Antimicrobial Agents (Dr. Rolfe)

Front 1

Penicillin: structure required for activity

Back 1

Beta-lactam ring

Front 2

Penicillin: Mechanism of Action and is it bactericial or bacteristatic

Back 2

Interferes with peptidoglycan synthesis and releases autolytic enzymes. Cells eventually burst due to osmotic pressure
-bactericidal

Front 3

Penicillin: List the naturally occure Penicillin and what bacteria types they affect

Back 3

-Penicillin G (acid labile, inc. potency, and narrow spectrum)
-Pen V (acid stable, low potency, narrow spectrum)
-affects GPC, GNC, GPB, and spirochetes

Front 4

Penicillin: Side effects

Back 4

-hypersensitivity (Haplens, skin testing, IgE mediated, Anaphylaxis is rare) and GI problems

Front 5

Penicillin: Mechanism of Resistance

Back 5

-Beta lactamase
-altered cell wall formation
-mutation of PBP
-Tolerance (autolytic enzymes not activated giving it)

Front 6

Cephalosporins: structure

Back 6

Dihydrothiazide ring and 7-Aminocephalosporanic acid (it is Beta lacatamase sensitive)

Front 7

Cephalosporins: Mechanism of Action and is it bactericidal/static

Back 7

MOA-same as penicillin, will bind PBP and inhibit peptidoglycan synthesis. It produces autolysins.
-bactericidal

Front 8

Cephalosporins: Side Effects

Back 8

-hypersensitivity
-GI problems

Front 9

Cephalosporins: Mechanism of Resistance

Back 9

-Beta lactamase
-altered cell wall formation
-mutation of PBP
-Tolerance (autolytic enzymes not activated giving it)

Front 10

Name all Beta-lactam Antimicrobials

Back 10

-Penicillin
-Cephalosporin
-Monobactams (Aztreonam, narrow spectrum, works on aerobic GNR)
-Carbapenems (Imi-, mero-, and ertapenem)

Front 11

What is Clavulanic Acid and what does it combine with?

Back 11

It is a beta lactamase inhibitor with no antimicrobial effects.
-Augmentin= CA + Amoxycillin
-Timentin= CA + Ticarcillin

Front 12

What is sulbactam and what does it combine with?

Back 12

-It is a beta lactamase inhibitor with no antimicrobial effects.
-Unasym= Sul + Ampicillin

Front 13

What is Tazobactam and what does it combine with?

Back 13

It is a beta lactamase inhibitor with no antimicrobial effects.
-Zosyn= Taz + Piperacillin

Front 14

Vancomycin: Mechanism of Action and is it Bactericidal/static

Back 14

Inhibits linking of peptidoglycan chains.
-Bactericidal

Front 15

Vancomycin: Spectrum, affect bacteria, and common administration

Back 15

-Narrow Spectrum (GP)- due to its large size
-IV administration

Front 16

Vancomycin: Side Effects

Back 16

-Initial preparations were nerotoxic, but more recently purified versions were not.

Front 17

Vancomycin: Mechansim of Resistance

Back 17

-Alteration of cell wall

Front 18

Bacitracin: Mechanism of action and is it bactericidal/static

Back 18

Inhibits transfer of peptidoglycan precursors through Cell Membrane and Cell Wall.
-Bactericidal

Front 19

Bacitracin: Spectrum, affected bacteria, and application

Back 19

-Narrow (GP)
-topical application and oral
-It is not absorbed through the GI so is used to treat GI disease and sterilize the stomach before surgery.

Front 20

Bacitracin: side effects

Back 20

-Nephrotoxic (DO NOT give IV) but orally is okay because it is not absorbed in the GI.

Front 21

Cycloserine: Mechanism of Action

Back 21

-Inhibits incorporation of D-alanine into peptidoglycan

Front 22

Cycloserine: What is it used to treat

Back 22

-Mycobacterium tuberculosis
-it is ALWASY used in combo with other anti-TB agents because TB grows so slowly it builds resistance easily

Front 23

Cycloserine: side effects

Back 23

-CNS toxicity
-Usually only used when other treatments fail

Front 24

Isoniazid (INH): mechanism of action

Back 24

-blocks mycolic acid synthesis (mycolic acid is used in M. tuberculosis, but not in other bacteria)

Front 25

Isoniazid (INH): what does it treat

Back 25

M. tuberculosis

Front 26

Name all Antimicrobials that deal with peptidoglycan synthesis

Back 26

Penicillin, cephalosporin, Beta lacatams (monobactans and carbapenems), Vancomycin, Bacitracin, cycloserine

