Microbiology Ch5: Biological Basis For Antibacterial Action

Front 1

antimetabolite effective against a streptoccal infection in mice

Back 1

prontosil

Front 2

prontosil was the precursor to what drug

Back 2

sulfonamides

Front 3

substance in yeast that counteracts the actions of sulfonamides

Back 3

PAB, p-aminobenzoic acid

Front 4

relationship between amounts of sulfonamides administered and amounts of PAB created is called what

Back 4

competitive inhibition

Front 5

PAB is a constituitent of what vitamin

Back 5

folic acid

Front 6

antagonism of sulfa by folic acid is what

Back 6

noncompetitive

Front 7

what is unique about body folic acid requirements

Back 7

body requires preformed folic acid

Front 8

what effect do sulfonamides have on folic acid

Back 8

affect the synthesis, not the utilization, thats why body cells are not harmed

Front 9

why can't bacteria use preformed folic acid

Back 9

they do not contain a mechanism to uptake it

Front 10

how and why do sulfoniamides work for bacterial killing

Back 10

inhibits formation of folic acid, can take 16 daugter cells for effect to become evident because has enough preformed folic acid

Front 11

bactericidal

Back 11

kills immediately

Front 12

bacteriostatic

Back 12

inhibit growth reversibly

Front 13

when are bactericidal drugs better to use

Back 13

when the body defenses are insufficient to clear the invading agents

Front 14

what conditions are better for bactericidals

Back 14

bacterial endocarditis, meningitis and agranulocytopenia

Front 15

erythromycin is what class

Back 15

bactericidal, inhibits protein synthesis

Front 16

in what case would you want a static agent

Back 16

when you would want to give the body defenses a chance to eliminate the organisms on its own with help

Front 17

is static vs cidal concrete for all organisms?

Back 17

no

Front 18

spectinomycin

Back 18

static for e coli, cidial for gonococci

Front 19

what is effective against e coli invivo

Back 19

rifampin

Front 20

every agent is responsive against a broad ____ of what

Back 20

spectrum

Front 21

aminoglycosides are taken up poorly under what conditions

Back 21

anerobic

Front 22

what antibiotic for UTI

Back 22

nitrofurantoin

Front 23

theraputic index

Back 23

ratio between the effective and toxic dose

Front 24

methotrexate

Back 24

inhibitors of folic acid metabolism

Front 25

topical antibiotics that harm host cell membranes

Back 25

polymyxin and antifungal nystatin

Front 26

sulfonamide side effect

Back 26

blood acidosis and alkaline urine, some also cause hypoglycemia

Front 27

function of trimethoprim

Back 27

blocks the function rather than the synthesis of folic acid

Front 28

what enzyme does trimethoprim deactivate

Back 28

dihydrofolate reductase

Front 29

what is the principle behind the mechanism of tetracycline

Back 29

relative sensitivity, bacteria will concentrate the antibiotic, mammal cells will not

Front 30

how is extreme selectivity achieved

Back 30

when the target is not present in the host, only the target organism

Front 31

B-lactam and extreme selectivty

Back 31

murein target is only present in bacterial cells walls

Front 32

B lactam antibiotics are known as what class of drugs

Back 32

broad spectrum antibiotics

Front 33

what type of microbes are B-lactams effective against

Back 33

gram negative

Front 34

3rd gen cephalosporins have what advantages

Back 34

works on pseudomonas, h. influenzae and penetrate CNS - useful for gram negative meningitis

Front 35

what is the principle mechanism of b-lactam resistance

Back 35

inactivating enzymes

Front 36

what kind of b-lactamaes do gram positive produce

Back 36

extracellular

Front 37

why is b-lactam ineffective against gram positive

Back 37

because they release and produce more lactamases the more antibiotic comes into contact with positive wall

