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Infectious Disease > Week 4 > Flashcards

Week 4 Flashcards

1
Q

Immunity

A

protection against disease (not necessarily infection)

More rapid and greater response to subsequent exposure (e.g. vaccin)

“Natural” and acquired

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2
Q

Immunology

A

study of the mechanisms of immunity against infection and adverse effects of immune response

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3
Q

Components of immune function: (4)

A

1) Anatomic (skin, mucosal barriers)
2) Phagocytes (neutrophils, macrophages)
3) Cellular immunity (CD4+, CD8+ T cells, NK cells)
4) Humoral immunity (specific antibodies, B cells, complement)

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4
Q

HIV/AIDS:

what are the immune defects? (4)

A

1) Low CD4+ T cell number, decreased CD4+ T cell function
2) NK cell dysfunction

3) B cell dysfunction:
- Hypergammaglobulinemia, increased activation
- Decreased memory B cells
- Decreased response to new antigens
- High rates of autoimmunity

4) Phagocytic function: PMN and macrophages OK

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5
Q

3 stages of HIV/AIDs infection in terms of T cell number

A

Early stage = > 500
Intermediate = 200-500
Advanced, AIDS = < 200

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6
Q

Complement

A

Classical, Alternative, and Lectin converge at C3 → C5-C9 (MAC) and C5a

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7
Q

C1-C4 deficiency

A

classical pathway, present with PYOGENIC infections

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8
Q

C5-C9 deficiency

A

terminal pathway, show serious Neisseria infections

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9
Q

Most common complement deficienct

A

C2 deficiency

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10
Q

Antibody structure and function: Fc vs. Fab

A

Variable region F(ab): antigen binding region, each is unique

Constant region: Fc

  • Defines isotype (IgG, IgM, IgA, IgE)
  • Activates complement
  • Binds phagocytes via Fc receptors
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11
Q

C5a

A
  • potent chemoattractant
  • promote anaphylactic activity
  • recruit neutrophils and other inflammatory cells.
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12
Q

Classical complement pathway

A

Immune complex (IgG or IgM) + C1 activation —> C2, C3, C4 activation –> C5-C9

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13
Q

Alternative complement pathway

A

C3b + microbial surface, endotoxin, aggregated IgA –> C5-C9 activation

DOES NOT require C1, C4, or C2

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14
Q

C3 deficiency can predispose to what kinds of infections?

A

severe, recurrent pyogenic sinus and respiratory tract infections

increased risk for type III hypersensitivity reactions

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15
Q

Mannose-binding lectin pathway

A

mannose-binding lectin replaces C1 and does not require the presence of ab to be activated –> C2, C3, C4 –> C5-C9

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16
Q

Decay accelerating factor (DAF)

-responsible for what disease?

A

aka CD55

inhibits C3 and C5 convertases, prevents inappropriate complement activate

Paroxysmyl nocturnal hemoglobinuria due to GPI anchor defect that attaches DAF (CD55) and prevents complement activation –> complement mediated lysis of RBCs, WBCs, and platelets

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17
Q

Selective IgA deficiency

A

LOW IgA, NORMAL IgG, IgM

-can see increased airway and GI infections

  • limited increase in infection due to protection by compensatory IgM
  • majority asymptomatic
  • Increased autoimmune +/- malignancy
  • Increased risk of atopy and anaphylaxis
  • Susceptible to transfusion reactions (with anti-IgA)
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18
Q

Primary immunodeficiency:

disease of adult (3) vs. childhood (3) presentation

A

Usually due to single gene defects

Most present in childhood:

1) X-Linked Agammaglobulinemia
2) SCID
3) Wiskott-Aldrich

Most common in adults:

1) CVID
2) IgG(2) subclass deficiency
3) Hyper-IgE syndrome (Job’s Syndrome)

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19
Q

Secondary immunodeficiency:

A

Developing country: Malnutrition, HIV/AIDS, Age (very young, very old), Measles

Developed country: chronic corticosteroids, chemotherapy, anti-TNF antibodies, HIV/AIDS, transplantation

Other causes: CLL (low Igs due to B “arrest”), multiple myeloma (high IgG but monoclonal, low IgM, IgA), renal and GI loss

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20
Q

Common variable immunodeficiency (CVID)

epidemiology
defect in what?

