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Microbiology & Immunity > 13- Antibiotics > Flashcards

13- Antibiotics Flashcards

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Biology 101 flashcards
1
Q

what is an antimicrobial?

A

substances that kill or inhibit the growth of microorganisms

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2
Q

what is an antibiotic?

A

substances produced by living organisms - natural products of fungi and bacteria - with activity against bacteria

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3
Q

describe the production of antibiotics

A

most antibiotics are completely or partly synthetic

some are produced by fermentation and then chemically modified to enhance their pharmacological and antimicrobial properties

some - e.g. sulphonamide - are completely synthetic

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4
Q

what are the three main principles of therapeutic antibiotic agents?

A

selective toxicity
therapeutic margin
effect on normal microbiota

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5
Q

what is selective toxicity?

A

ability of a drug to selectively inhibit/ kill pathogens or abnormal cells without causing significant harm to the host’s normal cells

exploits differences between microbes and host cells for targeted killing

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6
Q

how is selective toxicity with antibiotic agents ensured?

A

specific metabolic pathways or structures absent/ lacking in the host but present in microbes are targeted

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7
Q

what’s the importance of selective toxicity?

A

to minimise side effects, toxicity or harm to normal commensal/ beneficial microbes (e.g. gut flora) present in the host

prevent developing secondary conditions by killing off beneficial bacteria - e.g. dysbiosis/ imbalance in gut microbiome

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8
Q

why is selective toxicity harder to ensure with viruses? how do antivirals work around this?

A

harder with viruses they’re intracellular pathogens - they hijack host cell machinery

antivirals aren’t as selective but target specific stages of the viral replication cycle - minimise harm to host

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9
Q

what is a therapeutic margin with antibiotics?

A

difference between the minimum therapeutic dose and minimum toxic dose

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10
Q

what’s the importance of a wider therapeutic margin?

A

drugs with a wider therapeutic margin = safer

have a greater margin for safety, can be administered at higher doses without risking toxicity

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11
Q

what’s the danger of a narrower therapeutic margin?

A

smaller difference between therapeutic and toxic doses = less safe, higher risk of adverse effects and require careful monitoring upon administration

reserved for when the benefits outweigh risk

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12
Q

how do the antibiotic effects on normal microbiota affect antibiotic development?

A

some antimicrobials kill off normal/commensal bacteria - leads to microbial imbalance, can cause dysbiosis which is an imbalance in the gut microbiome

dysbiosis provides an opportunity for the overgrowth and colonisation of more harmful micro-organisms such as C. difficile - affects health, digestive and immune function

C. difficile infection causes inflammation, ulcerations, severe diarrhoea, antibiotic- associated/ pseudomembranous colitis

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13
Q

examples of drugs more associated with antibiotic-associated colitis

A

fluoroquinolones
broad-spectrum lactams
clindamycin

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14
Q

what’s the importance of immune system function in relation to antibiotics?

A

antibiotics and immune system work together for bacterial clearance - healthy immune system is needed

affected immune function influences the type of antibiotic administered

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15
Q

how are antibiotics classified? (3)

A

type of activity
structure
target site for activity

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16
Q

what are the two main types of antibiotic activity?

A

bacteriostatic
bactericidal

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17
Q

describe bactericidal antibiotics - function? when are they used?

A

directly kill bacteria = leads to decline in the bacterial popl overtime

preferred when host’s immune defences are reduced or during severe infections -rapid bacterial eradication is necessary

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18
Q

describe bacteriostatic antibiotics - function? when are they used?

A

halt the growth and replication of bacteria without directly killing them

preferred when host’s immune system is healthy and can clear the infection itself, used in a wide range of non life-threatening conditions

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19
Q

what affects the effectiveness of bacteriostatic drugs?

A

the specific drug

bacterial species involved

conc of the antibiotic - higher concentration may convert its activity from bacteriostatic to bactericidal

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20
Q

what are the two types of antibiotic spectrum activity?

A

broad spectrum
narrow spectrum

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21
Q

describe broad spectrum antibiotics - function? use?

A

effective against a wide range of bacterial types

used when the infecting organism is unknown or there’s a need to cover multiple types of bacteria

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22
Q

describe broad spectrum antibiotics - function? use?

