3 Hospital Acquired Infection and Antibiotic Resistance Flashcards
(36 cards)
Q: What is an antibiotic? Produced by? today?
A: -antimicrobial agent produced by a microorganism that kills or inhibits other microorganisms
-produced by soil-dwelling fungi/bacteria -> those used today have been altered eg semi-synthetic chemicals with antimicrobial activity
Q: What are antibiotics used for?
A: treating and preventing infection (eg in those that are immunosuppressed)
Q: What is an antimicrobial? Compared to antibiotics?
A: chemical that selectively kills or inhibits microbes (bacteria, fungi, viruses)
-broader target than antibiotics
Q: What is bactericidal behaviour? bacteriostatic? Relationship?
A: -kill bacteria
-stops bacterial growth
bactericidal activity is dose dependant (lower= bacteriostatic behaviour)
Q: What is an antiseptic?
A: chemical that kills or inhibits microbes that is usually used topically to prevent infection
Q: What does it mean for a bacteria to become resistant to antibiotics? (2) Spectrum?
A: that antibiotic can no longer be used against that bacteria // ability of an organism to replicate in the presence of an antibiotic at a particular concentration
there is a spectrum for different strains: the antibiotic concentration required to inhibit growth is different for different strains
Q: What is breakpoint? In relation to resistance?
A: an estimate of the reasonable concentration that might be achieved clinically
Any organism that can grow at a concentration of the breakpoint or greater than the breakpoint is resistant
Q: What is Minimal Inhibitory Concentration (MIC)?
A: the lowest concentration of the antibiotic required to inhibit growth
*Q: What occurs with greater use of antibiotics? Why? (2)
A: ->higher prevalence of resistance (less effective)
- bacteria constitute as a moving target -> rapidly evolving and changing -> come up with new methods not to be killed
- routine antibiotic use provides a selective pressure for the acquisition and maintenance (if a strain is already resistant) of resistant genes
*Q: Explain resistance in terms of natural selection. (3)
A: in any population-> get some variation
- absence of selection pressures-> said diversity is maintained
- presence of selection pressures-> allows specific phenotypes to thrive
*Q: What occurs soon after the arrival of a new antibiotic in hospitals? When is this not the case? Possible reason?
A: Resistance
Exceptions: Erythromycin and Vancomycin
Vancomycin - is toxic and not hugely effective so it wasn’t used much at the time of discovery so it took longer for resistance to develop
*Q: What does antibiotic resistance lead to? (3) Give 5 reasons for one. (5)
A: -increased mortality
- increased morbidity
- increased cost:
- increased time to find a effective therapy therefore longer stay
- use of less effective ‘second choice’ antibiotic therefore longer stay
- use of more toxic drugs that need need additional supported therapy
- use of more expensive therapy (newer drugs)
- requirement of different approaches entirely eg surgery
*Q: What is a possible way around antibiotic resistance?
A: using vaccinations so that you prevent the infections from even occurring and therefore preventing the need of them
*Q: How are antibiotics often categorised? Name 7 classes. Which is the most commonly used class? Which is the only synthetic class of antibiotics?
A: according to their mechanism of action
- Beta-lactams **
- Tetracycline
- Chloramphenicol
- Quinolones (s)
- Sulphonamides
- Aminoglycosides
- Macrolides
*Q: What is the overall mechanism of action of beta-lactams? Explain. (3) 2 examples. Why is MRSA resistant to it?
A: Interfere with synthesis of the PEPTIDOGLYCAN component of the bacterial cell wall
- beta-lactam ring is similar in structure to a precursor of peptidoglycan = AB mimics precursors for bacterial cell wall
- once enzymes tries to use the AB (bind to Penicillin Binding Proteins (PBP)) they become deactivated
- when bacteria are exposed to AB they lyse and die
Examples: Penicillin and methicillin
MRSA has a different PBP (PBP2a) which doesn’t bind with high affinity to beta-lactams
*Q: What is tetracycline? What is the overall mechanism of its action? Explain. (3)
A: -Bacteriostatic, broad spectrum
-Inhibits PROTEIN SYNTHESIS
- Binds to the 16S component of the 30S ribosomal subunit thus
- preventing charged aminoacyl tRNAs from binding to the mRNA/ribosome complex
- prevents elongation of the polypeptide
*Q: What is chloramphenicol? What is the overall mechanism of its action? Explain. (2) How is it often used? Current use?
A: -Bacteriostatic, broad spectrum
-Inhibits PROTEIN SYNTHESIS
- Binds to 50S subunit and blocks peptidyl transfer step
- prevents elongation of the polypeptide
Often used topically due to toxicity
as other drugs have become resistant-> it has been increasingly used as a systematic therapeutic
*Q: What are quinolones? What do they represent? What is the overall mechanism of its action? Explain. (3)
A: Bactericidal, broad spectrum -only synthetic class of AB
disrupt DNA replication
-targets DNA gyrase (in Gram NEGATIVE) and topoisomerase (in Gram POSITIVE)
(-DNA gyrase and topoisomerase is responsible for unravelling DNA)
-prevents DNA from sticking back together during unwinding process
*Q: What are sulphonamides? (2) What is the overall mechanism of its action? Used to treat? (3) Give example and explain how it’s used. Use today?
A: Bacteriostatics that are not strictly antibiotics (synthesised)
Interferes with the folate pathway
-UTI, Reproductive Tract Infection (RTI) and bacteraemia
sulpha-methoxazole
-sometimes used with trimethoprim (co-trimoxazole) as they target separate components of the folate pathway
becoming more common despite some toxicity due to resistance to other antimicrobials
*Q: What are aminoglycosides? What is the overall mechanism of its action? (3) Causes? 2 examples.
A: Bactericidal
-Target PROTEIN SYNTHESIS (30S ribosomal unit), RNA proofreading and cause damage to cell membrane
causes aberrant proteins and misfolding
EXAMPLES: Gentamycin, Streptomycin
Q: What do macrolides treat? Method of action? (2) Example.
A: gram positive infections
- Targets 50S ribosomal subunit preventing aminoacyl transfer
- Causes truncation of polypeptides
EXAMPLE: Erythromycin
*Q: What are the 4 distinct mechanisms of antibiotic resistance?
A: 1 Altered Target Site
2 Inactivation of Antibiotic
3 Altered Metabolism
4 Decreased Drug Accumulation
Q: How can a bacteria ‘alter a target site’ in terms of antibiotic resistance? (2) Explain. 2 examples.
A: -arise from acquisition of an alternative gene or
-a gene that encodes a target-modifying enzyme (mutation)
You can acquire a gene which performs the same function but has a different structure and hence is not susceptible to the AB.
- MRSA acquired a gene which produces an alternative penicillin binding protein (PBP2a) - it performs the same function but has lower affinity to beta-lactams so methicillin is ineffective
- Streptococcus pneumoniae is resistant to erythromycin because it has acquired a gene which encodes an enzyme that methylates the AB target site in the 50S ribosomal subunit (ribosome still works) - this changes its structure so erythromycin can no longer act
Q: How can a bacteria ‘inactivate an antibiotic’ in terms of antibiotic resistance? 4 examples. Alternative?
A: Acquire gene for an enzyme which breaks down the antibiotic (degradation or alteration)
- chloramphenicol acetyl-transferase (cat)
- beta-lactamase (bla)
- ESBL and NDM-1 are examples of broad spectrum beta-lactamases
enzyme-independent: bacterium releases fragments of membrane that sequester antibiotic (act as decoy) and inactivate it