A

most common serious primary defect in adults (Onset in teens or 20’s)

Defect in B cell differentiation (many causes)

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21
Q

Common variable immunodeficiency (CVID)

labs and presentation

A

Recurrent PYOGENIC sinopulmonary infections (especially S. pneumoniae)

  • bronchiectasis
  • lymphoma
  • increased risk of autoimmune disease

Chronic diarrhea with GI lymphoid hyperplasia and increased risk of bacteremia

Some PCP, fungi, mycobacteria, recurrent HSV

Labs: low IgG, IgM, IgA. NORMAL B cells, “NORMAL” T cells, LOW plasma cells

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22
Q

Chronic Granulomatous Disease (CGD)

A

sufficient phagocyte number but decreased function (NADPH oxidase deficiency = oxygen radicals decreased)

NBT negative

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23
Q

Chronic Granulomatous Disease (CGD)

increased susceptibility to…

A

Increased susceptibility to: “CATs Need PLACES to Belch Hairballs” = catalase + organisms

Nocardia
Pseudomonas
Listeria
Aspergillus
Candida
E. Coli
Serratio, Staph
B. cepacia
H. pylori

Recurrent skin abscesses, severe prolonged pneumonia, bone infections

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24
Q

If you have a cell mediated immunodeficiency, then you are more suscpetible to what bugs:

1) Bacterial (5)
2) Fungal (5)
3) Viral (4)
4) Protazoan (2)
5) Helminths (1)

A

*=TMP/SMX prophylaxis

Bacterial: Listeria, Nocardia, Mycobacterium, Salmonella*, Legionella

Fungal: Cryptococcus, Pneumocystis*, Aspergillus, Cocci. Immitis, Candida

Viral: HSV, Varicella, CMV, adenovirus
-Acyclovir prophylaxis for HSV and Varicella

Protozoan: Toxoplasma*, Cryptosporidium

Helminths: Strongyloides

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25
Q

TRECs

A

pieces of DNA cut out during intrathymic T-cell receptor gene rearrangement

V(D)J Recombination: take pieces of VDJ gene segments to generate a T cell receptor
D→ J and then V → DJ

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26
Q

SCID: Severe Combined Immunodeficiency

Possible defects: (2)

A

1) Defective IL-2R gamma chain (XR, most common)

2) Adenosine deaminase deficiency (AR)

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27
Q

Pediatric emergency to recognize SCID early: why?

A

Exposure to non-irradiated blood product transfusions, live vaccines, and common infections in patients in SCID can be life-threatening

Less complications, better prognosis, save money

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28
Q

Clinical presentation of SCID child

A

Failure to thrive, diarrhea, recurrent pulmonary infections

Opportunistic infections: viruses, fungi, intracellular bacteria
-PJP, Candida, Aspergillus, CMV, Enteroviruses, Mycobacteria

Absence of lymphoid tissue - ABSENT thymus

Alopecia, erythroderma, hepatosplenomegaly

Decreased TRECs

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29
Q

Genome structure of retroviruses

Structural proteins (4)
Viral enzymes (3)
Viral genome?
A

Structural proteins:

  • Envelope (gp120, gp41)
  • Gag = matrix (p17) and capsid (p24)

Viral enzymes:

  • Reverse transcriptase: inefficient and error-prone
  • Integrase: required for virus replication and transcription
  • Protease: required for viral maturation

Viral genome: two RNA molecules

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30
Q

Retroviruses accessory proteins (6)

A

Tat (Tax): transactivator - required for viral gene transcription*

Rev (Rex): nuclear exporter

Vif: blocks APOBEC3G restriction

Vpr: multiple functions, nucleus importer

Vpu: multiple functions, virus assembly

Nef: multiple functions, host immune invasion

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31
Q

Long terminal repeats (LTRs)

A

cis elements required for reverse transcription, viral gene transcription, splicing, virus integration, and packaging

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32
Q

Life cycle of retroviruses (6 steps)

