S2 I&i Exam 5: Commonly Used Antimicrobials

Front 1

what is the essential feature of effective antimicrobial agents?

Back 1

the ability to inhibit the growth of microorganisms at concentrations tolerated by the host.

Front 2

what do antimicrobial agents generally target?

Back 2

anatomic (cell) structures or biosynthetic pathways unique to microorganisms

Front 3

what are the four classes of antimicrobial agents?

Back 3

antibacterial, antiviral, antifungal, and antiparasitic

Front 4

what are the two subcategories given for antifungals?

Back 4

fungistat and fungicide

(stats suppress, cides kill)

Front 5

what are the two subcategories given for antiparasitic?

Back 5

antiprotozoal (inhibits DNA synth or carb metab)
&
antihelminthic (inhibits glycolysis or neuromusc)

Front 6

define antibiotic.

Back 6

antimicrobials of microbial origin, most of which are produced by fungi or by bacteria of the genus Streptomyces

Front 7

what are antibiotic made from?

Back 7

microbes (fungi or bacteria), commonly streptomyces


(genetically modify microbe to make it antimicrobial- usable to tx infectious disease)

Front 8

define chemotherapeutic.

Back 8

not an antibiotic

-used for the treatment of cancer as well as for infectious disease

Front 9

define Minimal inhibitory concentration (MIC)

Back 9

the lowest drug (antimicrobial) concentration (ug/mL) able to inhibit growth of the microorganism.

Front 10

T/F
Sensitivity & susceptibility are the same thing

Back 10

TRUE

Front 11

define sensitive/susceptible

Back 11

microorganisms that will be inhibited by concentrations of the antimicrobic that can be achieved clinically.

Front 12

define resistant.

Back 12

organisms that are NOT inhibited by clinically achievable concentrations of an antimicrobial agent.

(= OPPOSITE sensitive/susceptible)

Front 13

define spectrum.

Back 13

the variety of categories of microorganisms against which an antimicrobial is typically active

(wide= wide variety, narrow= few microorganisms)

Front 14

what are the five considerations that determine which antimicrobial is appropriate for the infection?

Back 14

1) infecting organism's antimicrobial sensitivities
2) type of infection
3) host factors (age, drug allergies, renal fxn, etc)
4) factors associated w/ antimicrobial agent (dosage, routes of administration, etc)
5) public health considerations (likelihood of widespread resistance)

Front 15

what are the three possible sources of antimicrobial agents?

Back 15

biological origin, chemically synthesized and molecular manipulation

Front 16

what common antimicrobial has a biological origin?

Back 16

penicillin (from mold)

Front 17

T/F
benzyl penicillin is a narrow-spectrum agent.

Back 17

TRUE

(works on gram (+) better)

Front 18

what affect does benzyl penicillin have on gram positive cocci, gram negative cocci and enteric gram negative bacilli?

Back 18

Gram positive cocci- highly active
Gram negative cocci- highly active
Gram-negative bacilli- little activity

Front 19

If you needed an antibacterial antimicrobic that would inhibit cell wall synthesis, what are your two choices?

Back 19

B-lactams (penicillin) and glycopeptides.

Front 20

If you needed an antibacterial antimicrobic that would inhibit cell Protein synthesis, what are your four choices? what is the acronym?

Back 20

MCAT: Macrolides, Chloramphenicol, tetracyclines, and aminoglycosides

Front 21

If you needed an antibacterial antimicrobic that would inhibit nucleic acid synthesis, what are your four choices? What is the mnemonic?

Back 21

Queen Folate Married Rifampin:
Quinolones
folate inhibitors
metronidazole
rifampin

Front 22

If you needed an antibacterial antimicrobic that would act on the outer and cytoplasmic membrane, what are your two choices?

Back 22

polymyxin B and Colistin

Front 23

what are four subcategories of B-lactam?

Back 23

penicillins, cephalosporins, carbapenems, monobactams

Front 24

what are the two subcategories of glycopeptides?

Back 24

Vancomycin and teicoplanin

Front 25

what enzyme catalyzes the cross-linking of the amino acid side chains?

(cross-linking necessary for cell wall synthesis)*

Back 25

transpeptidase

Front 26

what category of antimicrobials binds to transpeptidase preventing it from carrying out its function?

Back 26

B-lactams

Front 27

which antimicrobial binds directly to the amino acid of the cell wall preventing the binding of transpeptidase?

Back 27

vancomycin

Front 28

what infection is vancomycin used to treat?

Back 28

MRSA: methicillin Resistance Staphylococcous aureus

Front 29

T/F
the ring of the B-lactam is not essential for antibacterial activity.

Back 29

FALSE

It is absolutely essential!

Front 30

T/F
B-lactams can only affect bacteria with cell walls.

Back 30

True.

Front 31

what is the classic example of a bacteria that is not sensitive to B-lactams?

Back 31

mycoplasm

Front 32

from what bacterial genus is penicillium derived from?

