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2a - microbiology and IDs > Antibiotics; types, sites of action, organisms they are effective against, antibiotic resistance mechanisms > Flashcards

Antibiotics; types, sites of action, organisms they are effective against, antibiotic resistance mechanisms Flashcards

1
Q

what are antibiotics?

A

agents produced by microorganisms that kill or inhibit the growth of other microorganisms in high-dilution.

They are molecules that work by binding a target site to a bacteria.

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2
Q

what are antimicrobials?

A

semi-synthetic derivatives of antibiotics

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3
Q

which type of antimicrobial ( antifungals, antibacterials, antihelminthics, antiprotozoals, antiviral agents ) is what’s thought of as antibiotics?

A

antibacterials

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4
Q

what are the 3 main target sites of antibiotics?

A

within the bacterium:

  1. cell wall (peptidoglycan) synthesis
    - PBPs in cell wall
    - cell membrane
  2. nucleic acid synthesis
    - DNA
    - topoisomerase Iv or DNA gyrase
  3. protein synthesis
    - ribosomes
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5
Q

how do antibiotics inhibit cell wall synthesis?

A

These disrupt peptidoglycan production (for cell envelope)

They do this by binding covalently and irreversibly to the penicillin binding proteins (PBSs)

Cell wall is disrupted, lysis occurs

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6
Q

what are the main group of antibiotics that target cell wall synthesis?

these are the most commonly prescribed antibiotics

A

beta lactams

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7
Q

what are the subcategories of antibiotics within beta lactams?

A

penicillins

Carbapenems

Monobactams

Cephalosporins

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8
Q

list 3 penicillins

A

Penicillin V
Flucloxacillin
Amoxicillin
Penicillin G
Piperacillin

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9
Q

give an example of a Carbapenem (beta lactam, targets cell wall)

A

Meropenem

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10
Q

give examples of Cephalosporins (beta lactams, target cell wall)

A

Cefuroxime
Ceftriaxone
Cefotaxime

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11
Q

why/when are Cephalosporins used over penicillins?

A

Still beta lactams

But good for people with non-severe penicillin allergy

Work against some resistant bacteria too

Can get into different parts of the body eg. CNS, to treat meningitis

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12
Q

name the category of antibiotics that target cell wall synthesis but are not beta lactams ?

why/when are these used?

A

GLYCOPEPTIDES

Use for gram positives that are resistant to beta lactams eg. MRSA, enterococci and some coagulation negative staph

and for people with penicillin allergies

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13
Q

name 2 examples of glycopeptides

A

vancomycin bacitracin

teicoplanin (IV)

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14
Q

are antibiotics that target cell wall synthesis better suited to treating gram positive or gram negative bacteria?

A

Gram positive bacteria → thick cell wall therefore use beta lactams (they are the main cell wall weapons)

Gram negative bacteria → additional wall reduces antibiotic penetration/diffusion therefore don’t tend to use cell wall weapons

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15
Q

which antibiotic would you prescribe to treat cellulitis? (skin and soft tissue infection)

A

commonly caused by these bacteria : S.aureus and group A,C,G strep

these are gram positive

flucloxcalccin

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16
Q

which antibiotic would you prescribe to treat strep throat?

Group A,C,G strep

A

oral penecillin V

or

IV benzylpeneckllin

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17
Q

which antibiotic would you prescribe to treat pneumonia ?

A

caused by S.pneomniae

oral amoxilcin or IV benzylepenecillin

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18
Q

which antibiotic would you prescribe to treat MRSA caused cellulitis?

A

vancomycin bacitracin and teicoplanin (IV)

these are glycopeptides

can’t use beta lactams because MRSA in resistant

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19
Q

how do antibiotics that taste protein synthesis work ?

A

target ribosomes

prevent synthesis of subunits eg. 50S and 30S

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20
Q

list the types of antibiotic that target protein synthesis

A

macrolides

lincosamides

tetracyclines

aminoglycosides

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21
Q

protein synthesis inhibitors: macrolides

  • give an example
  • when/why used?
A

Eg. Clarithromycin – oral (& IV)

Use on gram positives

Eg. S. aureus, β haemolytic strep

Use if penicillin allergy

Use if severe pneumonia

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22
Q

why use Clarithromycin to treat sever pneumonia

why. not a cell wall weapon?

A

Atypical pneumonia eg, legionella

multiply inside cells,

therefore no good having a cell wall active antibiotics as can’t get to it if it’s hiding inside a cell

So use protein synthesis inhibitors instead

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23
Q

protein synthesis inhibitors: lincosamides

  • give an example
  • when/why used?
A

Eg. Clindamycin = oral (& IV)

Use on gram positives

Eg. S. aureus, β haemolytic strep , anaerobes

Use for cellulitis if penicillin allergy
Ues for necrotising fasciitis
Turns off toxins made by gram positive bacteria

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24
Q

protein synthesis inhibitors: tetracyclines

  • give an example
  • when/why used?
A

Eg. Doxycycline = oral

Broad but mainly use for gram positives

Eg ​​S. aureus and streps

Use for cellulitis if penicillin allergy
Use for pneumonia

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25
Q

what group of antibiotics that target protein synthesis are used to treat gram negative bacteria? and why?