A

effective against a limited range of bacterial types

reserved for when the infecting organism is known to be susceptible to the antibiotic - helps reduce antibiotic resistance, minimise effects on normal microbiota

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23
Q

what type of antibiotic are penicillins?

A

beta lactams = contain a beta-lactam ring in their chemical structure

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24
Q

list the types of penicillins & examples

A

basic penicillins - e.g. Pen G, Pen V

anti-staphylococcal penicillins - e.g. flucloxacillin

broader spectrum penicillins - e.g. ampicillin

anti-pseudomonal penicillins - e.g. piperacillin

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25
Q

what are basic penicillins? - properties?

A

penicillins effective against gram-positive bacteria - e.g. streptococci, pneumococci, meningococci, treponemes

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26
Q

examples of basic penicillins?

A

Penicillin G/ benzylpenicillin
Penicillin V

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27
Q

properties of penicillin G/ benzylpenicillin?

A

not acid stable, given via i.v. or i/m routes

effective against gram positive and negative bacteria

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28
Q

properties of penicillin V?

A

more acid stable than Penicillin G, given orally

less active against gram negative bacteria, still effective against gram positive

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29
Q

what are anti-staphylococcus penicillins - properties?

A

narrow spectrum, target gram-positive bacteria

beta-lactamase resistant = effective against penicillinase-producing bacteria

30
Q

what is beta-lactamase?

A

structural enzyme present in bacteria that confers resistance to beta-lactam antibiotics like penicillins and cephalosporins - can break down the beta-lactam ring, refer beta-lactam ineffective

31
Q

what is penicillinase?

A

specific type of beta-lactamase - specifically targets and inactivates penicillin antibiotics

resistance mechanism in certain strains of bacteria

32
Q

describe basic penicillins

A

active against gram pos and neg bacteria - e.g. streptococci, pneumococci…

e.g. - Penicillin G = effective against gram pos & neg bacteria, not acid stable, given by intravenous or muscular injection

e.g. - Penicillin V = effective against gram pos, less against gram neg, given orally, acid stable

33
Q

describe anti-staphylococcal penicllins

A

narrower spectrum of activity, target gram pos bacteria

they’re beta-lactamase and penicillinase resistant - effective against these bacteria

e.g. flucloxacillin

34
Q

describe broader-spectrum penicillins

A

similar spectrum of activity to basic penicillins, includes some gram negative bacteria and enterococci

e.g. ampicillin

35
Q

describe beta-lactams - molecular structure? how does this affect their antibiotic activity?

A

structure - beta lactam ring, structural mimic for the natural substrate of penicillin-binding protein enzymes (PBPs) = substrate being D-Ala-D-Ala dipeptide terminus

activity: PBPs and D-Ala-D-Ala are involved in bacterial cell wall synthesis
- beta lactam enters bacterial cell, binds to PBP active site
- interferes with the transpeptidation reaction to form cross-links between peptidoglycan strands via their DADA dipeptide terminus
- prevents proper assembly of bacterial cell wall = leads to cell lysis and death

36
Q

what is beta-lactamase resistance? how is this resistance being combatted?

A

some bacteria produce beta lactamase which hydrolyse the beta-lactam ring, inactivates antibiotic

newer beta-lactam antibiotics are being developed with modifications in chemical structure - e.g. adding side chains - to enhance stability against beta-lactamase

37
Q

list the target sites for antibiotic activity

A

50s subunit protein synthesis inhibitors
30s subunit protein synthesis inhibitors
cell wall synthesis
DNA and RNA processing
folic acid metabolism
cell membrane inhibitors

38
Q

50s inhibitors - reason for targeting 50s? mechanism of action?

A

reason - largest ribosomal human subunit is 60s, in bacteria its 50s = exploiting differences to inhibit protein synthesis

mechanism - inhibit 50s, prevent initiation/ elongation phases of protein synthesis

39
Q

examples of 50s inhibitors?

A

macrolides / erythromycin
chloramphenicol

40
Q

30s inhibitors - reason for targeting 50s? mechanism of action?

