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Microbiology > Antibiotics I > Flashcards

Antibiotics I Flashcards

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1
Q

What are Abx and where do they come from?

A

molecules produced by one organism which inhibit the growth of another organism.

most are originally produced by fungi or bacteria, a few are purely synthetic

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2
Q

5 major classes of Abx

A
  1. Antimetabolites (inhibit synthesis of nucleotides)
  2. Inhibitors of Peptidoglycan Synthesis
  3. Inhibitors of Protein Synthesis
  4. Inhibitors of DNA-stability
    Inhibitors of RNA synthesis
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3
Q

what is meant by selective toxicity, in terms of Abx

A

Abx need to be toxic to something in the bacteria, that is not toxic to the host

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4
Q

What are the two things Abx target in order to be selectively toxic (toxic to bacteria but not to the host)

A
  1. something in the bacteria, but not in the host (ie enzymes to make peptidoglycan)
  2. something that differs from the corresponding molecule in the host (i.e. ribosome)
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5
Q

Therapeutic index

A

The Toxic Dose for 50% of people/the Effective dose for 50% of the people (TD50/ED50)

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6
Q

define the “spectrum” of Abx

A

the species against which an Abx is typically effective

- it can be associated with characteristics of a bact (gram pos. v gram neg., aerobic vs anaerobic, specific species)

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7
Q

3 determinants of Abx efficacy

A
  1. ability of abx to reach target
  2. ability to bind target and inhibit function
  3. ability of abx to resist inactivation
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8
Q

when is Abx susceptibility testing performed (2 times)?

A
  1. when the abx has therapeutic potential for that organism at that infected body site
  2. if the susceptibility can’t be predicted from the species of organism
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9
Q

Minimum Inhibitory Concentration (MIC) for Abx

A

the concentration of Abx which inhibits the visible growth of the bacteria (found by putting the bacteria in vials with increasing levels of Abx). this is the common method for determining abx susceptibility

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10
Q

Minimum Bactericidal Concentration (MBC)

A

the concentration of Abx which kills 99.9% of the bacteria (found by growing the subculture on an agar). this is rarely used to determine abx susceptibility

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11
Q

Disk Diffusion Abx Susceptibility Testing/Aka a Kirby Bauer Test

A

put many Abx onto a plate and try to culture bacteria. Abx that are effective agst the bacteria will form clear circles around them. The bigger the clear circle, the more effective the Abx and so the lower the Minimum Inhibitory Concentration (MIC)

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12
Q

Baceriostatic Abx

A

block the growth of bacteria (so that the immune system can kill them)

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13
Q

Bactericidal Abx

A

kill the bact

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14
Q

Bacteriostatic Abx are effective agst most infections, but bactericidal Abx are better for the treatment of what two diseases and in what type of person?

A

bactericidal Abx = better for:

  1. endocaritis
  2. meningitis
  3. immunocompromised pts (ie on steroids or HIV +)
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15
Q

Indifference vs antagonistic vs synergistic combos of Abx

A

indifference: when the combination of both is no different than the effectiveness of 1
2. antagonistic: when using both gives worst results than using one (ie you give a bactericidal Abx which can only be effective during replication, but you also give a bacteriostatic which halts replication)
3. synergistic: the combo of drugs is more effective than either alone

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16
Q

5 classes that are usually bactericidal

A
  1. aminoglycosides
  2. Rifamycins
  3. cell-wall synthesis inhibitors
  4. daptmycin
  5. flouroquinolones
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17
Q

3 classes of usually bacteriostatic Abx

A
  1. protein-synthesis inhibitors other than aminoglycosides
  2. trimethoprim (antimetabolites)
  3. sulfonamides (antimetabolites)
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18
Q

4 mechanisms of synergy

A
  1. one abx allows second abx to reach a greater concentration at site of activity
  2. one abx enhances binding of the second
  3. one abx blocks destruction of the second
  4. two abx partially inhibit separate steps of a synthetic pathway
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19
Q

Pharmacokinetics

A

the absorption, districution, metabolism and excretion of drugs

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20
Q

4 means of administering Abx

A
  1. topical
  2. oral
  3. IV
  4. intramuscular
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21
Q

what are topical abx used for?

