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microbiology final > chapter 28 - antimicrobial therapy > Flashcards

chapter 28 - antimicrobial therapy Flashcards

1
Q

What are two disorders of the immune system?

A
  1. hypersensitivity
  2. autoimmunity
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2
Q

What are the 4 subsets of hypersensitivity?

A
  1. allergies /immediate hypersensitivity / Type 1
  2. cytotoxic / Type 2
  3. immune complex / Type 3
  4. Delayed-type hypersensitivity / Type 4
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3
Q

What are the symptomatic treatment of hypersensitivity?

A
  1. mild symptoms: antihistamines (OTC/prescription)
  2. severe symptoms: epinephrine
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4
Q

What are the long term treatments of hypersensitivity?

A

desensitization: small, increasing doses of allergen shifts Ig interaction from IgE to IgA and IgG.

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5
Q

What is the mechanisms of hypersensitivity of immediate hypersensitivity/Type I

A
  1. allergen bound by B cell
  2. allergen processed and presented to Th2 cell
  3. Th2 cell provides B cell help
  4. B cell forms plasma cells
  5. plasma cell produces IgE
  6. IgE sensitizes tissue mast cells by binding to surface IgE receptors
  7. subsequent exposure to antigen
  8. antigen cross-links two antibody molecules
  9. release of allergic mediators
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6
Q

What are the delayed-type hypersensitivty (DTH) and what are the treatments?

A
  1. maximal response in 24/48h (swelling, reddening)
  2. DTH antigens are often non-immunogenic but can react with skin proteins to form novel immunoreactive antigens
  3. local immune response to antigens encountered before also causes DTH symptoms
  4. treatment is often symptomatic.
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7
Q

What are the treatments to autoimmunity for organ/site-specific disorders?

A
  1. type 1 diabetes: supple insulin
    hyperthyroidism: supply thyroxine
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8
Q

What are the treatments to autoimmunity for multi-organ/site disorders

A
  1. general immunosupression (weakening the immune system)
  2. monoclonal antibodies are emerging as attractive options. (antibodies to neutralixe inflammatory cytokines
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9
Q

What are superantigens?

A

they bring together APC and T-cells, byt bypass the antigen-TCR complementarity by targeting conserved regions outside the antigen-binging sites.
This activates a large fraction of T cells.

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10
Q

What are the two types of immunodeficiencies?

A
  1. genetic; severe combined immune deficiency, cannot form B and T cells.
  2. infections; AIDS, HIV infects and kills macrophages and T-helper cells.
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11
Q

What are the treatments for genetic immunodeficiency?

A
  1. bone marrow transplant
  2. gene therapy
  3. continuous antibiotic therapy
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12
Q

What are the treatments for infection immunodeficiency?

A

antiretroviral therapy

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13
Q

How do vaccines work?

A

Person gets an inactivated pathogen or pathogenic epitope that causes the production of memory cells which can mount a swift and strong response of actually infected.

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14
Q

What are the different types of vaccines?

A
  1. Inactivated: heat/chemical treated pathogens
  2. Attenuated: avirulent strains of a pathogen
  3. Subunit: component of pathogens like toxoids, isolated virulence antigens
  4. Conjugate: genetically engineered antigens (polysaccharides) coupled with large harmless proteins that elicits and effective immune response
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15
Q

What are the different nucleic acid vaccines?

A
  1. DNA vaccines: antigens delivered to cells directly in plasmids. Host cells transcribe and translate the antigen to produce the antigen
  2. mRNA vaccines: antigens delivered as pre-processed mRNA for translation in the host cells.
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16
Q

What are the advantages of nucleic acid vaccines?

A

virtually zero risk of infection from the vaccine itself. mRNA vaccines also have short half life.

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17
Q

What are the disadvantages of nucleic acid vaccines?

A

vaccine delivery and host cell update, mRNA vaccines can be unstable

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18
Q

How do plant-based vaccines work?

A

antigen delivered into plants.
Antigen can be extracted from plant cells in the form of virus-like particles (VLP): antigens embedded in phospholipid vesicles.
it elicits a strong immune response, but lacks pathogen DNA, hence cannot cause disease

19
Q

What are immunotherapy treatments?

A

anticancer vaccines

20
Q

What are the 2 different anticancer vaccines?

A
  1. prophylactic: preventive; target oncogenic pathogens like HPV (cervical cancers)
  2. therapeutic: immune cells can be sensitized to tumor antigens to mount a response against cancer cells.
21
Q

What are checkpoint inhibitors?

