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Microbiology summer 2015 Midterm 2 > Antibiotics lecture > Flashcards

Antibiotics lecture Flashcards

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1
Q

Prokaryotes

Mycobacteria causes tuberculosis, what antibiotics work against it?

A

1) isoniazid 2) streptomycin

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2
Q

Prokaryotes

what antibiotics work against gram negative?

A

1) Polymyxin
2) Streptomycin
3) Erythromycin
4) Tetracycline
5) Sulfonamides (works on eukaryotes protozoa)
6) Isoniazid (slightly gram negative, mostly mycobacteria)
7) pencilin (slightly gram negative, mostly gram positive)

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3
Q

Prokaryotes

what antibiotics work against gram positive?

A

1) pencilin
2) erythromycin
3) tetracycline
4) sulfonamides

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4
Q

Prokaryotes

what antibiotis work against Chlamydias and rickettsias?

A

1) Erthromycin
2) Tetramycin
3) Sulfonamides

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5
Q

Eukaryotes ( complex like us)

what antibiotics work on protozoa and Fungi?

A

Azoles

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6
Q

Eukaryotes

what antibiotics work against Helminths?

A

1) Niclosamide
2) Praziquantel

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7
Q

what antibiotics are used against viruses? (we have to target our cells)

A

1) Arildone
2) Ribavirin
3) Acyclovir

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8
Q

Mechanisms of Action

-inhibit/interfere with cell wall synthesis means

A

stoping cell walls from being made, which will result in no growth.

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9
Q
  • B-lactam antibiotics have beta lactam ring that __________________________
  • ex: __________________________________________
A

1) inhibit peptidoglycan synthesis
2) Penicillin derivatives (produced by fungi) , cephalosporin, monobactams, carbapenems

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10
Q

B-lactamase is produced by bacteria and it __________________________

A

cuts the little beta lactam rings making antibiotics no longer effective

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11
Q

B-lactamase inhibitors inhibits the bacteria that cuts the beta lactam rings

ex. __________________ and ___________________

A

1) clavulanic acid
2) guacomin

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12
Q

B-lactam ring is the ______________________________

A

functional portion that messes up the peptidoglycan layer

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13
Q

Antibiotics side effects

1) ______________________
2) ______________________

A

1) Ciprofloxacin
2) Doxycycline

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14
Q

Examples of glycopeptides antibiotics that ( Inhibit/interfere with Cell Wall Synthesis)

1)

2)

3)

4)

5)

A

1) Vanomycin
2) Teicoplanin
3) Oritavancin
4) Telavancin
5) Dalbavancin

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15
Q

Glycopeptides prevents the _________________________ making it ______________.

A

1) Addition of new peptidoglycan subunits
2) Bacteriastatic

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16
Q

inhibit protein synthesis —> different numbers! (80s Ribosomes)

  • ______________ : prevent formation of initiation complex (shuts off protein synthesis at that site.
  • _______________ & ______________ ; blocks A (arrival) site (new amino acid can’t be brought in, poly chain cut off)
A

1) Linezolid
2) Tetrecycline
3) Tigecycline

17
Q

Aminoglycosides; interfere with proofreading (incorrect amino acids brought in)

(producer of antibiotics) -Streptomyces; _________, _________, _________.

(producer of antibiotics) -Micromonospora; _____________.

A

1) streptomycin
2) kanamycin
3) neomycin
4) gentamicin

18
Q
  • _________________; block peptidyl transfer step of elongation on 50S subunit in bacteria and mitochondria ——> first _____________________
  • Adverse effects (not a “go-to” any more): _______________________________
A

1) Chloramphenicol
2) LARGE SCALE ANTIBIOTIC
3) aplastic anemia, bone marrow suppression, leukemia, neurotoxicity

19
Q

Chloramphenicol is still around because it crosses ____________________________

A

blood brain barrier; meningitis; tradeoff

20
Q

aminoglycosides: ___________________________
- macrolides
ex) _______________, _________________.
- lincosamide
ex) __________________