A

topical infections only!

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22
Q

advantages, disadvantages and uses of oral abx

A

advantages: convenient, some drugs aren’t absorbed, so you can treat bacteria in the gut
disadvantages:
- systemic levels are variable (depends on absorption, breakdown and exretion)
- some might not get absorbed
uses:
-most outpt care

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23
Q

advantages, disadvantages and uses of IV abx

A 
advantages:
- bypass absorption
disadvantage: 
- inconvenient (has to be administered at medical facility, or have a nurse sent to a home)
uses:
-serious infections
- organisms resistant to oral meds
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24
Q

advantages, disadvantages and uses of intramuscular abx

A 
advantage:
- bypass absorption
disadvantage:
- inconvenient
- painful
uses:
-occasional outpt txt
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25
Q

what effect does the anatomic separation between circulation and the CNS or prostatic tissues have on Abx concentrations

A

it reduces diffusion of most abx into these tissues

26
Q

what sorts of drugs will reach high concentrations in prostatic tisues? why?

A

basic drugs like trimethoprim and fluoroquinolones because they’re attracted to the acidic prostatic secretions

27
Q

how is abx concentration regulated in the CNS when there’s no infection? when there is infection?

A

when there is no inflammation in the CNS, penicillin will diffuse in low concentrations across the blood brain barrier (BBB), pass through the choroid plexus and is sent back out into systemic circulation, keeping penicillin concentrations very low.

If there is inflammation in the choroid plexus, however, the penicillin stays inside the CSF and so concentrations of peicillin quickly increase

28
Q

which 3 abx reach adequate levels in the CNS in the presence of inflammation?

A
  1. penicillin
  2. ampicillin
  3. 3rd and 4th generation cephalosporins
29
Q

2 antimetabolite abx

A
  1. trimethoprim

2. sulfonamides

30
Q

the importance of folic acid, and where does it come from in bacteria?

A

folic acid is needed for the synthesis of DNA because it allows the transfer of 1 Carbon to form thymidine, purines and some aa

bacteria are capable of making folic acid themselves (mammals bring it into the cell from EC sources)

31
Q

tetrahydrofolate

A

a folic acid derivative necessary to make thymidine, purines and aa

32
Q

what enzyme that is only present in bacteria do sulfamides work on?

A 
dihydropteroate synthase (which converts pteridine and PABA into Dihyropteroic acid
(on the pathway to make a folic acid derivative)
33
Q

what enzyme that is present in hmans and bacteria does trimethoprim work on?

A

dihydrofolate reductase which converts dihydrofolate into tetrahydrofolate (which can add single carbons to make thymidine, purines and aa)

34
Q

sulfonides and trimethoprim are synergistic because they

A

are a sequential blockade of the pathway to synthesizing tetrahydrofolate, which inhibits thymidine, purine and aa synthesis

35
Q

Sulfonides are analogues of what and work on what enzyme?

A

PABA analogues that inhibit dihydroperoate synthase from making dihydropteroate out of pteridine and PABA

36
Q

trimethoprim are analogues of what, and they work on which enzyme to inhibit production of tetrahydrofolate?

A

Pteridine analogues that work o dihydrofolate reductase

37
Q

what class of drugs are dihydropteroate synthase (DS) inhibitors?