A

aminoglycosides

Gram negative bacteria → additional wall reduces antibiotic penetration/diffusion therefore don’t tend to use cell wall weapons, favour protein synthesis method

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26
Q

name an amminoglycoside that is used to treat gram negative bacteria

what diseases can It treat?

A

gentamicin - IV only

Use for UTIs

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27
Q

can amminoglycosides be used to treat gram positive?

A

mainly used for gram negatives

but can be used synergistically for streps (which are gram positive)

Use for infective endocarditis (synergistically)

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28
Q

list specific protein synthesis inhibitors

A

Examples that synthesis 505 subunits

Clarithromycin
Clindamycin
Linezolid
Chloramphenicol
Streptogramins

Examples that synthesis 305 subunits

Doxycycline
gentamicin

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29
Q

give examples of nucleic acid synthesis inhibitor antibiotics

A

DNA gyrase eg. quinolines
RNA polymerase eg. rifampin

folate synthesis inhibitors

30
Q

name a quinoline and what its used for?

A

Eg. ciprofloxacin - oral and IV

Better for gram negative then positive

Use if penicillin allergy

Use on UTIs

Use on intra-abdominal infections

31
Q

name 3 folate syyntheisis inhibitors

how do they work?

what are they used for?

A

these are anti-metabolites that stop folic acid synthesis

Synthesis sulfonamides
Synthesis trimethoprim
Co-trimoxazole

Mainly used for gram negative
Use for UTIs

32
Q

name a membrane inhibitor antibiotic

A

nitrofurantoin

Used for gram negative and gram positives
Use for lower UTIs when resistant to trimethorpims
Fist in to cell wall category

33
Q

can beta lactams be used to treat gram negative?

A

sometimes

if they have specific side chains that make their range broader

34
Q

give 3 examples of beta lactams that can treat gram negative

(1 penicillin, 1 Carbapenem, 1 Cephalosporin)

these are really important and useful antibiotics with low resistance

A

Piperacillin-tazobactam

Meropenem

Cefuroxime

35
Q

what are the 2 categories of antibacterials antibiotics?

A

Bacteriostatic

bactericidal

36
Q

what are the main differences between Bacteriostatic and bactericidal antibiotics ?

A

Bactericidal antibiotics
- Kill bacteria

Bacteriostatic antibiotics
- Inhibit bacterial growth

37
Q

what does MIC mean?

A

Minimum inhibitory concentration,

defines in vitro levels of susceptibility or resistance of specific bacterial strains to applied antibiotics.

38
Q

is an antibiotic with a really low MIC always the most effective?

A

a lower MIC value indicates that less of the drug is required in order to inhibit growth of the organism, drugs with lower MIC scores are more effective antimicrobial agents

However this isnt always true because there are other factors to consider

39
Q

what are the 2 major determinants of antibacterial effects?

A

Concentration at binding sites
- Drug must occupy an adequate number of binding sites, to create a sufficient concentration to have sufficient effect

Time at binding site
- Antibiotic must remain at binding site for sufficient period of time in order for the metabolic process of the bacteria to be sufficiently inhibited

40
Q

how do pharmokinetics affect antibiotics?

A

A

absorption from site of administration into bloodstream

41
Q

how do pharmokinetics affect antibiotics?

D

A

Distribution to site of infection -

Consider the pH of the site? Is the antibiotic lipid soluble? Can it penetrate the site (get through memebranes?) How fat is a patient?

Antibiotic must reach the site of bacterial infection

42
Q

how do pharmokinetics affect antibiotics?

M + E

A

rate of elimination from body via metabolism (liver) or excretion (kidney)

Half life of antibiotic helps us to decide dosage

43
Q

briefly, what are the 4 mechanisms of antibiotic resistance?

A

Change antibiotic target/ masking

Destroy antibiotic

Prevent antibiotic access

Remove antibiotic from bacteria

44
Q

explain the mechanism of resistance and give examples:

  1. Change antibiotic target/ masking
A

Bacteria mask or change the molecular configuration of antibiotic binding site

eg. MRSA resistant to flucloxacillin

Enterococci resistant to vancomycin

TB resistant to rifampicin

45
Q

explain the mechanism of resistance and give examples:

  1. Destroy antibiotic
A

The antibiotic is destroyed or inactivated

Examples:

Beta lactam ring of penicillins + cephalosporins hydrolysed by bacteria enzyme beta lactamase, so it is unable to bind to penicillin binding sites (PBP)

46
Q

explain the mechanism of resistance

  1. prevent antibiotic access
A

Modify the bacteria membrane porin channel (size, number and selectivity)

47
Q

explain the mechanism of resistance

  1. Remove antibiotic from bacteria
A

Proteins in bacterial membranes act as an export or efflux pumps
So the level of antibiotic is reduced by removing it

48
Q

what does MRSA stand for and which antibiotic is it resistant to?

how has it become resistant?

