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phase 2a > antibiotics symposium > Flashcards

antibiotics symposium Flashcards

1
Q

what is an antibiotic?

A

agents produced by micro-organisms that kill or inhibit the growth of other micro-organisms in high dilution

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2
Q

how do antibiotics work?

A

by binding a target site on a bacteria
this crucial binding site will vary with the antibiotic class

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3
Q

what are antimicrobials?

A

semi-synthetic derivatives of antibiotics
Defined as points of biochemical reaction crucial to the survival of the bacterium
HOWEVER IN PRACTISE
ANTIBIOTIC= ANTIBRACTERIAL

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4
Q

give examples of antimicrobials

A

antifungal, antibacterial, antihelminthic,
antiprotozoal and antiviral agents

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5
Q

what do beta lactam antibiotics do ?

A

disrupt peptidoglycan production by binding convalently and irreversibly to the penicillin binding proteins- causing cell Wass to disrupt-lysis occurs- resulting in hypo-osmotic or iso-osmotic environment

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6
Q

what are beta lactic antibodies active against?

A

only rapidly multiplying organisms

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7
Q

in order to bind to the penicillin binding proteins, what must the beta lactam antibodies do first?

A

diffuse through the bacterial wall

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8
Q

what do gram negative organisms have that decreases antibiotic penetration?

A

an additional lipopolysaccharide layer

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9
Q

what are the differences in the activity of beta lactam antibodies due to?

A

their relative affinity for different Penicillin Binding Proteins

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10
Q

why are beta lactams innefective in the treatment of intracellular pathogens?

A

because penicillins poorly penetrate mamlilan cells

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11
Q

describe the bacterial agenda

A
  1. attach and enter
  2. local spread
  3. multiply
  4. evade host defences
  5. shed from body
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12
Q

what are the direct consequences of bacteria?

A

destroy phagocytes or cells in which bacteria replicate

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13
Q

what are the indirect consequences of bacteria?

A

inflammation- e.g necrotic cells
immune-pathology- e.g antibody

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14
Q

what are the toxin related consequences of bacteria?

A

Exotoxin - Protein production
Endotoxin - Gram negative

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15
Q

what are bactericidal antibiotics?

A

agents that kill the bacteria
are antibiotics that inhibit cell wall synthesis

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16
Q

when are bactericidal antibiotics useful?

A

Useful if poor penetration (Endocarditis),
when it is difficult to treat infections or need to eradicate infection quickly (meningitis)

17
Q

define bacteriostatic antibodies

A

defined as a ratio of Minimum Bactericidal Concentration (MBC) to Minimum inhibitory Concentration (MIC) of > 4
Antibiotics that Inhibit protein synthesis, DNA replication or metabolism

18
Q

what do bacteriostatic antibodies do?

A

Reduce toxin production and Endotoxin surge less likely
they prevent growth of bacteria

19
Q

what are the two major detriments of anti bacterial effects?

A

concentration
time
( that the antibiotic remains on these binding sites

20
Q

what does the antibiotic drug do?

A

drug must not only attach to its binding target but also must occupy an adequate number of binding sites, which is related to its concentration within the microorganism.

21
Q

in order to work effectively what does the antibiotic have to do?

A

the antibiotic should remain at the binding site for a sufficient period of time in order for the metabolic processes of the bacteria to be sufficiently inhibited.

22
Q

describe time dependent killing

A

Key parameter is the time that serum concentrations remain above the MIC during the dosing interval
t>MIC

23
Q

describe concentration dependant killing

A

Key parameter is how high the concentration is above MIC
peak concentration/MIC ratio

24
Q

what is the antibiotic dependant on?

A

pharmokinetics- The movement of a drug from its administration site to the place of its pharmacologic activity and then its elimination from the body

25
Q

how do bacteria resist antibiotics?

A
  • change antibiotic target
  • destroy antibiotic
    -prevent antibiotic access
    -remove antibiotic from bacteria
26
Q

resist antibiotics-describe change antibiotic target

A

Bacteria change the molecular configuration of antibiotic binding site or masks it
e.g- Flucloxacillin (or methicillin) is no longer able to bind PBP of Staphylococci – MRSA*
Wall components change in enterococci and reduce vancomycin binding – VRE#
Rifampicin activity reduced by changes to RNA polymerase in MTB – MDR-TB$

27
Q

resist antibiotics-describe destroy antibiotic

A

The antibiotic is destroyed or inactivated e.g.
Beta lactam ring of Penicillins and cephalosproins hydrolysed by bacterial enzyme ‘Beta lactamase’ now unable to bind PBP

28
Q

resist antibiotics-describe-prevent antibiotic access

A

modify the bacterial membrane porin channel size, numbers and selectivity e.g.
-Pseudomonas aeruginosa against imipenem,
-Gram negative bacteria against aminoglycosides

29
Q

resist antibiotics-describe-remove antibiotic from bacteria

A

Proteins in bacterial membranes act as an export or efflux pumps - so level of antibiotic is reduced

30
Q

why do bacteria develop resistance?

A

intrinsic- naturally resistant
acquired- spontaneous gene mutation
-horizontal gene transfer- conjugation
-transduction
-transformation

31
Q

intrinsic resistance

A

All subpopulations of a species will be equally resistant
e.g. Aerobic bacteria are unable to reduce metronidazole to its active form
-Vancomycin cannot penetrate outer membrane of gram negative bacteria

32
Q

acquired 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

33
Q

name two Important resistances in Gram positive bacteria

A

MRSA
VRE

34
Q

describe MRSA

A

Methicillin resistant Staphylococcus aureus
Bacteriophage mediated acquisition of Staphylococcal cassette chromosome mec (SCCmec)
contains resistance gene mecA
encodes penicillin-binding protein 2a (PBP2a)
confers resistance to all β-lactam antibiotics in addition to methicillin (= flucloxacillin)

35
Q

describe VRE

A

vancomycin-resistant enterococci
Plasmid mediated acquisition of gene encoding altered amino acid on peptide chain preventing vancomycin binding
Promoted by cephalosporin use

36
Q

Name an important resistance in Gram-negative bacteria

A

ESBL

37
Q

describe ESBL

A

extended spectrum beta lactamase (ESBL) inhibition
These hydrolise oxyimino side chains of cephalosporins: cefotaxime,ceftriaxone, andceftazidime and monobactams: aztreonam

phase 2a (67 decks)

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