A

1) Binding and Entry
2) Reverse transcription
3) Genome integration
4) Viral gene transcription
5) Virus assembly and release
6) Viral maturation

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33
Q

Genome integration requires _______

Viral gene transcription requires ________

Virus assembly and release requires ______

Viral maturation requires _______

A

Genome integration (viral integrase)

Viral gene transcription (Tat transactivator)

Virus assembly and release: (Vpu required for virus release)

Viral maturation requires protease

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34
Q

protease in retroviruses

A

protease required for virus maturation and cleaves proteins in multi-linked chain to individual proteins

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35
Q

HERV: Human Endogenous Retrovirus

A

Comprises 8-10% of human genome

Most HERVs are defective and cannot produce infectious viruses but may be associated with human cancers

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36
Q

AIDS defining cancers: (3)

A 
Kaposi sarcoma (HHV8)
Non-hodgkin’s lymphoma (HHV8, EBV)
Cervical cancer (HPV)
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37
Q

Non-AIDS defining cancers (7)

A

Anal cancer (HPV)

Hodgkin’s lymphoma (EBV)

Liver cancer (HBV, HCV)

Skin cancer (HPV?)

Head and neck cancer (HPV)

Lung cancer

Kidney cancer

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38
Q

What are the unique characteristics of HIV-positive cancers

A
  • HIV associated cancers are more aggressive and progress faster
  • Atypical pathology, higher tumor grade
  • Poorer outcomes
  • Higher rate of relapse
  • Rapidly invasive
  • Develops at a younger age

Significant improved survival rate of persons with HIV due to HAART → shift spectrum of HIV diseases from AIDS defining cancers to more Non-AIDS defining cancers

Antiretrovirals and chemotherapeutic agents have interactions and overlapping toxicities making therapy challenging

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39
Q

Potential contributing factors of HIV-positive cancers

A

1) Behavior risk factors

2) Direct effects of HIV:
- Transactivation of proto-oncogenes by HIV Tat
- Inhibition of tumor suppressor genes (p5s) by HIV
- Endothelial abnormalities by HIV (pro angiogenesis)

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40
Q

HTLV: Human T Cell Lymphocytic Virus

A

Oncovirus

Causes lymphoproliferative disorders

Epidemiology: Japan, Caribbean, South America, Africa, Iran

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41
Q

Lymphoproliferative disorders caused by HTLV

A

Adult T cell leukemia/Lymphoma (ATL)

HTLV-1-associated myelopathy (HAM)

Uveitis

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42
Q

Origins of AIDS epidemic

A

HIV entered human pop. from chimps in east central Africa

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43
Q

Markers of HIV disease and response to treatment: (2)

A

1) CD4+ lymphocytes = main host cell for HIV
CD4+ count correlates with disease progression

2) Plasma HIV RNA level - viral load is a measure of the extent of ongoing replication in lymphoid tissue

44
Q

CCRH-d32 mutation

A

naturally occurring human genetic polymorphism

32 base pair deletion in CCR5 gene

Causes translational frameshift and protein truncation → CCR5 NOT expressed on cell surface

45
Q

Initial infection with HIV presents with what symptoms?

A

acute febrile illness, mononucleosis-like illness +/- aseptic meningitis

Usually occurs 2-3 weeks after HIV exposure

Occurs in > 50% of patients (usually unrecognized)

Signs and Symptoms: fever, fatigue, maculopapular rash, myalgia, headache, pharyngitis, cervical lymphadenopathy, arthralgia, oral ulcers, odynophagia, weight loss, diarrhea, oral candidiasis, photophobia

46
Q

Opportunistic infection

A

Infection that takes advantage of weakened immune system to cause an illness

Many only occur when CD4 < 200

Restoring CD4 count with antiretrovirals can minimize opportunistic infections

47
Q

Opportunistic infection - 6 common ones with HIV/AIDS patients

A

1) Pneumocystis Pneumonia (PCP)
2) Kaposi Sarcoma
3) Thrush (mouth and esophagus)
4) CMV retinitis
5) CNS Toxoplasmosis (ring enhancing abscess)
6) Extrapulmonary TB