A

reason - smallest ribosomal human subunit is 40s, in bacteria its 30s = exploiting differences to inhibit protein synthesis

mechanisms:
1. block synthesis and access of aminoacyl-tRNAs to the ribosome = inhibits protein synthesis
2. inhibit 30s activity

41
Q

examples of 30s inhibitors?

A

blocking synthesis and access to tRNAs - Mupirocin

inhibiting 30s activity - aminoglycosides

gentamicin

tetracycline

42
Q

targeting cell wall synthesis - reason for targeting? mechanism of action?

A

reason - bacterial cells have cell walls, eukaryotic cells don’t

mechanism - inhibiting enzymes involved in bacterial cell wall synthesis like PBPs to prevent cross-linking of peptidoglycans = induces cell lysis

43
Q

examples of bacterial cell wall synthesis inhibitors?

A

Vancomycin
Penicillins
Cephalosporins

44
Q

targeting bacterial DNA and RNA processing - reason for targeting? mechanism of action?

A

reason - bacterial DNA gyrase and DNA-directed RNA polymerase is structured different to human variations

mechanism:
- interfere with DNA gyrase activity from unwinding DNA before replication
- interfere with DNA-directed RNA polymerase to prevent RNA template synthesis from DNA

45
Q

examples of antibiotics that target DNA and RNA processing?

A

Quinolones - target DNA gyrase

Rifampin, Fidaxomicin - target DNA-dependent RNA polymerase

46
Q

targeting bacterial folic acid metabolism - reason for targeting? mechanism of action?

A

reason - bacteria synthesise their own folate, humans get it from diet

mechanism:
- target different bacterial enzymes involved in folic acid synthesis, metabolism and conversion

47
Q

examples of antibiotics that target folic acid metabolism?

A

Trimethoprim
Sulphonamides

48
Q

bacterial cell membrane inhibitors - reason for targeting? mechanism of action?

A

reason - exploiting differences in human vs bact. cell membranes

mechanism - generating free radicals within bacterial cells, causing oxidative stress and cell damage, especially in anaerobes

49
Q

examples of bacterial cell membrane inhibitors

A

Metronidazole
Nitrofurantoin

50
Q

describe the process of bacterial cell wall synthesis/ transpeptidation

A

during transpeptidation, new peptidoglycan units are added to the cell wall

terminal D-alanyl-D-alanine peptide side chain of one peptidoglycan strand is linked to the side chain of another

penicillin-binding proteins/ PBPs/ transpeptidases catalyse the cross-linking of peptidoglycan strands via their terminal D-alanyl-D-alanine peptide side chains

51
Q

describe how beta-lactams target bacterial cell wall synthesis for gram POSITIVE bacteria

A

penicillins structurally mimic D-alanyl-D-alanine substrate for PBPs - bind to PBP active site, prevents cross-linking of terminal DADA side chains = prevents cell wall synthesis

no cell membrane = no inhibition for penicillin entry

52
Q

describe how beta-lactams target bacterial cell wall synthesis for gram NEGATIVE bacteria

A

gram neg bacteria has an extra impenetrable outer membrane which regulates passage of molecules through porins

porins allow beta lactam antibiotic (e.g. penicillin, cephalosporins) based on size and charge - enter periplasmic space

beta lactam binds to PBP active site - prevents binding of peptidoglycan peptide terminus D-alanyl-D-alanine

prevent cross-linking of peptidoglycan strands = prevents cell wall synthesis

triggers autolytic enzymes - autolysins - which break down cell wall and trigger cell lysis

53
Q

compare gram positive and negative bacterial cell wall structure

A

gram positive - thick peptidoglycan cell wall, lacks outer membrane

gram negative - thin peptidoglycan cell wall, outer membrane serves as an impenetrable layer antibiotics would need to get through first

54
Q

name three drugs that inhibit bacteiral folate synthesis

A

trimethoprim
dapsone
sulphonamide

55
Q

how do each of the three drugs (sulphonamide, dapsone and trimethoprim) inhibit folic acid synthesis