Front 27

Ethionamide: mechanism of action

Back 27

-blocks mycolic acid synthesis (it is a more potent derivative of INH)

Front 28

Ethionamide: what does it treat

Back 28

M. tuberculosis

Front 29

Ethambutol: Mechanism of Action

Back 29

Interferes with synthesis of rabinogalactam (important in M. tuberculosis but not other bacteria)

Front 30

Ethambutol: what does it treat

Back 30

M. tuberculosis

Front 31

Ethambutol: side effects

Back 31

-retinal damage/optic neuritis

Front 32

List all antibiotics that inhibit cell wall synthesis

Back 32

-beta lactams (penicillin, cephalosporins, monobactams, carbapenems), vancomycine, bacitracin, cycloserine, isoniazid, ethionamide, ethambutol

Front 33

List all antibiotics used to treat M. tuberculosis

Back 33

Cycloserine, Isoniazid, ethionamide, ethambutol, Rifampin

Front 34

List all Aminoglycosides

Back 34

-Streptomyces (streptomycin, neomycin, kanamycin, tobramycin, amikacin)
-Micromonosporum (Gentamicin and sisomicin)
-Synthetic derivatives (Amikacin, Netilmicin)
--Tobramycin, Gentamicin, and Amikacin are the three most used. Amikacin is held on reserve in case the other two fail.

Front 35

Aminoglycosides: mechanism of action, bactericidal/static

Back 35

Irreversible bind to ribosome
-bactericidal (except streptomycin)
-It is taken up by energy dependent process and uses porins.
-Not good agains anaerobic bacteria

Front 36

Aminoglycosides: Spectrum, bacteria affected, administration

Back 36

-Narrow (except kanamycin and gentamicin)
-GN bacteria
-Given IV (poor GI absorption)

Front 37

Aminoglycosides: side effects

Back 37

-ototoxicity (reversible)
-nephrotoxic (irreversible)
-the theraputic and toxic doses are close together. When administered, the concentration in the blood must be monitored to ensure that no kidney damage is being done.

Front 38

Aminoglycosides: Mechanism of Resistance

Back 38

-Enzymatic Modification (acetyltransferase, phosphotransferase, and nucleotidyl transferase)
-mutatation to ribosomal binding site
-If the resistance to one is enzymatic, you can use another one.
-If the resistance to one is due to binding site alteration, then the bacteria will be resistant to all

Front 39

Tetracyclines: Name all forms

Back 39

-Streptomyces
-semisynthetic (Chlortetracycline, Tetracycline, doxycycline, minocycline, and tigecycline)

Front 40

Tetracylcine: mechanism of Action, bactericidal/static

Back 40

-Taken up by active transport and reversibly binds ribosome
-bacteriostatic (because it reversibly binds)

Front 41

Tetracycline: spectrum, administration

Back 41

-broad spectrum
-oral absorption

Front 42

Tetracycline: advantages/disadvantages over aminoglycosides

Back 42

-It has a broader spectrum and you can take orally. However, it is only bacteriostatic.

Front 43

Tetracycline: Side Effects

Back 43

-discoloration of teeth (does not damage, just discolors)
-GI problems (due to broad spectrum of bacteria affected)
-Should never be given to pregnent women or children under eight

Front 44

Tetracycline: Mechansim of Resistance

Back 44

-Decrease permeability
-Active Efflux
-Alteration of Ribosome binding site
-Enzymatic Modification

Front 45

Tetracycline: True/False:
If a bacteria is resistant to one, they are resistant to all.

Back 45

True

Front 46

Chloramphenicol: Mechanism of Action, Bactericidal/static

Back 46

-Reversible binding to Ribosome
-Bacteriostatic

Front 47

Chloramphenicol: Spectrum, administration

Back 47

-Broad
-Oral

Front 48

Chloramphenicol: Side Effects

Back 48

-Reversible bond marrow depression (dose dependent) leading to anemia, leukopenia, and thrombocytopenia.
-Aplastic Anemia (Dose Independent, affects 1:20,000)

Front 49

Chloramphenicol: Mechanism of Resistance

Back 49

-Acetyltransferase alteration
-altered cell wall (porin alteration)

Front 50

Macrolides (Erythromycin): Mechanism of Action, bactericidal/static

Back 50

-Binds ribosome
-Bacteriostatic (depending on the species, growth phase, # of bacteria-it may be bactericidal)