Back 32

streptomyces


(penicilin originally derived from penicilum genus of mold)

Front 33

which type of penicillin is injectible? which can be taken orally?

Back 33

injectible: Penicillin G
Orally: Penicillin V

Front 34

what is penicillin G active against?

Back 34

gram positive organisms, gram negative cocci, and some spirochete

(narrow range)

Front 35

what can broad spectrum penicillins do?

Back 35

penetrate the outer membrane of some Gram-negative bacteria

*Ampicillin

Front 36

what are the four types of penicillins?

Back 36

penicillin G, Penicillin V, broad spectrum penicillins and penicillinase-resistance pencillins

Front 37

how do cells have penicillin resistance?

Back 37

by releasing penicillinase enzyme (destroys penicllin)

Front 38

How do penicillinase-resistant penicillins work?

Back 38

inhibit pencillinase!

*methicillin (treats penicillin resistant staphylococcus aureus)

Front 39

how are cephlosporins classifed?

Back 39

by generation


(which ones were made first & later, each generation side chains are modified to expand spectrum)

Front 40

what does a fourth generation cephalosporin have in relation to a first generation?

Back 40

a wider spectrum

Front 41

what is the activity of the first generation cephalosporins (cephazolin, cephalexin?

Back 41

gram positive organisms that resembles that of penicillinase-resistance penicillin, some enterobacteriacea

Front 42

what is the activity of the second generation cephalosporins (cefoxitin, cefaclor)?

Back 42

-expanded activity against B-lactams producing Gram-negative organisms.
-Expanded activity against enterobacteriacea species - activity against anaerobes (including normal gut flora- bacteroides fragilis)

Front 43

what are the three third generation cephalosporins?

Back 43

ceftriaxone, cefotaxime and cetazidime

Front 44

what is ceftazidime used against? what is the clinically correlation?

Back 44

pseudomas aeruginosa; chosen in a febrile bone marrow transplant patient.

Front 45

what can ceftriaxone or cefotaxime be used against?

Back 45

childhood meningitis

Front 46

what are the three major causes of childhood meningitis?

Back 46

Neisseria meningitidis, streptococcus pneumoniae, and hemophilus influenzae

Front 47

what is the most common cause of meningitis in neonatals?

Back 47

steptocococcus pneumoniae

Front 48

what is the most common cause of meningitis period?

Back 48

neisseria meningitidis

Front 49

what is the activity of a fourth generation cephalosporin (cephepime)?

Back 49

wide spectrum antimicrobial effects:
-enhanced ability to penetrate gram-negative bacteria;
-resistant to many Gram-negative B-lactamases.
-active against wide spectrum of enterobacteriaceae.

*overall best/most effective & expensive drug

Front 50

what are the two types of carbapenems? which one requires a coadministration of cilastatin and why?

Back 50

imipenem & meropenem;

imipenem requires cilastatin to prevent imipenem rapid hydrolysis by renal tubular dehydropeptidase-1, cilastatin inhibits this enzyme.

Front 51

which B-lactam has the broadest spectrum? why?

Back 51

carbapenems:
easily penetrate gram-negative & gram-positive
& highest level of resistance to B-lactamases.

Front 52

Aztronam was the first monobactum liscensed in the US. What is the spectrum of aztreonam limited to?

Back 52

aerobic and facultatively anaerobic gram-negative bacteria

Front 53

why are anaerobic superinfections and major distortions of the bowel flora less common with aztreonam?

Back 53

because aztreonam does not produce a general suppression of gut anaerobes

Front 54

what is the main use of glycopeptides?

Back 54

against multiresistant Gram-positive infections (especially staphylococci that are resistant to the penicillinase resistant penicillins and cephalosporins)
*inhibit linear peptidoglycan assembly
(vancomycin & teicoplanin)

Front 55

where do the aminoglycosidases bind to in order to prevent protein synthesis of microbials?

Back 55

bind to multiple sites on both the 30S and 50S ribosomes--> preventing tRNA from forming initiation complexes.

(steptomycin, gentomyocin and aminocasin)

Front 56

where do tetracyclines bind in relation to protein synthesis?

Back 56

30S ribosomes

Front 57

what does chloramphenicol block?

Back 57

formation of the peptide bond between the amino acids

Front 58

what does erythomycin and macrolides block?

Back 58

translocation of tRNA from the acceptor to the donor side on the ribosome.

Front 59

what do sulfonamides block?

Back 59

folate precursors of DNA synthesis

Front 60

what affect does metronidazole have on DNA?

Back 60

inflicts breaks in the DNA itself

Front 61

what does rifampin inhibit?

Back 61

synthesis of RNA from DNA by inhibiting RNA polymerase

(R goes w R)

Front 62

what do quinolones inhibit?

Back 62

DNA topoisomerase and thus prevent the supercoiling required for the DNA to "fit" inside the bacterial cell.

Front 63

what affect to polymyxin B and colistin have on cell membranes?

Back 63

they bind to cell membranes of susceptible Gram-negative bacteria and alter their permeability resulting in loss of essential cytoplasmic components (organelles exit cell)--> bacterial death.