A

MRSA = Methicillin Resistant Staphylococcus Aureus

resistant version of staph A

MRSA resistant to flucloxacillin or methicillin →
antibiotics are no longer able to bind to PBP of staphylococci

acquired resistance

49
Q

explain how enterococci has become resistant to vancomycin

A

Enterococci resistant to vancomycin →
enterococci have changed their wall components which has reduced vancomycin binding

50
Q

explain how TB has become resistant to rifampicin

A

TB resistant to rifampicin →
multi drug resistant TB (MDR-TB) changes its RNA polymerase which reduces rifampicin activity

51
Q

what are the 2 types of antibiotics resistance

(development)

A

intrinsic

acquired

52
Q

describe intrinsic resistance

do all populations of a species have equal resistance?

A

when a bacterial species is naturally resistant to a certain antibiotic or family of antibiotics, without the need for mutation or gain of further genes

All subpopulations of a species will be equally resistant

53
Q

describe acquired resistance

do all populations of a species have equal resistance?

A

A bacterium which was previously susceptible obtains the ability to resist the activity of a particular antibiotic

Only certain strains or subpopulations of a species will be resistant

54
Q

give 2 examples of antibiotics that certain bacteria are resistant to?

A

aerobic bacteria is resistant to Metronidazole

gram negative bacteria is resistant to Vancomycin

55
Q

explain Metronidazole resistance

A

Metronidazole can treat anaerobic bacteria - by become its active, toxic form

but Metronidazole cannot treat aerobic bacteria.

Because it doesn’t get reduced by bacteria to form its active, toxic, bacteria killing form

56
Q

explain how gram negative bacteria is resistant to Vancomycin

A

Vancomycin cannot penetrate outer membrane of gram negative bacteria

57
Q

what are the 2 mechanisms of acquired resistance?

A

Spontaneous gene mutation

Horizontal gene transfer

58
Q

how does spontaneous gene mutation lead to acquired resistance to antibiotics?

A

There is spontaneously a new nucleotide base pair

This changes the amino acid sequence

This changes to enzyme of the cell structure

This can cause reduced affinity of activity of the antibiotic to this bacterium

59
Q

name the 3 ways Horizontal gene transfer leads to acquired resistance to antibiotics?

A
  1. conjugation
  2. transduction
  3. transformation
60
Q

how does Horizontal gene transfer via conjugation lead to acquired resistance to antibiotics?

give example

A

bacterial sex,

where plasmids are shared between bacteria.

Plasmids contain extrachromosomal DNA

eg. new delhi meallo-beta-lactamase

61
Q

how does Horizontal gene transfer via transduction lead to acquired resistance to antibiotics?
give example

A

TRANSDUCTION - when bacteriophages (viruses that infect bacteria) mediate transfer of DNA between bacteria (by packaging donor bacterium in a virus particle and transferring into a recipient bacterium during infection)

eg. mecA genes for MRSA

62
Q

how does Horizontal gene transfer via transformation lead to acquired resistance to antibiotics?
give example

A

TRANSFORMATION - when naked DNA is picked up

eg. when foregin DNA from S.mitis is picked up by S.pneumonia it becomes penicillin resiistnat

63
Q

Examples of gram-positive bacteria that have acquired resistance:

A

MRSA

VRE

64
Q

MRSA:

  • through which type of acquired resistance does MRSA form from?
  • name gene involved
  • what is MRSA resistant to?
A

Transduction occurs,

insertion of staphylococcal cassette chromosome mec (SCCmec)

This contains the resistant gene mecA

It encodes PBP2a

Confers resistance to all beta-lactam antibiotics eg. flucloxacillin

65
Q

VRE:

  • through which type of acquired resistance does VRE form from?
  • what is VRE resistant to?
A

VRE = Vancomycin Resistant Enterococci

Conjugation occurs,

acquired a gene encoding altered AA on peptide chain that prevents vancomycin binding

66
Q

what are ESBLs?

what type of resistance is this an example of?

A

ESBL = Extended Spectrum Beta Lactamase

enzymes that allow for resistance to most beta-lactam antibiotics

example of gram negative acquired resistance

67
Q

how do ESBLs form?

A

Mutation at active site causes extended range of antimicrobial resistance to form ESBL

68
Q

how do ESBLs cause antibiotic resistance?

A

ESBL hydrolyse oxyimino side chains of cephalosporins, cefotaxime, ceftriaxone, and ceftazidime and monobactams: aztreonam

69
Q

what antibiotics are capable of treating ESBLs?

A

Can pair together antibiotics to enhance effect eg.
Amoxicillin + Clavulanate = Co-Amoxiclav
Pipericillin + Tazobactam = ‘Tazocin’

70
Q

Carbapenems (eg. Meropenem) were the last resort to treat infections due to ESBL. It remained highly resistant to beta lactamase. however why this no longer the case?

A

recently Carbapenem resistant enterobacteriaceae (CRE) formed. It produces carbapenemases which breaks down the antibiotics, so this treatment no longer works.

71
Q

where is CRE common?

A

hospitals

2a - microbiology and IDs (13 decks)

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