48
Q

Effects of antiretroviral therapy:

  • Virologic and immunologic effect (3)
  • Clinical effects?
A

Virologic and immunologic effect:

  • Potent inhibition of viral replication
  • Early HIV → prevent immunologic deterioration
  • Advanced HIV → allows immunologic recovery

Clinical effect:

  • Prevent opportunistic infections, improve existing OIs
  • Reduce hospitalizations, long-term care facility use, medications for OIs, and cost
49
Q

Expected response to antiretroviral therapy (5)

A
  • Reduces plasma HIV RNA levels (viral load)
  • Increase CD4 count
  • Improve existing OIs, prevent new OIs
  • Decrease morbidity and mortality
  • Reduced HIV transmission
50
Q

HIV evolution

A

leads to increased pathogenicity, and drug resistance

-Genetic diversity (introduction of mutations)

Error-prone nature of viral replication → genetically distinct viral variants evolve from initial virus inoculum

Fast replication rate

Selective pressures (genetic bottlenecks)

51
Q

Retroviral targets

A

1) Protease inhibitors
2) Entry inhibitors: target fusion, CD4, or CCR5
3) Reverse transcriptase (RT) inhibitors (includes NRTIs and NNRTIs)
4) Integrase inhibitors

52
Q

HIV Prevention Strategies

A

Abstention and other behavioral changes

Male circumcision

Condoms

Pre-exposure prophylaxis

Post-exposure prophylaxis
ART in HIV+ patient

HIV vaccine

Microbicides

53
Q

Diagnosis of HIV

A

initial ELISA, positive tests confirmed by Western blot

Viral load from qRT-PCR → help monitor efficacy of drug therapy

54
Q

ELISA and Western Blot for diagnosis of HIV

False negative/False positive can be seen in what situations?

A

Can be falsely negative in first 1-2 months post HIV infection

Can be falsely positive in infants born to HIV+ mothers (anti-gp120 crosses placenta)

55
Q

Diseases seen when CD4 < 500 (6)

A

1) Candida albicans
2) EBV
3) Bartonella Henselae
4) HHV-8
5) Cryptosporidium
6) HPV

56
Q

Diseases seen when CD4 < 500

EBV vs. Candida

A

Candida albicans: oral thrush (scrapable plaque)

EBV: oral hairy leukoplakia (unscrapable plaque on lateral tongue)

57
Q

Diseases seen when CD4 < 500

Bartonella Henselae vs. HHV-8

A

Bartonella Henselae: bacillary angiomatosis with neutrophilic inflammation on biopsy

HHV-8: Kaposi sarcoma, lymphocytic infiltrate on biopsy

58
Q

Diseases seen when CD4 < 500

Cryptosporidium

  • sx?
  • what do you see in stool?
A

chronic, watery diarrhea, acid-fast oocysts in stool

59
Q

Diseases seen when CD4 < 500

HPV

A

resulting in squamous cell carcinoma (anus or cervix)

60
Q

Diseases seen when CD4 < 200 (3)

A

1) Pneumocystis jirovecii
2) JC virus reactivation
3) HIV dementia

61
Q

Diseases seen when CD4 < 200

Pneumocystis jirovecii

  • sx?
  • appearance on imaging?
  • increased value on what lab?
A

pneumonia, ground-glass appearance on imaging, elevated serum lactate dehydrogenase

62
Q

Diseases seen when CD4 < 200

JC virus reactivation

  • disease it causes?
  • appearance on MRI?
A

resulting progressive multifocal leukoencephalopathy with nonenhancing areas of demyelination on MRI

63
Q

Diseases seen when CD4 < 100 (8)

A

1) Aspergillus fumigatus
2) Histoplasma capsulatum
3) Candida albicans
4) Cryptococcus neoformans
5) CMV
6) Mycobacterium avium-intracellulare (MAC)
7) EBV
8) Toxoplasma gondii

64
Q

Diseases seen when CD4 < 100

Aspergillus fumigatus

  • sx
  • appearance on chest imaging?
A

hemoptysis, pleuritic pain, cavitation or infiltrates on chest imaging

65
Q

Diseases seen when CD4 < 100

Histoplasma capsulatum

  • sx?
  • appearance on histology?
A

nonspecific symptoms - fever, weight loss, fatigue, cough, dyspnea, nausea, vomiting, diarrhea

Oval yeast cells within macrophages

66
Q

Diseases seen when CD4 < 100

Candida albicans
sx?
appearance on microscopy?