Front 51

Erythromycin: spectrum

Back 51

-broad

Front 52

Erythromycin: Side Effects

Back 52

-GI problems due to broad spectrum

Front 53

Erythromycin: Mechanism of Resistance

Back 53

-Cross resistance with lincosamides
-Altered ribo binding site
-Esterase-inactivates the antibiotic
-GN bacteria develop resistance fairly quickly

Front 54

Lincosamides (Clindamycin): Mechanism of Action, bactericidal/static

Back 54

-Binds ribosome
-can be both cidal/static

Front 55

Clindamycin: what bacteria does it treat

Back 55

-used to treat anaerobic bacteria
-used to treat MRSA

Front 56

Clindamycin: side effects

Back 56

-High GI problems because it acts on anaerobic bacteria and allows for colonization of C. dificile.

Front 57

What antimicrobials are used to treat MRSA

Back 57

Clindamycin and Oxazolidinones (linezolid)

Front 58

What antimicrobials are used to treat VREF

Back 58

-Streptogramins (synercid) and Oxazolidinones (linezolid)

Front 59

What are the two Streptogramins, what is the antimicrobial agent called when they are combined, and why are they combined

Back 59

-Quinupristin and Dalfopristin
-Synercid= Quinu + Dalfo
-Alone they are bacteriostatic, but combined they are bactericidal

Front 60

Synercid: Mechanism of Action

Back 60

-Inhibits protein synthesis
-Dalfopristin binds ribosomes and Quinupristin causes the premature release of peptides

Front 61

Synercid: What bacteria do they affect, how is it administered, and what disease is it frequently used against

Back 61

-GP bacteria
-IV administration
-used to treat VREF

Front 62

Synercid: Side effects

Back 62

-venous irritation
-vomiting/diarrhea
-rash
-hepatoxicity
- athralagia and myalgia

Front 63

Oxazolidinones (linezolid): mechanism of action, bactericidal/bacteriostatic

Back 63

-Binds to Ribosomes
-bacteriostatic

Front 64

Oxazolidinones (linezolid): what does it treat and how is it given

Back 64

-VREF and MRSA
-oral and IV

Front 65

Oxazolidinones (linezolid): side effects

Back 65

-If taken with over the counter medicine, it causes increased Blood Pressure

Front 66

Name all antibiotics that inhibit protein synthesis

Back 66

-Aminoglycosides (streptomyces, Micromonosproum, synthetic derivatives)
-Tetracycline
-chloramphenicol
-Macrolides
-Erythromycin
-Lincosamides
-Streptogramins (synercid)
-Oxazolidinones (linezolid)

Front 67

Sulfonamides: mechanism of action

Back 67

-It resembles PABA and blocks the synthesis of folic acid (and ultimately DNA) by competing with PABA for Tetrahydropteroic Acid synthetase.

Front 68

Sulfonamides: Spectrum, bactericidal/static

Back 68

-Broad
-Bacteriostatic

Front 69

Sulfonamides: what is it used to treat

Back 69

-GI
-UTI
-Topical
-it must concentrate in the cells in high concentrations

Front 70

Sulfonamides: side effects

Back 70

-hypersensitivity
-blood abnormalities (hemolytic and aplastic anemia, leukopenia, agranulocytes, thrombocytopenia)
-reversible
-All based on metabolic pathways

Front 71

Sulfonamides: Mechanism of Resistance

Back 71

-overproduce PABA
-Alter Tetrahydropteroic Acid synthetase
-Develop ways to use exogenous folic acid
-decrease permeability

Front 72

Dapsone and Para-Aminosalicylic Acid: Mechanism of Action

Back 72

-Mechanism similar to sulfonamides

Front 73

Dapsone/Para-Aminosalicylic Acid: what is it used to treat

Back 73

-mycobacterium leprae (leprosy)

Front 74

Dapsone/Para-Aminosalicylic Acid: Spectrum

Back 74

-Narrow, used to treat leprosy. Will not repair damage already done.

