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POM Week 2 > Hospital acquired infection and antibiotic resistance > Flashcards

Hospital acquired infection and antibiotic resistance Flashcards

1
Q

What is Prontosil?

A

First example of an effective and safe anti-bacterial therapeutic

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2
Q

What are the main features of Prontosil?

A

Bacteriostatic
Synthetic
Used to treat UTI’s, RTI’s, bacteraemia and prophylaxis for HIV+ individuals
Sometimes used together with Trimethoprim- work better together
Becoming more common due to resistance to other anti-bacterials

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3
Q

What was the issues with Prontosil?

A

Only effective with Gram-positive bacteria (single outer membrane)

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4
Q

Why is it difficult to develop drugs against Gram-negative bacteria?

A

To get a drug across the outer layer it must be hydrophilic

And hydrophobic for the inner layer

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5
Q

What was the issue with early penicillin?

A

Excreted from the body very rapidly WH

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6
Q

What is a Beta-lactam?

A

Most commonly prescribed type of antibiotic
E.g pencilling and methicillin
Has a characteristic Beta-lactam ring
Chemically mimic components of peptidoglycan cell wall
Competitive inhibitor of enzymes involved in cell wall synthesis

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7
Q

What is an antibiotic? (strictly speaking)

A

Agent produces by microorganism the kills or inhibits another microorganism
However many are semi-synthetic or synthetic

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8
Q

What are the 4 types of antibiotic?

A

Antimicrobial
Bactericidal
Bacteriostatic
Antiseptic

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9
Q

Why did antibiotic discoveries slow down?

A

Economic factors

Already so many, why spend money acquiring more?

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10
Q

What did Flemming predict?

A

Resistance primarily due to misuse

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11
Q

What are the main features of resistance?

A

Constantly changing landscape- problems we face today are not what we will face tomorrow
Countries that use the most antibiotics have the most resistance
Resistance usually emerges soon after the new arrival of the new AB

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12
Q

Why is the market for antibiotics different from any other type of drug?

A

Newest drugs are kept sparingly for the most severe of cases- small market
Older drugs are in more demand

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13
Q

How does resistance come about?

A

Evolution by natural selection

Routine use of antibiotics provides selection pressure

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14
Q

What were the misconception at the dawn of the antibiotic era?

A

Resistance against more than one class of antibiotics would not occur at the same time
Horizontal gene transfer would not occur
Resistance organisms would be significantly less ‘fit’

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15
Q

What are the consequences of resistance?

A

Increased mortality, morbidity and cost
Increased time for effective therapy, requirement for additional approaches
Use of expensive therapy
More toxic drugs

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16
Q

Name some gram-negative resistant bacteria

A

Pseudomonas aeruginosa
E. coli
Salmonella
Acinetobacter

17
Q

Name some gram-positive resistant bacteria

A

Staphylococcus aureus
Streptococcus pneumonias
Clostridium difficle
Myobacterium tuberculosis

18
Q

What are Aminoglycosides?

A 
E.g. Gentamicin, streptomycin
Bactericidal 
Targets proteins synthesis, RNA proofreading and causes damage to cell membrane
Toxic- limited use 
Increasing due to resistance to others
19
Q

What is Rifampicin?

A

Bactericidal
Targets RpoB subunit of RNA polymerase
Spontaneous resistance frequent
Makes secretions go red

20
Q

What is Vancomycin?

A

Bactericidal
Targets lipid II components of cell wall biosynthesis
Toxic
Increasing use due to resistance to others

21
Q

What is Linezolid?

A

Bacteriostatic
Inhibits the imitation of protein synthesis
Gram-positive

22
Q

What is Daptmycin?

A

Bactericidla
Targets cell membrane
Gram positive
Toxicity limits dose

23
Q

What principle do antibiotic works on?

A

Selective toxicity

24
Q

What are the 4 mechanisms of antibiotic resistance?

A

Altered target site
Inactivation of antibiotic
Altered metabolism
Decreased drug accumulation

25
Q

How does the altered target site mechanism work?

A

Gene encodes a target-modifying enzyme
e.g MRSA encodes alternative enzyme with low affinity for Beta-lactams
Streptococcus pneumoniae encodes enzyme that methylates the AB target site

26
Q

How does the inactivation of antibiotic mechanism work?

A

Enzymatic degradation or altering rendering antibiotic ineffective

27
Q

How does the altered metabolism mechanism work?

A

Increased production of enzyme substrate can out-compete antibiotic inhibitor
Bacteria south to other metabolic pathways

28
Q

How does the decreased drug accumulation mechanism work?

A

Reduced penetration of AB into bacterial cell
Increased efflux of AB out of cell
Drug does not reach concentration to be effective

29
Q

What macrocolides?

A

E.g. erythromycin, azithromycin
Gram-positive and some gram-negative
Targets ribosomal sub-unit preventing amino-acyl transfer

30
Q

What are quinolones?

A

Synthetic, broad spectrum, bactericidal
Target DNA gyrase in GM-ve
Toposomerase on GM+ve

31
Q

What are the sources of antibiotic resistance genes?

A

Plasmids
Transposons
Naked DNA

32
Q

What are transposons?

A

They integrate into chromosomal DNA allowing transfer of genes from plasmin to chromosome and vice versa

33
Q

What are the non-genetic mechanisms of resistance?

A 
Biofilm
Intracellular location
Slow growth
Spores
Persisters
34
Q

What are other reasons for failure of antibiotics?

A

Wrong for organism
Poor penetration to target site
Wrong dose
Wrong administration

35
Q

Why do hospitals provide strong elective pressure for AB resistance?

A

Large number so infected people receiving high doses of antibiotics
Strong selective pressure

36
Q

What are some risk factors for HAI?

A 
High no. of immunosuppressed
Crowded wards
Presence of pathogens 
Broken skin
AB therapy may suppress normal flora
Transmission by staff with contact with multiple patients
37
Q

What can be done to address resistance?

A 
Prescribing strategies 
Reduce broad-spectrum use
Quicker identification 
Combination therapy
Knowledge of strains and resistance patterns

POM Week 2 (12 decks)

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