A

esophagitis, white plaques on endoscopy, yeast/pseudohyphae on microscopy

67
Q

Diseases seen when CD4 < 100

Cryptococcus neoformans

sx?
appearance on microscopy?

A

meningitis, thickly encapsulated yeast on India ink stain on microscopy

68
Q

Diseases seen when CD4 < 100

CMV

A

retinitis, esophagitis

Retinitis → cotton-wool spots on fundoscopy

Esophagitis → linear ulcers on endoscopy

Biopsy with intranuclear (owl eye) inclusion bodies

69
Q

Diseases seen when CD4 < 100

Mycobacterium avium-intracellulare (MAC)

  • sx?
  • which two labs will be elevated?
A

anemia, increased alk phosphatase, increased lactate dehydrogenase, hepatosplenomegaly

70
Q

Diseases seen when CD4 < 100

EBV

  • sx?
  • appearance on brain imaging?
A

B cell lymphoma with single or multiple ring enhancing lesions on brain imaging (fewer that Toxoplasma)

71
Q

Diseases seen when CD4 < 100

Toxoplasma gondii
-appearance on MRI?

A

brain abscesses that appear as multiple ring-enhancing lesions on MRI

72
Q

HHART includes what combination of drugs?

A

2 NRTIs + Integrase inhibitor, protease inhibitor, or NNRTI

73
Q

Nucleoside reverse transcriptase inhibitors (NRTIs):

Mechanism of action

A

prodrug activated by cellular kinases to triphosphorylated active form → inhibit reverse transcription by competing with host cell triphosphate nucleotides for access to active site of HIV reverse transcriptase
→ Prevents genome replication and establishment of provirus

74
Q

Nucleoside reverse transcriptase inhibitors (NRTIs):

Mechanism of resistance

A 
high rate of resistance, associated with mutations in amino acid positions of HIV reverse transcriptase
CROSS RESISTANCE within class is common
75
Q

Nucleoside reverse transcriptase inhibitors (NRTIs):

what happens if levels are too low? too high?

A

Levels fall too low → increase resistance developing, levels too high → toxicity

76
Q

Nucleoside reverse transcriptase inhibitors (NRTIs):

Drug names (6)

A

1) *Tenofovir AF
2) *Emtricitabine
3) Abacavir
4) *Lamivudine
5) Stavudine
6) Zidovudine (formerly AZT)

77
Q

*Tenofovir AF

mechanism? ADR? metabolism?

TDF vs. TAF?

A

NRTI

Mechanism: nucleoTIDE reverse transcriptase inhibitor
-*Does NOT require intracellular phosphorylation to be active

ADRs: Fanconi syndrome

Renal excretion

Lower systemic exposure than TDF because action primarily intracellular

78
Q

*Emtricitabine

A

Best tolerated NRTI
Also active against HBV
Renal excretion

79
Q

Abacavir

-metabolism?

  • ADRs?
  • what can you screen for to prevent ADR?
A

NRTI

Hepatic metabolism

ADRs: hypersensitivity reactions
HLAB*57:01 screening performed prior to initiating treatment with abacavir to avoid Type IV hypersensitivity reaction

80
Q

*Lamivudine

A

Best tolerated NRTI
Also active against HBV
Renal excretion

81
Q

Zidovudine

-main use?

