoles
  2. Altered nucleus
  3. Indented cell margin
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35
Q

How can we prevent mono? Is there a vaccine?

A

No vaccine

antivirals to inhibit the viral pol

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36
Q

Are antivirals effective in EBV?

A

Yes, but symptoms remain unchanged b/c of immune response

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37
Q

Who usually gets oral hairy leukoplakia?

A

Immunosuppressed population

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38
Q

What causes oral hairy leukoplakia?

A

EBV shedding

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39
Q

What is the treatment for oral hairy leukoplakia? (2)

A
  1. Antiherpetic drugs

2. Podophyllin resin

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40
Q

What is Burkitt’s lymphoma caused by?

A

EBV

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41
Q

Where in the body does Burkitt’s lymphoma present? Symptoms?

A

B cells in the Jaw of children

CA of the jaw

42
Q

Where is the world is Burkitt’s lymphoma found?

43
Q

What causes Burkitt’s lymphoma?

A

Myc gene on ch14 translocated to ch8, changes E2F expression

44
Q

What is the pathophysiology of Burkitt’s lymphoma?

A

Increase in E2F d/t translocation of the Myc gene

45
Q

What is the treatment for Burkitt’s lymphoma?

46
Q

What are the two cofactors of Burkitt’s lymphoma?

A

Chronic malaria

Immune suppression

47
Q

What is Hodgkin’s disease?

A

EBV caused B cell disruption

48
Q

What are the symptoms of Hodgkin’s disease?

A

Nontender, lymphadenopathy in the neck and/or axilla

Fever, weight loss, night sweats

49
Q

What is a Reed-sternberg cell? What is this diagnostic of?

A

A large cell with two or more nuclei or nuclear lobes, each of which has eosinophils

This is associated with Hodgkins’ disease

50
Q

What is the treatment for Hodgkin’s?

A

Radiotherapy or chemo

51
Q

What is the cause of nasopharyngeal carcinoma?

52
Q

What are the symptoms of nasopharyngeal carcinoma?

A

Facial pain/fullness

hearing loss

53
Q

What cells are affected in nasopharyngeal carcinoma?

A

Epithelial cells

54
Q

What is the treatment for nasopharyngeal carcinoma?

A

Chemo/radiation

55
Q

What is PTLD (post transplantation lymphoproliferation disorder)?

A

Abnormal proliferation of lymphoid cells in a transplant pt d/t EBV

56
Q

What are the symptoms of PTLD?

A

Fever, weight loss, progressive encephalopathy

57
Q

What is the major risk factor for PTLD?

A

EBV infection at the time of transplant

58
Q

How do you diagnose PTLD?

A

Histological analysis

59
Q

What is the treatment for PTLD? (3)

A
  1. reduce immunosuppression
  2. Rituximab (binds CD20)
  3. Conventional chemo
60
Q

What is the family of CMV? Enveloped? Genome?

A

Herpesviridae
Enveloped
dsDNA

61
Q

Most infections with CMV lead to what?

A

Asymptomatic to mono-like

62
Q

CMV infections with AIDs pts result in what?

A

Mutlisite symptomatic disease

63
Q

Primary CMV infections of new mothers lead to what?

A

Developmental problems (cytomegalic inclusion disease)

64
Q

Where does the CCMV replicate? Where is it latent?

A

Mucosal epi/viremia

Latet in monocytes

65
Q

Reactivation of CMV is (always/rarely) symptomatic in immunocompetent pts?

66
Q

How is CMV transmitted?

A 
Saliva
Breast milk
Urine
Fomites
Sex
67
Q

How do you diagnose CMV?

A
  1. Detection of viral DNA in diseases tissue

2. Seroconversion

68
Q

Why is it hard to diagnose CMV?

A

virus can shed for year after initial infection during other infections

69
Q

What is the 1st line treatment for CMV?

A
  1. Gancyclovir

2. Valganciclovir

70
Q

What is the MOA of Ganciclovir?

A

Converted to viral pol inhibitor by CMV enzymes

71
Q

What is the MOA of valganciclovir?

A

Converted to ganciclovir within the body

72
Q

What is the toxicity associated with Ganciclovir?

A

Bone marrow toxicity

Neutropenia

73
Q

What is the 2nd line treatment for CMV? Why are they second line?

A
  1. Cidofovir
  2. Foscarnet

2nd b/c IV, and renal toxic

74
Q

What is the MOA of cidofovir?

A

Converted to a viral pol inhibits by cellular enzymes

75
Q

What is the MOA of Foscarnet?

A

Direct inhibitor of the CMV pol

76
Q

What is the primary disease caused by CMV

A

CMV mono-like illness

77
Q

What are the symptoms of CMV IM-like illness?

A

fever, fatigue

NON-exudative pharyngeitis

78
Q

What is the etiology of CMV IM-like illness?

A

Primary infection with CMV

79
Q

Is there heterophile antibody production with CMV IM-like illness?

80
Q

How do you differentiate between CMV IM-like illness and IM caused by EBV? (2)

A

EBV has exudative pharyngitis and heterophile production

CMV IM-like illness does not

81
Q

When is CMV inclusion body disease found in babies? Does it cross the placenta

A

Most common with primary infections of mother during prego

Crosses placenta

82
Q

What are the symptoms of CMV inclusion body disease in newborns?

A
  1. Hepatosplenomegaly
  2. Jaundice
  3. Petechial rash
83
Q

What is the most common congenital viral infection in the US?

A

CMV inclusion body disease

84
Q

How does congential CMV infection occur? How often is this passed on from mothers?

A

Mother exposure to primary CMV virus

33% of the time passed onto child

85
Q

How do you prevent CMV inclusion disease?

A

Prevent seronegative pregnant women from coming into contact with babies or other infected with CMV

86
Q

What is the treatment for maternal treatment with CMV?

A

CMV immunoglobin

87
Q

What is the most common viral pathogen complicating organ transplant?

88
Q

When do AIDS patient present with CMV diseases?

A

between 50-100 CD4 count

89
Q

What are the symptoms of CMV in immunocompromised pts?

A

Spiking fever, followed by hypothermia

90
Q

What are the two ways that transplantation result in a CMV infection?

A

Reactivation d/t immunosuppression

From organ

91
Q

What are the usual diseases associated with CMV transplantation? For HIV pts?

A

CMV penumonitis = transplant

GI tract illness = HIV, CMV retinitis

92
Q

What is the complication risk in CMV transplant infection?

A

Perforation and hemorrhage of GI epithelium

Graft vs host disease

93
Q

What are the symptoms of CMV in AIDS pts?

A

CMV retinitis, GI tract illnesses

94
Q

What are the symptoms of CMV retinitis?

A
  1. Blurred vision
  2. Floaters
  3. White, necrotic lesions on fundoscopic exam
95
Q

How do you prevent CMV in organ transplants?

A

Seronegative matching donors

96
Q

How do you diagnose CMV retinitis?

A

Fundoscopic exam seeing necrotic lesions

97
Q

What is the treatment for CMV in immunocompromised pts?

A

Prophylaxis with antivirals

98
Q

What are the general characteristics of viral diseases of the systemic circulation?

A

Hide and lay dormant

99
Q

What abx is associated with a rash if given to pts with mono?

A

Ampicillin

100
Q

What is the CA caused by EBV that is the result of a translocation of a gene: Hodgkin’s lymphoma, or Burkitt’s lymphoma? What is the gene that is translocated?

A

Burkitt’s lymphoma

Gene for E2F translocated to Chromosome 8 to 14

Microbio (50 decks)

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