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MICR 3050 > Vaccines and Antimicrobial Drugs > Flashcards

Vaccines and Antimicrobial Drugs Flashcards

1
Q

vaccination

A
  • inoculation of a living host with inactive or attenuated (weakened) pathogens, or pathogen products, to stimulate protective active immunity
  • active immunity means that your body is making the antibodies
  • passive immunity involves obtaining antibodies from a different organism
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2
Q

vaccine

A
  • the substance given to a host (usually by injection) that induces artificial active immunity
  • acts as an antigen, but does not cause disease
  • stimulates the production of antibodies
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3
Q

herd immunity

A
  • resistance in a population to a pathogen (disease) as a result of the immunity of a large portion of the population
  • breaks the chain of pathogen transmission from one susceptible host to another
  • the more highly infectious a pathogen, the greater the proportion of immune individuals needed to prevent disease spread
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4
Q

How do vaccines stimulate active immunity?

A
  • the initial exposure to the antigen from the vaccine causes the primary immune response
  • the primary immune response causes a rise in antibody concentration that decreases over time
  • when exposed to the antigen a second time, the secondary immune response occurs
  • the secondary immune response causes a rise in antibody concentration that is higher and faster
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5
Q

What are the different types of SARS-CoV-2 vaccines being used or in development?

A
  • mRNA vaccines (Pfizer and Moderna): mRNA that codes for spike protein is purified and injected, body produces spike protein
  • adenovirus vector vaccine (Johnson and Johnson): spike protein gene is purified and put inside an adenoviral vector, body produces spike protein
  • protein based: spike protein is purified and injected
  • all cause the immune system to produce the antibody against the spike protein antigen
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6
Q

antimicrobial drugs

A
  • compounds used to treat disease by destroying or inhibiting the growth of pathogenic microbes within a host (in vivo)
  • synthetics, antibiotics, semi-synthetics
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7
Q

What are synthetics?

A

chemicals

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8
Q

antibiotics

A
  • naturally produced antimicrobial agents (microbial products)
  • produced by bacteria and fungi
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9
Q

semi-synthetics

A

chemically modified antibiotics

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10
Q

How are antimicrobials classified?

A
  • molecular structure
  • mechanism of action
  • spectrum of antimicrobial activity
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11
Q

selective toxicity

A
  • ability of a drug to kill or inhibit the pathogen while damaging the host as little as possible
  • ex: penicillin goes after peptidoglycan
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12
Q

therapeutic (effective) dose

A

drug level required for clinical treatment

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13
Q

toxic dose

A

drug level at which drug becomes too toxic for the patient (produces side effects)

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14
Q

therapeutic index

A
  • ratio of toxic dose to therapeutic dose

- the larger the therapeutic index, the better

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15
Q

narrow spectrum drugs

A

attack only a few different pathogens

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16
Q

broad spectrum drugs

A

attack many different pathogens

17
Q

cidal agent

A

kills microbes

18
Q

static agent

A

inhibits growth of microbes

19
Q

side effects

A

undesirable effects of drugs on host cells

20
Q

growth factor analogs

A
  • structurally similar to an essential growth factor
  • disrupt cell metabolism
  • ex: isoniazid (narrow spectrum, cidal if actively growing, static if dormant)
21
Q

quinolones

A
  • interfere with bacterial DNA gyrase
  • prevent DNA packaging
  • ex: ciprofloxacin (narrow spectrum, cidal)
22
Q

macrolides

A
  • target the 50S ribosomal subunit
  • ex: erythromycin (broad spectrum, static)
  • ex: azithromycin (Z-pack) (semisynthetic)
23
Q

tetracyclines

A
  • target the 30S ribosomal subunit

- ex: tetracycline (broad spectrum, static)

24
Q

lipid biosynthesis disruptors

A
  • target fatty acid biosynthesis

- ex: platensimycin (broad spectrum, static, effective againt MRSA and VRE)

25
Q

beta-lactam antibiotics (from fungi)

A
  • include penicillins and cephalosporins
  • target cell wall synthesis
  • effective primarily against gram-positive bacteria
  • cidal against actively growing cells
26
Q

isoniazid

A
  • type: synthetic
  • mode of action: lipid synthesis (especially mycolic acid)
  • effect: cidal if actively growing, static if dormant
  • spectrum of activity: narrow
27
Q

ciproflaxin

A
  • type: synthetic
  • mode of action: bacterial DNA gyrase (prevents DNA packing)
  • effect: cidal
  • spectrum of activity: narrow
28
Q

penicillin

A
  • type: antibiotic
  • mode of action: cell wall synthesis
  • effect: cidal (if actively growing)
  • spectrum of activity: narrow
29
Q

erythromycin

A
  • type: antibiotic
  • mode of action: 50S ribosomal subunit
  • effect: static
  • spectrum of activity: broad
30
Q

tetracycline

A
  • type: antibiotic
  • mode of action: 30S ribosomal subunit
  • effect: static
  • spectrum of activity: broad
31
Q

platensimycin

A
  • type: antibiotic
  • mode of action: fatty acid biosynthesis (MRSA and VRE)
  • effect: static
  • spectrum of activity: broad
32
Q

Why is antimicrobial resistance a threat to public health?

A
  • once resistance originates in a bacterial population, it can be transmitted to other bacteria
  • resistance mechanisms are not confined to a single class of drugs
  • erroneous practices select for the growth of resistant bacteria
33
Q

What are the mechanisms of bacterial resistance?

A
  • target modification
  • preventing entrance
  • inactivation
  • efflux pumps
  • alternate pathway
  • impermeability
34
Q

What is the origin of resistance?

A
  • natural immunity genes
  • spontaneous mutations
  • resistance genes are located in chromosome, plasmids (R factors), or mobile genetic elements such as transposons
35
Q

How is resistance transmitted?

A

horizontal gene transfer (transformation, conjugation, and transduction)

36
Q

How do drug resistant bacteria emerge?

A
  1. Prescription of antibiotics
  2. Antibiotic selective pressure
  3. Genetic factors
  4. Spread of antimicrobial-resistant bacteria in the community
37
Q

How can drug resistance be prevented?

A
  • give drug in high concentrations to destroy susceptible
  • use antimicrobials only when necessary
  • take full course of antimicrobial
  • use narrow spectrum antimicrobials
  • give a combination of unrelated drugs
  • possible future solutions: continued development of new antimicrobials and use of bacteriophages to treat bacterial disease
38
Q

How did MRSA become VRSA?

A
  • vancomycin was used to treat MRSA
  • increased selective pressure
  • VRSA strains have high resistance to vancomycin

MICR 3050 (18 decks)

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