A

NRTI
(formerly AZT):

Can be given prophylactically after birth along with Nevirapine to decrease risk of HIV acquisition from mom

82
Q

NRTIs:

Adverse Drug Reactions common to all the drugs in this class (4)

A

1) Some activity against mitochondrial DNA polymerase → Myopathy, anemia, granulocytopenia, neuropathy
2) Lactic acidosis
3) Hepatic steatosis
4) Renal impairment potential

83
Q

Non-Nucleoside Reverse Transcriptase Inhibitor (NNRTIs):

Mechanism

A

bind and directly inhibit reverse transcriptase (non-competitive inhibition)
Do NOT require phosphorylation to be active
Do NOT compete with nucleotides

84
Q

Non-Nucleoside Reverse Transcriptase Inhibitor (NNRTIs):

Mechanism of resistance

A 
single AA substitutions in binding site of NNRTIs on HIV reverse transcriptase
Resistance to one NNRTI → resistance to remaining class members

**Must be used with as least two other antiretroviral agents to prevent acquisition of strain resistance

85
Q

Non-Nucleoside Reverse Transcriptase Inhibitor (NNRTIs):

ADRs (2)

A

rash, hepatotoxicity

86
Q

Non-Nucleoside Reverse Transcriptase Inhibitor (NNRTIs):

Drug names (3)

A

1) *Efavirenz
2) Nevirapine
3) Delavirdine

87
Q

*Efavirenz

2 ADRs unique to this drug
contraindicated in who?

A

NNRTI

vivid dreams, CNS symptoms

CONTRAINDICATED in pregnancy

88
Q

Nevirapine can be given with Zidovudine to do what?

A

Can be given prophylactically after birth along with Zidovudine to decrease risk of HIV acquisition from mom

89
Q

Nevirapine

ADRs (3)

A

potential for severe hepatotoxicity, hepatic failure, and death - not used really anymore

NNRTI

90
Q

Delavirdine

A

NNRTI

CONTRAINDICATED in pregnancy
Least potent NNRTI, rarely used

91
Q

Fusion inhibitors

mechanism?

A

interfere with binding, fusion, and entry of HIV virion into CD4 cells

92
Q

Fusion inhibitors

2 drug names?

A

1) *Enfuvirtide

2) *Maraviroc

93
Q

Enfuvirtide

Mechanism?

A

blocks gp41 conformational change → prevent fusing with CD4 cells

94
Q

Enfuvirtide

Mechanism of resistance?

A

gp41 mutations

95
Q

Maraviroc

Mechanism?

A

CCR5 antagonists → prevent fusion between viral gp120 and CCR5 receptors on macrophages → prevent viral entry

96
Q

Maraviroc ADRs (1)

A

hepatotoxicity (with high dose treatment)

97
Q

Maraviroc

mechanism of resistance?

A

mutations in gp120, no cross resistance

98
Q

Maraviroc has no activity against what strain of HIV?

A

No activity against “X4” or “dual tropic” HIV-1 strains - HIV-1 virions that target CXCR4, associated with later stages of HIV infection and disease progression

Means CXCR4 used over CCR5 to enter cell

99
Q

Integrase inhibitors:

mechanism?

A

prevent insertion of viral dsDNA into host genome via reverse transcription of RNA, no action against human DNA polymerase

100
Q

Integrase inhibitors:

Mechanism of resistance

A

lower genetic barrier to resistance, single point mutation

101
Q

Integrase inhibitors:

Drug names? (3)

A

*Raltegravir
Elvitegravir
Dolutegravir

102
Q

Integrase inhibitors

ADRs (2)

A

hypercholesterolemia, increase in creatine kinase

Generally well tolerated

103
Q

Protease inhibitors

Mechanism of action

A

bind and prevent virally encoded proteases (HIV-1 protease, pol gene) from cleaving polyproteins into mature proteins

104
Q

Protease inhibitors:

Mechanism of resistance

A

single AA substitution, typically SPECIFIC for individual protease inhibitors

Resistance development is rapid when used as a single drug → must combine

105
Q

Protease inhibitors:

ADRs

A

1) Lipodystrophy (fat redistribution, central fat accumulation)
2) Hyperglycemia, hyperlipidemia, hyperinsulinemia

3) GI intolerance
4) QT prolongation
5) Hepatotoxicity
6) **Rifampin (CYP450 inducer) CONTRAINDICATED with protease inhibitors

106
Q

Protease inhibitors:

Drug names (4)

A

(-navir)

Darunavir
Atazanavir
Fosamprenavir
Ritonavir

Infectious Disease (9 decks)

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