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POM 3 G: IMMUNOLOGY AND INFECTION > 3.3 Antimicrobial Thewpies > Flashcards

3.3 Antimicrobial Thewpies Flashcards

1
Q

Prontosil

A

Sulphonamide antibiotic

Bacteriostatic
Synthetic

Gram +ve

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2
Q

Example of a prontosil

A

Sulpha methoxazole

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3
Q

Prontosil used in

A

UTI, RTI, bactaeremia

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4
Q

Beta lactams example

A

Penicillin methicillin

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5
Q

How do beta lactams work

A

Interferes with synthesis of peptidoglycan in cell wall by binding to penicillin binding proteins which catalysed many steps in its formation

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6
Q

Antibiotic

A

Antimicrobial agent produced by a microorganism that kills or inhibits other microorganisms

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7
Q

What produces majority of antibiotics

A

Bacteria or soil dwelling fungi

However some are synthetic or semi synthetic

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8
Q

Antimicrobial

A

Chemical that selectively kills or inhibits microbes

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9
Q

Bactericidal

A

Kills nacteria

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10
Q

Bacteriostatic

A

Stops bacteria growing

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11
Q

Antiseptic

A

Topically used chemical which kills or inhibits microbes

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12
Q

Why are antiseptics used topically

A

To prevent infection

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13
Q

MIC

A

Minimal inhibitory concentration

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14
Q

Minimal inhibitory concentration.

A

Lowest conc of AB required to inhibit growth

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15
Q

Wntibiotic resistance stems from

A

A selection pressure

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16
Q

No selection pressure with resistance

A

Resistant strains have no advantage and maintain a low prevalence

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17
Q

Presence of a selection pressure with resistance e

A

Resistant mutants outcompete giving a high prevalence in pt population

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18
Q

Misconception of AB

A

Resistance against multiple AB at same time wouldn’t occur

Horizontal gene transfer wouldn’t occur

Resistant genes would be lesss able to cause disease

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19
Q

AB resistance leads to

A

Inc mortality, morbidity and cost due to

Need for additional approaches
Expensive therapies
More toxic drugs
Use of more types of AB

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20
Q

Gram negative resistant bacteria examples

A

Ecoli

Salmonella spp

Meisseria gonorrhoeae

21
Q

Gram positive resistant bacteria

A

MRSA

Streptococcus oneumoniae

Clostridium difficile

Mycobacterium tuberculosis

22
Q

Ways AB can damage cell membrane

A

Target protein synthesis of 30s ribosome subunit or 50s

E.g. aminoglycosides, linezolid

23
Q

How can AB affect dna replication or transcription

A

Target RNA polymerase

E.g. rifampicin

24
Q

How can AB target cell wall synthesis

A

Bind to pbp which catalyses formation of peptidoglycan

Target lipid ii component of cell wall and it’s cross link in
E.g. penicillins, vancomycin

25
Q

What can AB target

A

Cell wall

Cell memb

Dan replication

Protein synthesis

26
Q

Cell wall ab

A

Penicillins

Vancomycin

27
Q

Cell memb ab

A

Daptomycin, aminoglycosides

28
Q

Linezolid

A

Inhibits p synthesis by binding 50s subunit

Gram positive Bacteriostatic

29
Q

Vancomycin

A

Targets lipid ii component of cell wall biosynthesis and its cross linkages

Bactericidal

30
Q

Rifampicin

A

Targets rna polymerase (dna replication and p synthesis and cell memb)

Bactericidal

31
Q

Aminoglycosides

A

Target 30s ribosomes in p synthesis damaging cell membrane

E.g. streptomycin

Bactericidal

32
Q

Daptomycin

A

Gram positive Bactericidal

Targets cell memb

33
Q

What are the mechanisms of antibiotic resistance

A

Altered target site

Inactivation of AB

Altered metabolism

Decreased drug accumulation

34
Q

Altered target site

A

Can alternate a gene or a gene encoding a target modifying enzyme

MRSA alternative pbp with low affinity for AB (works in its presence)

Or acquires a gene that encodes an enzyme which chemically modifies the target site

35
Q

Inactivation of AB

A

Enzymatic degradation or alteration making AB ineffective

36
Q

Altered metabolism

A

Inc production of enzyme substrate to out compete AB inhibitor

Or switch to other metabolic pathways

37
Q

Decreased drug accumulation

A

Reduced penetration of AB into cell

Increased effluent of AB out

38
Q

Sources of AB resistant genes

A

Plasmids
Transposons
Naked dna (from dead bacteria)

39
Q

How do ab resistant genes spread between bacteria

A

Transformation (uptake of Extracellular dna)

Conjugation (via pious)

Transduction (phage mediated dna transfer)

40
Q

Reasons for treatment failure

A

Wrong choice

Wrong dose

Poor penetration of ab

Wrong administration

41
Q

In vitro

A

In lab

42
Q

In Vivo

A

In Organism

43
Q

Macrolides examples

A

Erythromycin, azithromycin

44
Q

Macrolides

A

Target 50s ribosome subunit preventing polypeptides synthesis

45
Q

Quinolones

A

Synthetic
Broad spectrum
Bactericidal

Targets what holds together dna strands stopping replication

46
Q

Measuring resistance

A

Swabs onto diagnostic agar to identify causative agent then overlaid with AB containing strips

Or broth mjcrodilution and pcr detection

47
Q

why do hospitals proved a strong selection pressure

A

Large number of infected people receiving high doses of AB

48
Q

Addressing resistance

A

Combination therapy

Quicker identification

Reduce use of broad spectrum

Prescribing strategies

Kowledge

POM 3 G: IMMUNOLOGY AND INFECTION (10 decks)

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