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Year 1 POM > Hospital Acquired Infection and Antibiotic Resistance > Flashcards

Hospital Acquired Infection and Antibiotic Resistance Flashcards

1
Q

What is beta-lactams?

A
  • Interfere with the synthesis of the peptidoglycan component of the bacterial cell wall.
  • Examples include Penicillin and methicillin.
  • Bind to penicillin-binding proteins.
  • PBPs catalyse a number of steps in the synthesis of peptidoglycan.
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2
Q

Describe antibiotics

A
  • An antibiotic is an antimicrobial agent produced by a microorganism that kills or inhibits other microorganisms.
  • Most antibiotics in use today are produced by soil-dwelling fungi (Penicillium and Cephalosporium) or bacteria (Streptomyces and Bacillus).
  • However, antibiotics commonly used today encompass a range of natural, semi-synthetic and synthetic chemicals with antimicrobial activity.
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3
Q

What does antimicrobial mean?

A

chemical that selectively kills or inhibits microbes (bacteria, fungi, viruses).

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4
Q

What does bactericidal mean?

A

kills bacteria.

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5
Q

What does bacteriostatic mean?

A

stops bacteria growing.

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6
Q

What does antiseptic mean?

A

chemical that kills or inhibits microbes that is usually used topically to prevent infection.

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7
Q

Why does antibiotic resistance leads 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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8
Q

What are the major gram-negative antibiotic resistant bacterial pathogens?

A 
Pseudomonas aeruginosa
Cystic fibrosis, burn wound infections. Survives on abiotic surfaces.
E. Coli (ESBL)
GI infect., neonatal meningitis, septicaemia, UTI.
E. coli, Klebsiella spp (NDM-1) 
As above.
Salmonella spp. (MDR)
GI infect. , typhoid fever.
Acinetobacter baumannii (MDRAB)
Opportunistic, wounds, UTI, pneumonia (VAP). Survives on abiotic surfaces.
Neisseria gonorrhoeae
Gonorrhoea.
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9
Q

What are the major gram-positive antibiotic resistant bacterial pathogens?

A

Staphylococcus aureus (MRSA, VISA)
Wound and skin infect. pneumonia, septicaemia, infective endocarditis.
Streptococcus pneumoniae
Pneumonia, septicaemia.
Clostridium difficle
Pseudomembranous colitis, antibiotic-associated diarrhoea.
Enterococcus spp (VRE)
UTI, bacteraemia, infective endocarditis.
Mycobacterium tuberculosis (MDRTB, XDRTB)
Tuberculosis

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10
Q

What is ahminoglycosides?

A
  • E.g. Gentamicin, streptomycin.
  • Bactericidal.
  • Target protein synthesis (30S ribosomaml subunit), RNA proofreading and cause damage to cell membrane.
  • Toxicity has limited use, but resistance to other antibiotics has led to increasing use.
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11
Q

What is rifampicin?

A

•Bactericidal.
•Targets RpoB subunit of RNA polymerase.
•Spontaneous resistance is frequent.
Makes secretions go orange/red – affects compliance

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12
Q

What is vancomycin?

A
  • Bactericidal.
  • Targets Lipid II component of cell wall biosynthesis, as well as wall crosslinking via D-ala residues
  • Toxicity has limited use, but resistance to other antibiotics has led to increasing use e.g. against MRSA
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13
Q

What is linezolid?

A
  • Bacteriostatic.
  • Inhibits the initiation of protein synthesis by binding to the 50S rRNA subunit.
  • Gram-positive spectrum of activity.
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14
Q

What is daptomycin?

A
  • Bactericidal.
  • Targets bacterial cell membrane.
  • Gram-positive spectrum of activity.
  • Toxicity limits dose.
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15
Q

What are antibiotics?

A

Antibiotics target many different bacterial processes and are selectivity toxic
Large number of difference between mammals and bacteria result in multiple targets for antibiotic therapy - selective toxicity

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16
Q

What are the mechanisms of antibiotic resistance?

A
  1. Altered target site
  2. Inactivation of antibiotic
  3. Altered metabolism
  4. Decreased drug accumulation
17
Q

What happens in altered target site?

A
  • Can arise via acquisition of alternative gene or a gene that encodes a target-modifying enzyme.
  • Methicillin-resistant Staphylococcus aureus (MRSA) encodes an alternative PBP (PBP2a) with low affinity for beta-lactams.
  • Streptococcus pneumoniae resistance to erythromycin occurs via the acquisition of the erm gene, which encodes an enzyme that methylates the AB target site in the 50S ribosomal subunit.
18
Q

What happens in inactivation of antibiotic?