A

sulfonamides

38
Q

what class of drugs are dihydrofolate reductase inhibitors (DHFR)

A

trimethoprim

39
Q

sulfonomides are monotherapeautic for…

A

UTIs

40
Q

bacterial spectrum for sulfonamide (Dihydropteroate Synthase (DS) inhibitors) and trimethoprim (Dihydrofolate reductase (DHFR) inhibitors)

A

most bacteria

41
Q

TMP (trimethoprim)/SXT (sulfonomides) are used together for many infections, especially (2)

A
  1. GI infections (enterobacteriaceae are often susceptible)

2. S aureus (including MRSA)

42
Q

adverse effects of sulfonamides

A

adverse effects involve the skin:

  1. hypersensitivity is common (immune mediated itchy skin– usually not severe)
  2. rare severe adverse effects (stevens-Johnson syndrome (loss of superficial layers of skin and mucus), anemia due to hemolysis with G6PD)
43
Q

adverse effects of trimethoprim

A
  1. rarely causes bone marrow suppression by inhibiting human DHFR (people with low folate = more susceptible) leading to anemia, granulocytopenia, throbocytopenia
    * all = reversible by stopping the drug
44
Q

what is the folate pathway required for?

A

biosynthetic stepsperformed by all organisms

45
Q

Class of drugs that are Inhibitors of DNA-Stability

A

Flouroquinolones and Quinolones

46
Q

adverse effects of quinolones

A
  1. tendinitis and rupture occors rarely in adults
  2. may predispose to cardiac arrhythmias (avoid using with antiarrhythmics)

*cartilage erosion occurs in juvenile animals, but doesn’t seem to happen in children

47
Q

2 classes of inhibitors of RNA synth

A
  1. Rifamycins

2. Fidaxomicin

48
Q

mechanism of Fidaxomicin (and RNA synth inhibitor)

A

It binds the RNA-polymerase-DNA complex and blocks the separation of DNA strands

49
Q

Mechanism of Rifamycis (a DNA synth inhibitor)

A

It binds the Beta subunit of RNA polymerase in the RNA-Polymerase-DNA complex and blocks progression of nuc. acids through the DNA/RNA channel, inhibiting new bonds on the RNA chain (so RNA chain can’t be constructed)

50
Q

Rifamycin spectrum, and how it’s used

A

broad spectrum of activity and it’s highly lipid soluble leading to excellent tissue penetration, but resistance rapidly develops with monotherapy
- used in combination for txt serious infections like: myobacterial infections (tb) and staph endocarditis/joint infections

51
Q

adverse effects of rifamycin (3)

A
  1. tears, urine and saliva turn orange
  2. hepatic failure in pt with another source of injury (ie another drug)– this is rare
  3. increased expression of metabolic enzymes leading to increased metabolism of many drugs
52
Q

spectrum/use of fidaxomicin

A
  1. Poor lipid solubility, so poor PO adsorption, so it stays in the GI tract
  2. variable activity against Gram +, but as good as vancomycin to fight C diff
53
Q

even though fidaxomicin is as effective as vancomycin for curing C diff and relapse with fidaxomicin is less common, why is it not currently used for C diff generally?

A

too expensive and too new

54
Q

when is fidaxomicin used instead of vancomycin to treat c diff?

A

with people who either didn’t recover on vancomycin, or who relapsed after taking vancomycin

55
Q

two topoligical challenges faced by mammals and bacteria during transcription and DNA replication?

A
  1. separation of the two strands of DNA leads to supercoiling
  2. after DNA replication the parent and daughter strands are “catenated” (linked together)
56
Q

what are gyrase and topoisomerase IV?

A

two enzymes that work together to cut the double stranded parent DNA to release the daughter DNA, and then reform the bond in the parent DNA

57
Q

mechanism of Quinlones (DNA stability inhibitor)

A

block the activity of the Gyrase and topoisomerase activity IV after they have cut the parent DNA, so there is no repair of the parent DNA. The presence of the double stranded DNA leads to bacterial death

58
Q

spectrum of flouroquinolones

A

there are several available, each with a different spectrum: some gram pos, some gram neg, some for anaerobic bact and some for mycobact

59
Q

naladixic acid, a quinolone is used for txtmt of…

A

UTIs

60
Q

difference btwn quinolone and flouroquinolone

A

flouroquinolone has an added fluorine which increases the blood levels, penetration and half life of the quinolones

Microbiology (11 decks)

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