A

sulphonamide and dapsone
- inhibit first step of folate synthesis = act as structural mimics for PABA (folate precursor) and bind to dihydropteroate synthase active site
- prevent first step for forming dihydropteroate acid = prevent tetrahydrofolic acid synthesis = prevent DNA synthesis and production of nucleic acid
- prevent bacterial cell growth and synthesis = leads to cell death

trimethoprim
- inhibit dihydrofolate reductase - catalyses dihydrofolic acid to tetrahydrofolic acid conversion
- prevent folate synthesis = prevents DNA synthesis = induces bacterial cell death

56
Q

describe selective toxicity in antibiotics inhibiting bacterial folate synthesis

A

in humans, dihydrofolic acid is obtained form diet

in bacterial, it’s synthesised from precursors

57
Q

describe sulphonamide + trimethoprim combination therapy - advantage?

A

target sequential steps in folate synthesis pathway - sulphonamide targets first step with dihydropteroate synthase, trimethoprim targets dihydrofolate reductase

advantage: act in synergy with bactericidal action

58
Q

how do aminoglycosides act as 30s inhibitors?

A

prevents fMet RNA binding = prevents initiation complex forming = inhibits translation

59
Q

how does gentamicin act as a 30s inhibitor?

A

prevents fMet RNA translocation to ribosomal P site = causes misreading of mRNA sequence = produces defective proteins, inhibits protein synthesis

60
Q

how does tetracycline act as a 30s inhibitor?

A

competes with aminoacyl tRNA at the ribosomal A site = inhibits elongation = leads to production of non-functional proteins

61
Q

how does erythromycin/ macrolide act as a 50s inhibitor?

A

blocks translocation of peptidyl tRNA

62
Q

how does cloramphenicol act as a 50s inhibitor?

A

blocks formation of peptide bonds by peptidyl transferase

63
Q

why do we use antibiotics?

A

treating bacterial infections

prophylactic - minimises chance of developing infection/ carrier status with transmissible infections

peri-operative cover begore surgery for more vulnerable patients

64
Q

different methods for administering antibiotics, and for what? (route - why?)

A

topical - for burns, antiseptic creams, superficial skin infections

orally for community infections

intramuscular or intravenous for serious infections requiring hospitalisation

65
Q

why are some antibiotics combined together for treatment?

A

lower toxicity, allows for lower doses and less adverse effects when combined

synergistic effects of two antibiotics - e.g. sulphonamide and trimethoprim - improves efficacy

polymicrobial infections - involves many pathogens

combating antibiotic resistance

66
Q

what is MIC?

A

minimum inhibitory concentration

lowest conc of an antimicrobial agent that inhibits the visible growth of a microorganism

67
Q

what does MIC depend on?

A

age, weight
renal and liver function
severity of infection
properties of antibiotics - pharmacokinetics/ ADME of drug, pharmacodynamics

68
Q

what are pharmacodynamics? how do they affect the MIC and dosing of a drug?

A

pharmacodynamics - how the drug exerts its effects on bacteria/ microbes

pharmacodynamics are time and concentration dependent
- time dependence = some antibiotics are more effective being constantly kept above MIC = ensures effective killing of microbe
- require frequent dosing to not fall below MIC

  • concentration-dependence = some antibiotics are more effective with peak concs above MIC, don’t need frequent dosing

timing. frequency and concentration of drug doses are affected - important to keep drug conc above MIC in patient for effective killing of bacteria

69
Q

list three antibiotic susceptibility tests

A

Kirby-Bauer disk diffusion
MIC testing with broth/ agar dilution
E-test

70
Q

Kirby-Bauer disk diffusion - describe

A

standard bacterial culture inoculated on agar plate, antibiotic disks with specific antibiotics are placed on the surface

following incubation - zones of inhibition will form around each disk

greater one diameter = greater susceptibility o f the bacteria to the antibiotic

71
Q

what do the broth/ agar dilution methods determine?

A

MIC of an antibiotic - the lowest concentration of a drug that visibly inhibits growth after incubation

72
Q

what does the E-test determine?

A

quantitative test for determining MIC using pre-made gradient-containing strips with a predefined conc range of antibiotics

based on the elliptical zone of inhibition

Microbiology & Immunity (37 decks)

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