A
  • Enzymatic degradation or alteration, rendering antibiotic ineffective.
  • Examples include beta-lactamase (bla) and chloramphenicol acetyl-transferase (cat).
  • ESBL and NDM-1 are examples of broad-spectrum beta-lactamases (can degrade a wide range of beta-lactams, including newest).
19
Q

What is altered metabolism?

A
  • Increased production of enzyme substrate can out-compete antibiotic inhibitor (e.g. increased production of PABA confers resistance to sulfonamides).
  • Alternatively, bacteria switch to other metabolic pathways, reducing requirement for PABA.
20
Q

What is decreased drug accumulation?

A

•Reduced penetration of AB into bacterial cell (permeability) and/or increased efflux of AB out of the cell – drug does not reach concentration required to be effective.

21
Q

What are macrolides?

A
  • E.g. Erythromycin, azithromycin.
  • Gram-positive and some Gram-negative infections.
  • Targets 50S ribosomal subunit preventing amino-acyl transfer and thus truncation of polypeptides.
22
Q

What are quinolone?

A
  • Synthetic, broad spectrum, bactericidal.

* Target DNA gyrase in Gm-ve and topoisomerase IV in Gm+ve.

23
Q

What re the sources of antibiotic resistance?

A
  • Plasmids – extra-chromosomal circular DNA, often multiple copy. Often carry mutliple AB res genes – selection for one maintains resistance to all.
  • Transposons. Integrate into chromosomal DNA. Allow transfer of genes from plasmid to chromosome and vice versa.
  • Naked DNA. DNA from dead bacteria released into environment.
24
Q

How does the spread of antibiotic resistant genes occur?

A

-Genes responsible for conferring antibiotic resistance can be shared between bacteria via several different mechanisms

25
Q

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

A
  • Biofilm
  • Intracellular location
  • Slow growth
  • Spores
  • Persisters
26
Q

What are other reasons for treatment failure?

A
  • Inappropriate choice for organism
  • Poor penetration of AB into target site
  • Inappropriate dose (half life)
  • Inappropriate administration (oral vs IV)
  • Presence of AB resistance within commensal flora e.g. secretion of beta-lactamase
27
Q

What are hospital acquired infections (HAI)?

A
  • Hospitals provide strong selective pressure for antibiotic resistance
  • Large numbers of infected people receiving high doses of antibiotics - strong selective pressure for emergence/maintenance of AB resistance
28
Q

What are examples of HAI?

A
  • Methicillin-resistant S. aureus (MRSA)
  • Vancomycin-insensitive S. aureus (VISA)
  • Clostridium difficle
  • Vancomycin-resistant enterococci (VRE)
  • E. coli (ESBL/NDM-1)
  • P. aeruginosa
  • Acineterbacter baumannii
  • Stenotrophomonas maltophilia
29
Q

What are the risk factors for HAI?

A
  • High number of ill people! (immunosuppression)
  • 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
30
Q

How can AB therapy impair commensal flora (microbiota)?

A
  • In health communal organisms can out-compete pathogen WRT adhesion, metabolism, growth
  • Pathogen cannot colonise at levels sufficient for infection
31
Q

How are we addressing resistance?

A
  • Prescribing strategies – tighter controls, temporary withdrawal of certain classes. Restriction of ABs for certain serious infections
  • Reduce use of broad-spectrum antibiotics
  • Quicker identification of infections caused by resistant strains
  • Combination therapy
  • Knowledge of local strains/resistance patterns
32
Q

How can we overcome resistance?

A
  • Modification of existing medications to e.g. Prevent cleavage (beta-lactams) or enhance efficacy. E.g. Methicillin.
  • Combinations of antibiotic + inhibitor of e.g. Beta-lactamase. E.g. Augmentin.
  • However, this is a reactive approach in response to emergence of resistance!
33
Q

What is in the future?

A
  • New antibiotics
  • New vaccines
  • Better screening and decolonisation
  • Novel approaches – phage lysins, photo-active compounds, siRNA, Quorum Sensing inhibitors
  • Anti-infectives – MAb or peptide blocking
  • Use of non-pathogenic competitor strains

Year 1 POM (39 decks)

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