A

block the activity of these proteins to prevent neutralization of cytotoxic T cells.
(cancer cells over express immune-suppressing checkpoint proteins (programmed cell death))

22
Q

What are some anticancer therapies?

A
  1. tumor infiltrating T cells (TILs)
  2. Chimeric antigen receptor (CAR) T cells
23
Q

What is the mechanism of TILs?

A
  1. extract T-cells that have natural anticancer ability from within tumors
  2. propagate in the lab
  3. infuse back into patient
  4. in use to treat melanoma
24
Q

What is the mechanism of CAR T cells?

A
  1. T cells extracted from patient
  2. engineered using viral vectors too give cells enhanced receptors
  3. infuse back into patients
  4. in use to treat melanoma
25
What are Chimeric antigen receptor T cells?
T cells with engineered receptors that can recognize tumor antigens even without their presentation on MHC complexes.
26
What are the challenges of adoptive t-cell transfers?
overcoming immunosupressive tumor microenvironments. Checkpoint inhibitors often used in combination to improve this
27
What are the side affects of adoptive t cell transfers?
1. neurologic toxicity 2. inflammation 3. variation in treamtent outcome from person to person
28
What is the role of the gut microbiome in anticancer therapies?
beneficial gut bacteria like Bifidobacterium are thought to induce release of immune-stimulating cytokines, which enhance tumor clearance in mice.
29
What is the main target to kill bacterias
Cell wall synthesis - using B-lactams: inhibits transpeptidation reaction during peptidoglycan cross-linking.
30
What are the different inhibitors in cell wall synthesis?
- B-lactams: inhibits transpeptidation reaction during peptidoglycan cross-linking. - isoniazid: analog of nicotinamide, a vitamin rquired for mycolic acid essential for mycobacterium cell wall synthesis - vancomycin: akin to b-lactams, but binds to the two D-ala residues on the end of the peptide chains, preventing cross-linking of peptidoglycan. Only effective in Gram Positive bacteria
30
What is the second target to kill bacterias?
protein synthesis
31
What are the 3 inhibitors used during protein synthesis?
1. aminoglycosides: inhibits the 30s subunit. 2. tetracyclines: inhibitd the 30S subunits. 3. macrolides: inhibits 50S subunit
31
What is the third target to kill bacterias?
nucleic acid synthesis
32
What are the 3 inhibitors used during nucleic acid synthesis?
1. quinolones: Inhibits DNA gyrase, preventing DNA packaging and unpakcing in bacteria 2. Rifamycin: inhibits RNA polymerase 3. Actinomycin: blocks RNA elongation by binding to DNA
33
What is the fourth target to kill bacterias?
Folic acid synthesis inhibitors
34
What is used for folic acid synthesis inhibitors?
sulfonamides: growth factor analogs. folic acid is essential in nucleic acid synthesis. commonly used with trimethoprim, which inhibits another step of folic acid synthesis.
35
What is the most effective way to kill bacteria?
membrane disruptors.
36
What are the different types of molecules used for membrane disruption?
1. Daptomycin: binds to cytoplasmic membrane of bacteria and forms pores 2. Polymyxins: disrupts the outer membrane and forms pores in the cytoplasmic membrane of bacteria.
37
What are the different ways to kill antiviral drugs?
1. reverse transcriptase inhibitors (RTI): blocks reverse transcription that converts viral RNA genomes to DNA in retroviruses 2. nucleoside RTIs (NRTI): dideoxy analogs of nucleosides 3. non-nucleoside RTIs(NNRTI): non-competitive inhibitor of reverse transcriptase 4. protease inhibitors: inhibits viral protease required for viral protein processing 5. fusion inhibitors: binds to viral membrane proteins required for docking and host-cell entry
38
What are the anti-fungal drugs?
can target ergosterol synthesis can target microtubule formation can target cell wall synthesis
39
What are the different anti-protozoan drugs?
1. quinine and derivatives: blocks hemoglobin metabolisms in species of plasmodium that can cause malaria 2. artemisinin: antimalarial drug 3. metronidazole: blocks nucleic acid synthesis in anaerobic organisms 4. mebendazole: inhibits synthesis of microtubules
40
What are the drivers of antibiotic resistance?
1. widespread (mis) use of antibiotics - unnecessary prescriptions - self-prescriptions - patients not completing treatment regimens 2. use in animals in agriculture
41
What can we do to fight against antibiotic resistance?
1. proper use of antibiotics 2. limiting use in agriculture 3. incentives to discover and commercialize new antibiotics 4. enzyme inhibitors: B-lactamase inhibitors 5. drug combinations

microbiology final (20 decks)

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