Front 38

where are b-lactamses found in gram negative

Back 38

in the periplasm or bound to inner membrane

Front 39

why is it effective against gram negative

Back 39

b-lactamases are produced at a constant rate, cant be increased

Front 40

b-lactam resistance is common in what genus

Back 40

staphylococci

Front 41

how is b-lactamase resistance gene transferred from one bacteria to another

Back 41

transposon via plasmid bridge

Front 42

what do b-lactams have to pass through in order to hit PBP

Back 42

outer membrane pores in gram negative bacteria

Front 43

what is a PBP

Back 43

penicillin binding protein

Front 44

penicillin resistant step pneumoniae and methicillin resistant staph aureus come from what resistance mechanism

Back 44

modification of PBPs

Front 45

what are extensively modified PBP bacteria referred to as

Back 45

MRSA

Front 46

what is used to treat MRSA

Back 46

cell wall inhibiting glycopeptides, vancomycin

Front 47

why are some strains of pneumococci and staphylococci inhibited rather than killed by b lactam

Back 47

partial resistance called tolerance

Front 48

what type of bacteria is vancomycin used for

Back 48

gram positive

Front 49

how is vancomycin administered

Back 49

intravenously

Front 50

what is the vancomycin target

Back 50

d-alanine-d-lactate

Front 51

what bacteria has vancomycin resistance

Back 51

enterococcus

Front 52

VRE and VRSA

Back 52

vancomycin resistant enterococcus and s aureus, very hard to treat

Front 53

how do quinolone antibiotics work

Back 53

inhibit bacterial topoisomerases

Front 54

gram negative and gram positive topoisomerase

Back 54

negative - topoisomerase IV
positive - dna Gyrase

Front 55

quinolone used for gram negative and positive effectiveness

Back 55

fluoroquinolone

Front 56

what is one of the principle methods of quinolone resistance

Back 56

flux pumps

Front 57

what is the basis for the effectiveness against bacteria with antiribosomal antibiotics

Back 57

eukaryotic and bacteria have different ribosomes to enable different targets

Front 58

what are two major antiribosomal antibiotics

Back 58

erythromycin, streptomycin

Front 59

what does tetracycline target

Back 59

mammalian and bacterial ribosomes invivo

Front 60

how do oxazolidinones work

Back 60

bind to the 50s unit of bacterial ribosomes and prevent the assembly of the translation complex

Front 61

what is aminoglycoside toxicity

Back 61

renal tubules and inner ear

Front 62

method of action for aminoglycoside

Back 62

1. penetrate gram neg outer membrane
2. initiate two stage transport system
3. BINDS TO 30S ribosome and fucks up the initiation site

Front 63

two major resistance mechanisms for gram neg bacteria for aminoglycosides

Back 63

modifying enzymes and obligate anaerobes

Front 64

what is the most common method of tetracycline resistance

Back 64

actively pumping the drug out of the bacteria

Front 65

Fun Factoid: Macrolide antiobiotic names

Back 65

erythromycin, clindamycin, azithromycin, clarithromycin

Front 66

can macrolides be pumped out of bacteria a la tetracyclines?

Back 66

yesss

Front 67

what is the most dignificant degree of macrolide resistancre

Back 67

methylation of the 23s ribosomal RNA, this enables the 50s transcription unit to becomes resistant to drugs

Front 68

what antibiotic works inspite of the methylase produced by macrolide resistance

Back 68

telithromycin, binds to two separate sites on 23s, can still inhibit 50s unit

Front 69

what is the major completely synthetically derived antibiotic

Back 69

oxazolidinones

Front 70

how is oxazolidinone resistance mechanized

Back 70

point mutations in bacterial 23s RNA of the 50s subunit, prevent binding to riobosome

Front 71

why are therputics against animal parasites, viruses or fungi toxic

Back 71

target human ribosomes as well

Front 72

polyenes

Back 72

bind to egosterol in the membranes of fungi

Front 73

amphotericin B

Back 73

yeasts are about 200 fold more sensitive to this than are human cells

Front 74

imidazoles

Back 74

target p450 demethylase, involved with sterol synthesis

Front 75

echinocandins

Back 75

inhibit fungal cell wall B-glucan