Antibiotics Flashcards
What is the most common mechanism of antibiotic activity
Effects on cell wall integrity
- Interferes with cell wall synthesis
How do beta lactams work
Target serine proteases and penicillin binding proteins
- Inhibits assembly and degrade cell wall
Four different beta lactams
- Penicillin
- Cephalosporin
- Monobactams
- Carbapenems
What is commonly associated with Clostridium difficile infections?
3rd generation/broad spectrum cephalosporins
Penicillin effective against mostly…
Gram +
Cephalosporins mostly effective against…
G- with each generation, but also some G+
Monobactams mostly effective against
Aerobic G-
Carbapenems mostly effective against
G+, G-, anaerobes
Glycopeptides/vancomycin
Targets cell wall
- Targets G+
Lipopeptides/daptomycin
Cell membrane inhibitor
Disruption of ionic concentration gradiet of the cell membrane
- Targets G+
Polypeptides
2 types
Cell membrane target
Bacitracin: topical, G+
Polymyxins/colistin: topical or IV, G-
Antimycobacterial
2 types
Inhibit mycolic acid synthesis in cell wall
Isoniazid and ethambutol
Prokaryotic ribosomes are made up of what?
30s and 50s subunits on the mRNA that lead to translation of genetic message
What are the 3 antibiotics that target the 30s ribosomal subunit
- Aminoglycosides
- Tetracycline
- Glycylcycline
The six antibiotics that target the 50s ribosomal subunit
- Macrolides
- Lincosamide
- Chloramphenicol
- Oxazolidinone
- Streptogramins
- Ketolides
Aminoglycosides
30s
- Almost always used with cell wall synthesis inhibitors
- Anaerobes are usually resistant
- GNR, some GP, mycobacteria
Tetracyclines
30s
- G+, G-, mycoplasma, chlamydiae, rickettsiae
- Not give to <8 yo children, preg women
- Food decreases absorption
Glycylcyclines
30s
- Similar to tetracyclines
- More against G-, anaerobes, rapid growing mycobacteria
Macrolides
50s
- Aerobic and anaerobic G+ cocci
Lincosamides
50s
- G+ cocci, anaerobes
- C. difficile diarrhea
Chloramphenicol
50s
- G+, G-, anaerobes, chlamydiae, mycoplasma, rickettsiae
- Aplastic anemia risk, backfire against human protein synthesis
Oxazolidinones
50s
- Aerobic G+, mycobacteria, anaerobes
Streptogramin
50s
- G+, anaerobes
Ketolides
50s
- Similar to erythromycins from macrolides
- - G+ cocci
What was the first effective systemic antimicrobial used in the US in the 1930s
Essential metabolite antimicrobials
Sulfonamides
Essential metabolite inhibitor
Trimethoprim
Essential metabolite inhibitor
Inhibitors of DNA replication
Quinolones/fluoroquinolones
Interfere with DNA transcription
Rifampin
Causes breaks in DNA
Metronidazole
Drug of choice for bacterial vaginosis
Metronidazole
Group at the heart of multi drug antibiotic resistance
ESKAPE
- ENFA
- STAU
- KLPN
- ACBA
- PSAE
- Enterobacter species
Multi drug resistance
Resistance to at least 1 in 3 or more antimicrobial categories
Extensively drug resistant
Resistance in at least one in ALL but 1-2 antimicrobial categories
Pan drug resistant
Resistant to everything
Preventing resistance
Vaccination
Infection control
Protect food supply
Antibiotic responsibility
Screening, treatment, education
Intrinsic mechanisms of antimicrobial resistance
Impermeability barriers
Biofilms
Drug efflux
Enzyme inactivation or degradation
Horizontal gene transfer: transformation
Parts of DNA taken up by bacteria from outside environment
Horizontal gene transfer: conjugation
Cell to cell contact between two bacteria and transfer plasmids
Horizontal gene transfer: transduction
Bacteria specific viruses transfer DNA between 2 closely related bacteria
Bacteriophag
Intrinsic antimicrobial resistance: impermeability barriers
- LPS
- Can reduce the number of porins or change sructure to reduce affinity for antibiotics
Intrinsic antimicrobial resistance: biofilms
Motile bacteria attached to substrate
- Decreased penetration of antibiotic
- Slowed bacterial growth
Intrinsic antimicrobial resistance: drug efflux
Pumps that transport the antibiotic back out of the cell
Intrinsic antimicrobial resistance: enzyme inactivation/degradation
Self explanatory
Fourextrinsic antimicrobial resistance mechanisms
Efflux
Target site modification
Antibiotic alteration
Enzymatic inactivtion
How to combat beta lactam antibiotics
- Making enzyme beta lactamase
- alter antibiotic target site
- alter porin channels
How to combat glycopeptides
- Alter antibiotic target site
How to combat aminoglycosides
- Alter antibiotic target site
- Modify antibiotic
- Alter porin channels
How to combat quinolones
- Alter antibiotic binding site
- efflux
What is MIC?
Minimum inhibitory concentration that visibly inhibits growth of the test organism
