L3 Antibiotics and antibiotic resistance Flashcards
What are antibiotics?
Chemicals that kill or inhibit the growth of bacteria and are used to treat bacterial infections.
How are antibiotics classified? give some examples.
Antibiotics can be classified in various ways:
Mainly by their structure (same side groups). They can also be classified based on their activity so for example which bacteria they target specifically. Lastly, they can be categorized based on what part of the cell they target.
B-lactams: act as bacterial agents, causing bacterial cell death.
Sulfonamides: act as bacteriostatic agents, restriciting growth and reproduction.
What are the different mechanisms of action for antibiotics?
Interfering with cell wall synthesis
DNA and RNA synthesis: synthetic antibiotics prevent supercoiling of DNA
Preventing protein synthesis (folic synthesis acids)
Disruption of the cell membrane. Blocking permeability of the outer membrane.
Use of antibiotics for Gram + vs. - bacteria
Gram+: easier to kill with antibiotics
Gram-: two membrane, less sensitive (more protected against) antibiotics
What is MIC?
MIC: minimum inhibitory concentration
Minimum amount of antibiotic to kill/prevent growth of bacteria.
Growth curve
- Low conc: bacteria grow normal growth curve
- Intermediate and high conc: bacteria doesn’t grow (flat curve).
How is antibiotic resistance defined?
Antimicrobial resistance is the capacity of bacteria to survive exposure to a defined concentration of an antimicrobial substance (antibiotic)
How can bacteria protect themselves form antibiotics?
Preventing antibiotics from reaching target:
- Expulsions of antibiotics via efflux pumps (protein pumps in cell membrane, that pump various molecules out of the cell).
Protection of target molecule:
- Ribosomal methylation
- Topoisomerase mutations
- Cell wall structure alteration
- Proteins binding to the antibiotic or target molecule
Enzymatic deactivation of the antibiotic:
- Hydrolysis of penicillin catalyzed by beta-lactamases
How doe bacteria acquire antibiotic resistance?
Random mutations:
-AA substitution in target molecule (decreased affinity for antibiotic binding)
- Mutations or transportation in regulatory genes: upregulation of pumps, alterations of expression of target molecules, or modifications
Acquisition of genes encoding antibiotic resistance determinants:
- Enzymes catalyzing deactivation of antibiotics (e.g., beta-lactamases)
- Enzymes modifying target molecule (e.g., ribosomal methylation)
- Enzymes providing alternate biosynthetic pathways
- Efflux pumps
- Proteins shielding/protecting target molecule
How does antibiotic resistance spread?
Via horizontal gene transfer:
- Transformation (uptake of free DNA)
- Transduction (examine of genetic material between two bacterial cells)
Conjugation: (make pili, uptake of plasmid)
What are the different factors that drive antibiotic resistance?
Selective pressure: survival of the fittest
Overuse and misuse of antibiotics in clinical aspects:
- noncompliance to the antibiotic regimen
- easy access to antibiotics non-professional use
Overuse and misuse of antibiotics on environmental aspects:
- in animal feed
- contamination of the environment (aquatic)
Narrow-spectrum vs. broad-spectrum antibiotics?
Narrow-spectrum: target a few types of bacteria
Broad-spectrum: target many types of bacteria
Both can be used to treat bacterial infections, however, using broad-spectrum antibiotics when not needed can cause antibiotic-resistant bacteria that are difficult to treat.
Acquired vs. intrinsic antibiotic resistance
Intrinsic resistance: the antibiotic never possesses activity against the pathogen.
Acquired: achieved through the transfer of genetic material that confers resistance.