Front 75

Dapsone/Para-Aminosalicylic Acid: Mechanism of Resistance

Back 75

Same as sulfonamides

Front 76

Trimethoprim: Mechanism of Action, Bactericidal/static

Back 76

Inhibits dihydrofolate reductase (the 2nd step in folic acid synthesis)
-bacteriostatic

Front 77

Trimethoprim: What is it combined with and what does that create

Back 77

Cotrimoxazole (bactrim)= trimethoprim + sulfamethoxazole

Front 78

Trimethoprim: used to treat

Back 78

-UTI
-Traveler's Diarrhea

Front 79

Trimethoprim: side effects

Back 79

-hypersensitivity
-blood abnormalities (reversible)

Front 80

Trimethoprim: mechanism of resistance

Back 80

-overproduce dihydrofolic acid
-alteration of dihydrofolic reductase
-folic acid dependnecy
-decrease cell permeability

Front 81

Name the antibiotics that inhibit folic acid synthesis

Back 81

-sulfonamides
-Dapsone/Para-aminosalicylic acid
-Trimethoprim + sulfamethoxazole

Front 82

Metronidazole: What does it treat

Back 82

-is only active against anaerobes because it requires a reduced environment to work

Front 83

Metronidazole: spectrum, bactericidal/static

Back 83

-narrow spectrum (anaerobes)
-bactericidal

Front 84

Metronidazole: side effects

Back 84

-mutagenic and carcinogenic
-peripheral neuropathy
-used to treat trichomonas vaginalis

Front 85

Metronidazole: mechanism of action

Back 85

-passively diffuses into the cell. It gets reduced and produces short lived toxic intermediates that are toxic to nucleic acids (affecting DNA, RNA, and proteins).

Front 86

Rifampin(Rifabutin): Mechanism of Action

Back 86

-inhibits DNA-dependent RNA polymerase (which ultimately inhibits protein synthesis).

Front 87

Rifampin: spectrum, what is it used to treat

Back 87

-broad
-used to treat TB, but it builds a resistance so fast it needs to be used with another anti-TB agent

Front 88

Rifampin: side effects

Back 88

-Skin rash
-Thrombocytopenia (few blood platelets)

Front 89

Nalidixic Acid: Mechanism of Action

Back 89

-inhibits bacterial DNA gyrase/topoisomerase
-Prevents supercoiling
-must be used in high concentrations and resistance is formed quickly

Front 90

Nalidixic Acid: spectrum, bactericidal/static

Back 90

-narrow spectrum (GN)
-bactericidal

Front 91

Quinolones: what are the three quinolones and what are they derivatives of

Back 91

Gatifloxacin, levofloxacin, and ciprofloxacin.
-they are derivatives of nalidixic acid (just 1000x more potent)

Front 92

Quinolones: mechanism of action and what types of bacteria do they affect

Back 92

inhibits bacterial DNA dependent gyrase and topoisomerase
-affect mostly GN, but some GP

Front 93

Quinolones: spectrum, and administration

Back 93

-broad
-oral

Front 94

Quinolones: side effects

Back 94

GI due to the broad spectrum

Front 95

Quinolones: mechanism of resistance

Back 95

-alter gyrase/topoisomerase
-alter outer membrane
-increase efflux pumps

Front 96

name the antibiotics which inhibit nucleic acid function

Back 96

-metronidazole (toxic)
-Rifampin (RNA poly)
-Nalidixic Acid (gyrase/topoisomerase)
-Quinolones (gyrase/topoisomerase)

Front 97

Polymixin: Which forms are used and why

Back 97

Polymixin B and E are the only ones not to toxic to humans

Front 98

Polymixin: mechanism of Action, bactericidal/static

Back 98

cationic detergent (disrupts the cell membrane)
-bactericial

Front 99

True/False- Polymixin only works when the cell is dividing

Back 99

False
-It does not matter whether the cell is resting or multiplying

Front 100

Polymixin: spectrum, bacteria affected, administration

Back 100

-narrow (GN bacilli)
-topical ointments
-oral (it is not absorbed, used for gut sterilization)

Front 101

Polymixin: side effects

Back 101

-neuroxic (reversible, dose related)
-nephrotoxic (dose related)

Front 102

Polymixin: mechanism of resistance

Back 102

-alteration of cell wall

Front 103

Name the quantitaive procedures for antimicrobial testing

Back 103

-Agar dilution (will measure MIC)
-Broth diffusion (will give MIC, plate the MIC tube to get MBC)
-Microtiter Broth (first clear tubes is MIC, take MIC tube and get MBC, can test many different types of bacteria against the same antibiotic, or the same antibiotic against multiple bacteria)
-E-test (filter paper contains incrasing concentrations of antibiotic)

Front 104

What are the semiquantitative procedures and what do they tell us

Back 104

-Semi-quantitative only measures susceptibility:
-very susceptible (good at theraputic dose)
-moderately susceptible (high dose required)
-Moderately resistant (drug must be concentrated in cell to work)
-Very Resistant (Can't use)
-Agar diffusion susceptibility (place disks containing antibiotics on agar, measure zone of inhibition, refer to a chart that gives correlation between size and susceptibility)