Front 64

polymyxin B and colistin use are now limited to what kind of applications?

Back 64

topical

Front 65

what are the consequences of indiscriminate use of antibacterial drugs?

Back 65

- can lead to a plethora of side effects and drug interactions
- hypersensitivity reactions
- microbial superinfections
- drive up the cost of health care
- antagonisms between certain agents
- foster the emergence of bacterial resistance, rendering previously valuable drugs useless*

Front 66

what are the unique viral events that occur in viral replication?

Back 66

attachment, penetration, uncoating, RNA-directed DNA synthesis (reverse transcription) and assembly and release of the intact virion.

*any of these steps can be targeted by antiviral)

Front 67

how can viral attachment be inhibited?

Back 67

by having an antibody bind to the extracellular virus and prevent the attachment of the virus to a cell receptor on the host cell
(doesn't work well in practice)

Front 68

how can we inhibit penetration of the virus?

Back 68

by using a neuraminidase inhibitor which will inhibit the fusion of an viral enveloped protein with the host cell membrane.

Front 69

what are the 2 neuraminidase inhibitors that selectively inhibit the neuraminidase of influenza A and B viruses? which one is oral and which one is a spray?

Back 69

oseltamivir (oral) and zanamivir (spray)

Front 70

what does neuraminidase do?

Back 70

aids in the release of newly formed viral particles from infected cells

Front 71

what are the agents in the antiviral inhibiting viral uncoating group? which one should be used cautiously with renal impaired patients?

Back 71

Rimantadine and amantadine (cautious in renal impaired patients)

(work on influenza strain A only)

Front 72

what are idoxiuridine and trifluorothymidine used to treat? what type of treatment?

Back 72

herpetic keratitis; topical

*inhibit nucleic acid synthesis)

Front 73

what is acyclovir used to treat? how?

Back 73

best for-->herpes simplex viruses (1 and 2), varicella zoster virus (less than HSV)(shinlges)
(can do cytomegalovirus also(least).

Inhibits the thymidine kinase (purine analoge)

Front 74

what is gancyclovir used to treat? what is it in relation to acyclovir?

Back 74

best for-->cytomegalovirus
(can do other herpes viruses)

an analogue of acyclovir, inhibits thymidine kinase

Front 75

what is a classic example of an inhibitor of viral RNA synthesis?

What kinds of infections does it treat?

Back 75

ribavirin


standard tx for HCV, also beneficial in RSV for infants

Front 76

what is the job of foscarnet? how?

Back 76

to inhibit viral DNA polymerase by blocking the pyrophosphate-binding site of viral DNA polymerase.

Front 77

what are interferons?

What do they do?

Back 77

host cell encoded proteins synthesized in response to double stranded RNA.

inhibit viral protein synthesis & protects uninfected cells

Front 78

what are interferons effective against?

Back 78

hepatitis C and B and papilloma virus (locally) infections

Front 79

what are higher rates of replication associated with?

Back 79

higher rates of spontaneous mutation

Front 80

what is the selective pressure of the drug?

Back 80

probability of mutation is increased to the point that virus replication is substantially reduced

Front 81

T/F
single stranded RNA viruses have a slower rate of mutation than double.

Back 81

false.....

single has a higher rate.

Front 82

T/F
some genes within a virus are more susceptible than others.

Back 82

true

(in herpes thymidine kinase is most susceptible)

Front 83

what are arsenicals (heavy metal) used against?

Back 83

trypansomiasis

Front 84

How do heavy metals work?

Why are they not commonly used?

Back 84

binds and inactivates the SH group of parasitic enzyme

toxic to host & parasite

Front 85

what are the four antimalarial quinolones? which one is the safest?

Back 85

quinine,
4-aminoquionolines (safest),
8-aminoquionolines, and
4-quinolinemthanols

Front 86

what do antimalarial quinolones do?

Back 86

accumulate & inhibit nucleic acid synthesis in parasitized host cell (RBC), inhibit heme peroxydase leading to accumulation of heme metabolites lethal to parasites.

Front 87

which antimalarial quinolones is used against chloroquine resistant parasites?

Back 87

4- quinolinemethanols

Front 88

what does quinone inhibit?

Back 88

parasites electron transport chain resulting in specific blockade of pyrimidine biosynthesis.

(hydroxynapthoquinone- atovaquone)

Front 89

what are the two example of folate antagonists?

Back 89

sulfonamide and trimethoprim

(inhibit folic acid synthesis, affect DNA synthesis)

Front 90

what does benzimidazole inhibit? what does protozoan does this taregt?

Back 90

fumerate reductase and polymerization of tubulin (cytoskeleton protein); helminths

Front 91

what member of the benzimidazole group is used against intestinal nematodes and trichinosis?

Back 91

thiabendozole

Front 92

which member of the benzimidazole group is effective against cestodes (tapeworms, hymenolepis, and echinococcus)?

Back 92

mebendazole