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Principles of Medicine (POM) - Block 2 > Lecture 12: Antimicrobial Therapies > Flashcards

Lecture 12: Antimicrobial Therapies Flashcards

1
Q

How do Beta-lactam antibiotics work?

A

Interfere with synthesis of peptidoglycan component of bacterial cell wall.
Bind to penicillin-binding proteins —> catalyse no. Of steps in synthesis of peptidoglycan

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2
Q

Name some examples of beta-lactams.

A

Penicillin

Methicillin

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3
Q

What is an antibiotic?

A

An anti microbial agent produced by a microorganism that kills or inhibits other microorganisms.

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4
Q

What is an anti microbial?

A

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

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5
Q

What is the difference between bactericidal and bacteriostatic antibiotics?

A

Bactericidal - kills bacteria

Bacteriostatic - stops bacteria growing

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6
Q

What is antiseptic?

A

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

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7
Q

How does use of antibiotics lead to resistant strains of bacteria?

A

It is a selection pressure that selects for resistant strains. The resistant strains replicate whilst non resistant strains die out, so the process continues by natural selection.

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8
Q

Name some major antibiotic resistant bacterial pathogens. (Gram-negative)

A

Pseudomonas aeruginosa - CF, burn wound infections
E. Coli - GI infect, neonatal meningitis, septicaemia, UTI
Salmonella spp. - GI infect, typhoid fever
Acinetobacter Baumannii - opportunistic, wounds, UTI, pneumonia
Neisseria gonorrhoeae - gonorrhoea

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9
Q

Name some major antibiotic resistant bacterial pathogens. (Gram-positive)

A

staphylococcus aureus (MRSA, VISA) - wound + skin, pneumonia, septicaemia
streptococcus pneumoniae - pneumonia, septicaemia
clostridium difficle
enterococcus spp (VRE) - UTI, bacteraemia, infective endocarditis
mycobacterium tuberculosis - TB

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10
Q

How do aminoglycoside antibiotics work?

A

Bactericidal, target protein synthesis (30S ribosomal subunit), RNA proofreading and cause damage to cell membrane

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11
Q

What is a problem with aminoglycoside antibiotics?

A

They are quite toxic so they have limited use

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12
Q

How does Rifampicin work?

A

Bactericidal, targets RpoB subunit of RNA polymerase, spontaneous resistance is frequent, makes secretions go orange/red - affects compliance.

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13
Q

Name some examples of aminoglycoside antibiotics.

A

Gentamicin

Streptomycin

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14
Q

How does Vancomycin work?

A

Bactericidal, targets lipid II component of cell wall biosynthesis, as well as wall cross-linking via D-ala residues

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15
Q

How does Linezolid work?

A

Bacteriostatic - inhibits initiation of protein synthesis by binding to 50S rRNA subunit.
Gram-positive spectrum of activity

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16
Q

How does Daptomycin work?

A

Bactericidal, targets cell membrane, gram-positive spectrum of activity

17
Q

What is selective toxicity?

A

The large number of differences between mammals and bacteria result in multiple targets for antibiotic therapy, so antibiotics target many different bacterial processes and are selectively toxic.

18
Q

By what 4 mechanisms does antibiotic resistance occur?

A
  • Altered target site
  • Inactivation of antibiotic
  • Altered metabolism
  • Decreased drug accumulation
19
Q

How can an altered target site arise and cause antibiotic resistance?

A

via acquisition of alternative gene or gene that encodes a target-modifying enzyme e.g. MRSA encodes alternative Penicillin binding protein (PBP2a) w/ low affinity for beta lactams

20
Q

How can inactivation of antibiotics lead to resistance?

A

Enzymatic degradation or alteration, rendering antibiotic ineffective e.g. beta-lactamase (bla) and chloramphenicol acetyl-transferase (cat)

21
Q

How can altered metabolism lead to antibiotic resistance?

A

Increased production of enzyme substrate can out-compete antibiotic inhibitor e.g. increased production of PABA (acid) confers resistance to sulphonamides or switch to other pathways reducing requirement of antibiotic

22
Q

How can decreased drug accumulation lead to resistance?

A

reduced penetration of antibiotic into bacterial cell (permeability) and/or increased efflux of AB out of cell - can’t reach conc. required to be effective

23
Q

How do macrolides work?

A

They target 50S ribosome subunit preventing amino-acyl transfer and stop the polypeptide from being completed - the chain keeps growing so the shape of the protein is wrong. (gram -ve and +ve)

24
Q

How do quinolones work?

A

Bactericidal, target DNA gyrase in gram -ve and topoisomerase IV in gram +ve.

25
Q

Name some sources of antibiotic resistance genes.

A

Plasmids - circular piece of DNA, often multiple copies, often carry multiple AB resistant genes
Transposons - integrate into chromosomal DNA, genes from plasmid to chromosome and vice versa
Naked DNA - from dead bacteria, released into environment

26
Q

Name 3 ways genes responsible for resistance can be shared between bacteria.

A

Transformation (uptake of extracellular DNA)
Transduction (phage-mediated DNA transfer)
Conjugation (pilus-mediated DNA transfer)

27
Q

Name some non-genetic mechanisms of resistance/treatment failure

A
  • Biofilm
  • Intracellular location
  • Slow growth
  • Spores
  • Persisters
28
Q

Name some other reasons why antibiotic treatment might fail.

A
  • Inappropriate choice for organism
  • Poor penetration of antibiotic into target site
  • Inappropriate dose (half-life)
  • Inappropriate administration (oral vs IV)
  • presence of AB resistance in microbiota/flora
29
Q

Give some examples of HAIs

A 
MRSA
VISA
Clostridium difficle
VRE
E.coli (ESBL/NDM-1)
30
Q

Name some risk factors for HAIs

A
  • high no. ill people (immunosuppression)
  • crowded wards
  • presence of pathogens
  • broken skin
  • indwelling devices
  • AB therapy may suppress normal flora
  • transmission by staff - contact w/multiple patients
31
Q

Name some ways in which antibiotic resistance can be addressed.

A
  • prescribing strategies
  • reduce use of broad-spectrum antibiotics
  • quicker identification of infections caused by resistant-strains
  • combination therapy
  • knowledge of local strains/resistance patterns
32
Q

What Gram negative organism causes hospital acquired pneumonia, burn wounds, particularly affects immunocompromised hosts (e.g. chemotherapy, individuals with cystic fibrosis), and survives on abiotic surfaces?

A

Pseudomonas aeruginosa

33
Q

What is the abbreviation for extended spectrum beta-lactam resistant E. coli?

A

ESBL

34
Q

What Gram Negative organism causes UTI infections, and survives on abiotic surfaces?

A

N/A

35
Q

What Gram Positive organism colonises the nasopharynx, causes bloodstream infections, and disseminated spread (e.g. osteomyelitis & infective endocarditis)?

A

Staphylococcus aureus

36
Q

What Gram Positive organism is a commensal of gastrointestinal tract, but can cause bloodstream and urinary tract infections?

A

Enterococcus

37
Q

What Gram Positive organism is a major cause of antibiotic associated diarrhoea and mortality?

A

Clostridium difficile

38
Q

Why type antibiotic is prontosil and how does it work?

A

Sulphonamide antibiotic
Bacteriostatic
Used to rear UTIs, RTIs, bacteriaemia and prophylaxis for HIV+ individuals
Some host toxicity

Principles of Medicine (POM) - Block 2 (12 decks)

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