Antibiotics Flashcards
How are beta lactams excreted
In the urine
How do microbes develop resistance to beta lactams
Altered or different penicillin-binding proteins so antibiotic cant bind
Changes in specific pumps filtering out the drug
Changes in porin size or number (gram negative organisms) prevents drugs from gaining access to intracellular targets.
Inactivation by beta-lactamases – most common
Gram neg bacteria have it in their cell wall
Others get it induced after exposure to the drug
List major beta lactams
Cephalosporins, penicillins, carbepenems, and monobactams
Beta lactam MOA
Interferes with bacterial cell wall synthesis and causes cell wall degradation
Beta lactam time or concentration dependent
Time dependent
MRSA resistance MOA
Use of Beta lactamase protectors – clavulanic acid or sulbactam – led to adaptation by Staph by mutations in penicillin-binding proteins (PBP-2) encoded by mecA gene, located on the staphylococcal chromosomal cassette.
Expression of this gene prevents efficacy of any beta-lactam antibiotic
T/F: Beta lactams do not work well in hypoxic and hypertonic environments (e.g. abscesses)
True
Beta lactam - Efficacy in hypertonic environment
Does not work well in hypertonic environment (e.g. renal interstitium)
How to minimize nephrotoxicity associated with aminoglycosides
Add dietary calcium to protect against toxicity
Allow kidneys drug-free period (high once daily dosing)
Alkaline urine increases activity and decreases renal tubular cell uptake (reduces chance of tox)
List some aminoglycosides
Neomycin, gentamicin, amikacin, netilmicin, and streptomycin
Aminoglycosides MOA
Target bacterial ribosomes – 30s ribosomal subunit
Aminoglycosides bactericidal or static
Time or concentration dependent
Bactericidal and concentration-dependent
Aminoglycosides in purulent material
Not efficacious due to acidic environment
Is presence of renal disease a contraindication for administering aminoglycosides
No
Aminoglycosides and oxygen
Uptake depends on membrane bound respiratory protein therefore anaerobes are resistant - Lack of oxygen renders aminoglycosides ineffective
How do hyperosmolarity and decreased pH affect aminoglycosides
Hyperosmolarity and decreased pH also decrease drug movement into the cell
MOA of fluoroquinolones
Inhibits DNA synthesis via DNA gyrase – only veterinary microbial that does so
Benefits of fluoroquinolones
Still good in low oxygen tension
Accumulate in WBC
Broad gram-negative spectrum
Are fluoroquinolones bactericidal or static
time or concentration dependent
Bactericidal
Concentration dependent
Antibiotic recommended for hepatobiliary surgery
Cefoxitin
Which combination would be best for a gram positive aerobic and gram negative anaerobic infection
AGs or FQs are often combined with beta lactams, metro, or clindamycin to target both aerobic G+ and G- infections, or infections caused by both aerobes and anaerobes
Which antibiotics cross the blood-brain barrier in the presence of inflammation
Penicillins
Selected cephalosporins (e.g., cefotaxime, ceftriaxone, ceftazidime)
Fluorinated quinolones
Vancomycin
Which antibiotics cross the blood-brain barrier
Chloramphenicol
Doxycycline
FQ (for some organisms)
Metronidazole
Rifampin
Sulfonamides/trimethoprim
Which antibiotics DO NOT cross the blood-brain barrier
Aminoglycosides
Carbenicillin
Cephalothin
Cefazolin
Cefotetan
Clindamycin
Erythromycin
Tetracycline
hyperosmolar environment affects on drugs
Hyperosmolar environment: may occur in inflammatory debris – reduces osmotic destruction of the organisms and causes drugs that target cell walls (beta-lactams in particular) to be less effective.
