Antimicrobial Therapies Flashcards

1
Q

What is an antibiotic?

A

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

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2
Q

What does Antimicrobial mean?

A

Chemical that selectively kills or inhibits microbes

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3
Q

What does bactericidal mean?

A

Kills bacteria

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4
Q

What does bacteriostatic mean?

A

Stops bacteria growing

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5
Q

What does antiseptic mean?

A

Chemical that kills or inhibits microbes

Usually used topically to prevent infection

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6
Q

When is a bacterium considered resistant?

A

When it can grow at or above the breakpoint of the antibiotic conc. required to inhibit growth

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7
Q

What is the breakpoint?

A

Estimate of the clinically achievable conc of a given antibiotic in a host tissue

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8
Q

How does AB resistance lead to increased mortality, morbidity and cost?

A

Increased time to effective therapy

Requirement for additional approaches - e.g surgery

Use of expensive therapy (newer drugs)

Use of more toxic drugs e.g vancomycin

Use of less effective ‘second choice’’ antibiotics

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9
Q

What is the difference between positive and negative gram bacteria?

A

Gram-negative has 2 membranes but gram-positive has 1

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10
Q

What are the 4 distinct mechanisms of antibiotic resistance?

A

Altered target site

Inactivation of antibiotic

Altered metabolism

Decreased drug accumulation

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11
Q

What happens during the altered target site mechanism?

A

Acquisition of alternative gene —> drug no longer binds where
it wants to

Gene that encodes a target-modifying enzyme

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12
Q

What happens during the inactivation of antibiotic mechanism?

A

Enzymatic degradation or alteration —> rendering antibiotic
ineffective

—> enzyme cleaves antibiotic —> stops working

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13
Q

What happens during the altered metabolism mechanism?

A

Increased production of enzyme substrate can outcompete antibiotic inhibitor

Bacteria switch to other metabolic pathways

—> re-routes metabolism or massively increase expression of target
—> need more drug to inhibit it
—> may not be possible to give person that much drug

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14
Q

What happens in the decreased dug accumulation mechanism?

A

Reduced penetration of AB into bacteria cell or increased effluent of AB out of the cell

—> drug does not reach concentration required to be effective

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15
Q

What are the sources antibiotic resistance genes?

A

Plasmids —> can be moved around easily

Transposons —> can shuttle DNA

Naked DNA —> take up DNA from decade bacteria released into environment

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16
Q

What are non-genetic mechanism of resistance/treatment failure?

A

Biofilm

Intracellular location

Slow growths

Spores

Persisters

17
Q

What are others reasons fro treatment failure?

A

Inappropriate choice for organism

Poor penetration of AB into target site

Inappropriate does (half life)

Inappropriate administration (oral vs IV)

Presence of AB resistance within commensal flora
—> resistance mech of 1 bacteria can protect the other

18
Q

How do hospitals provide strong selective pressure for AB resistance?

A

Large numbers of infected people receiving high dose of antibiotics

19
Q

What are risk factors fro HAI?

A

High number of ill people

Crowded wards

Presence of pathogens

Broken skin —> surgical wound/IV catheter

Indwelling devices - intubation

AB therapy may suppress normal flora

Transmission by staff - contact with multiple patients

20
Q

How can we address resistance?

A

Prescribing strategies —> tighter controls, temporary withdrawal of certain classes, restriction of ABs for certain serious infections

Reduce use of road-spectrum antibiotics

Quicker identification of infections caused by resistant strains

Combination therapy

Knowledge of local strains/resistance patterns

21
Q

How can we overcome resistance?

A

Modification of existing medications

Combinations of antibiotics + inhibitors