A

1) inhibit ribosomal translocation
2) azithromycin, erythromycin
3) clindamycin

21
Q

_______________________ causes premature release of peptide chain.

A

streptogramins

22
Q

disrupt unique components of cytoplasmic membrane

  • ____________: causes charge to go away; ions aren’t moving in and out so cell can’t function. (binds to membrane casuses it to deplorize)
  • ____________: poke holes in membrane (binds to phospholipids distructing cell membrane)
A

1) Daptomycin
2) Polymyxins

23
Q

inhibit metabolic pathways

  • _____________: get folic acid in our diet (don’t produce); needed for nucleotide production. Sulfonamides & trimethoprim can block pathways!
  • _________________ inhibitors
A

1) Antifolates
2) Purine/Pyrimidine

24
Q

inhibit nucleic acid synthesis

-_____________: inhibits transcription

-_____________: interfere with DNA coiling
–Nalidixic acid
–Ciprofloxacin

-_____________: test used to identify types of stap

A

1) Rifampin
2) Quinolones
3) Novobioci

25
Q

Protein synthesis

A site- _____________________________________________

P site- _____________________________________________

E site- _____________________________________________

A

1) where the tRNA bring in the amino acid then,
2) the pepty bond is formed between the new amino acid and the growing poly peptide chain
3) Where tRNA exits the ribosomes

26
Q

Antibiotics should be…

A
  • Inexpensive
  • Readily available
  • Stabile (long shelf life)
  • Easily administered
  • Non toxic, non allergic
  • Selectively Toxic (harm whatever we’re trying to get rid of, no damage to us)
27
Q

Spectrum of Action

Narrow spectrum: _____________________________________

Broad spectrum: _________________________________________________

A

1) will only work on a limited number of organisms
2) will work on a large amount of organisms; not selectively toxic (used when you are unaware w/ what you are dealing with)

28
Q

Efficacy (to know whether it worked or not)

  • Diffusion susceptibility test (Kirby Bauer)
  • _______________: antibiotics works
  • _______________: antibiotic does not work
  • _______________: diameter of clearing that surrounds the disc
A

1) Susceptible
2) Resistant
3) Zone of inhibition

29
Q
  • Minimum Inhibitory concentration (MIC) : _______________________________
  • Minimum Bacteriocidal (MBC): ___________________________________
A

1) minimum amount of antibiotic we need to INHIBIT the growth (not kill it)
2) minimum concentration of a drug that kills the bacteria

30
Q

Routes of Administration

  • Topical/local - _______________________
  • Oral- _______________________________________
  • IM (intramuscular)- _____________________________________
  • IV (intravenous)- __________________________________
A

1) superficial infection
2) pill in your mouth (lower blood concentration takes time) no complience - we don’t finish it
3) slow diffusion into the blood vessels (fairly good concentration)
4) highest concentration (blood goes directly into a blood vessel)

31
Q

Safety & Side Effects

  • Toxicity
  • ______________ & _______________ (can be fatal on kidneys)
  • __________________ (black hairy tongue)
  • ___________________ (complex with calcium & gets incorporated into growing bone/teeth)
A

1) Polymyxin
2) aminoglycosides
3) Metronidazole
4) Tetracycline

32
Q

Safety & Side Effects

  • Allergies
  • __________________ ( when your trachea starts closing up) reactions to pinicillin; deadly, but only 0.1% Americans have it.
A

1) Anaphylactic

33
Q

Safety & Side Effects

  • Disruption to normal microbiota
  • Superinfections
  • ______________ (yeast infection (particulary females on antibiotics) , oral thrush (anybody)
  • C. diff (pseudomembranous colitis)
A

1) C. albicans

34
Q

How does antibiotics resistence become a problem?

1) Bacterial transformation ____________________________
2) Bacterial transduction ____________________________
3) Bacterial conjugation ____________________________

WE CALL THEM HORIZONTAL GENES TRANSFER BECAUSE THEY ARE ALL WITHIN THE SAME GENERATION.

A

1) DNA is released to env. and picked up by other bacteria
2) DNA is transfered via virus
3) Bacteria to Bacteria transfer via Pili

Microbiology summer 2015 Midterm 2 (5 decks)

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