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microbiology final > chapter 28 - antimicrobial therapy > Flashcards

chapter 28 - antimicrobial therapy Flashcards

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Biology 101 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
Q

What are Chimeric antigen receptor T cells?

A

T cells with engineered receptors that can recognize tumor antigens even without their presentation on MHC complexes.

26
Q

What are the challenges of adoptive t-cell transfers?

A

overcoming immunosupressive tumor microenvironments. Checkpoint inhibitors often used in combination to improve this

27
Q

What are the side affects of adoptive t cell transfers?

A
  1. neurologic toxicity
  2. inflammation
  3. variation in treamtent outcome from person to person
28
Q

What is the role of the gut microbiome in anticancer therapies?

A

beneficial gut bacteria like Bifidobacterium are thought to induce release of immune-stimulating cytokines, which enhance tumor clearance in mice.

29
Q

What is the main target to kill bacterias

A

Cell wall synthesis
- using B-lactams: inhibits transpeptidation reaction during peptidoglycan cross-linking.

30
Q

What are the different inhibitors in cell wall synthesis?

A
  • 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
Q

What is the second target to kill bacterias?

A

protein synthesis

31
Q

What are the 3 inhibitors used during protein synthesis?

A
  1. aminoglycosides: inhibits the 30s subunit.
  2. tetracyclines: inhibitd the 30S subunits.
  3. macrolides: inhibits 50S subunit
31
Q

What is the third target to kill bacterias?

A

nucleic acid synthesis

32
Q

What are the 3 inhibitors used during nucleic acid synthesis?

A
  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
Q

What is the fourth target to kill bacterias?

A

Folic acid synthesis inhibitors

34
Q

What is used for folic acid synthesis inhibitors?

A

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
Q

What is the most effective way to kill bacteria?

A

membrane disruptors.

36
Q

What are the different types of molecules used for membrane disruption?

A
  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
Q

What are the different ways to kill antiviral drugs?

A
  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
Q

What are the anti-fungal drugs?

A

can target ergosterol synthesis
can target microtubule formation
can target cell wall synthesis

39
Q

What are the different anti-protozoan drugs?

A
  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
Q

What are the drivers of antibiotic resistance?

A
  1. widespread (mis) use of antibiotics
    - unnecessary prescriptions
    - self-prescriptions
    - patients not completing treatment regimens
  2. use in animals in agriculture
41
Q

What can we do to fight against antibiotic resistance?

A
  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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