C-7 Flashcards
where do antibiotics come from
discovered in a contaminant - penicillium
natural antibiotics
Antimicrobial agents that are produced naturally by an organism (ex. Penicillin)
semi-synthetic antibiotics
Chemically altered antibiotics that are more effective, more stable, or easier to administer than their natural counterpart. (Ex. Can pass through the stomach without degradation)
synthetic antibiotics
Antimicrobials completely synthesized in a lab (Ex. Sulfonamides)
mechanism of action used by antimicrobial agents (what do they target inside the microbial cell)
- cell walls
- ribosomes
- cytoplasmic membranes
- metabolic pathways
- nucleic acid synthesis
- blocks attachment
selective toxicity and why it’s important
targeting structures unique to that microbe; antibiotic must be more toxic to the pathogen than the host
penicillin and cephalosporin
- Beta-lactam
- Cell wall biosynthesis inhibitor
- Gm+ mostly (hard to cross OM of Gm– bacteria) (bactericidal)
- some allergic reactions
Lipoglycopeptides
- Cell wall biosynthesis inhibitor
- Gm+ mostly (hard to cross OM of Gm– bacteria) (bactericidal)
- “red man syndrome” (RMS) –
flushing, hypotension, itching with
IV use, phlebitis
Macrolides
- Inhibit protein synthesis – bind large ribosomal subunit
- Broad spectrum - Gm+ and a few Gm- and fungi (bacteriostatic)
- Nausea, GI pain, vomiting
Aminoglycosides
- Inhibit protein synthesis – bind small ribosomal subunit
- Broad spectrum (usually Gm -) –
not effective against anaerobic
bacteria (bactericidal) - Toxic to kidneys (nephrotoxicity),
can cause deafness - inner ear and auditory nerves (ototoxicity)
Tetracyclines
- Inhibit protein synthesis – prevent tRNAs from binding small ribosomal subunit
- Broad spectrum: Gm+ and Gm-
and Mycoplasma (bacteriostatic) - Binds calcium – can stain fetus
teeth, nausea, diarrhea
Polymyxins
- Binds to and destroys LPS in outer membrane
- Gm- bacteria, (bactericidal)
- toxic to kidneys
Rifamycin
- Inhibits transcription (RNA polymerase)
- Broad spectrum - mycobacteria
and Gm+, (bacteriostatic) - no major side effects
Sulfonamides
- Inhibits folate biosynthesis, which inhibits DNA and RNA synthesis
- Broad spectrum Gm+ and Gm-
(bacteriostatic) - some allergic reactions and GI issues
Quinolones
- Inhibit DNA replication (gyrase)
- Broad spectrum Gm+ and Gm-
(bactericidal) - Tendonitis, tendon rupture
Echinocandins (mechanism of action)
- Fungal cell wall inhibitor
- affects fungi
Polyenes
- Fungal membrane inhibitor – bind ergosterols and form holes
- affects fungi and some protozoa
Azoles
- Fungal membrane inhibitor – prevent ergosterol synthesis
- affects fungi
Chloroquine/Quinine
- Inhibit metabolism (including nucleic acid synthesis) in
protozoa that cause malaria - affects protozoa
Nitroimidazoles
- Inhibits nucleic acid synthesis in protozoa
- affects protozoa
Nucleoside/Nucleotide analogs
- Inhibits viral nucleic acid synthesis
- affects viruses
Reverse Transcriptase inhibitors
- Inhibits replication of retroviruses
- affects viruses
Narrow-spectrum drugs
- Act on only a few kinds of pathogens
- use when the causative agent is known - decreases chances of killing normal bacteria
Why can’t you use antibiotics to treat viral infections?
viruses lack what antibiotics target
Differentiate between –cidal and –static antimicrobials. When might a -static antimicrobial be preferred over a -cidal one?
cidal: kills bacteria
static: inhibits growth
when we aren’t trying to kill off every bacteria - in Gm+ and Gm- situations when you aren’t wanting to get rid of one vs the other
Kirby-Bauer (disk diffusion test)
- given bacterial strain is spread on Petri dish
- Disks infused with various antibiotics are placed on the plate and incubated with the bacteria
- antibiotics then diffuse into media
MIC (minimum inhibitory concentration test)
- use broth dilution test
- bacteria is added to serial dilutions of given antimicrobial agent
- turbidity is measured to determine growth
MBC (minimum bactericidal concentration test)
- extension of MIC
- samples from clear wells are grown on plates without antimicrobial agent
- differentiates between bacteriocidal and static
topical route
- for external infections
- apply drug directly
intramuscular route
- allows drug to slowly diffuse into blood vessels
- doesn’t achieve doses as high as IV
- consider how drug affects liver and kidneys
intravenous route
- fastest delivery to blood
- continuous and steady concentrations
oral route
- easy to self-administer
- doesn’t achieve high blood concentrations
- easy for patients to miss doses
- have to consider how drug is metabolized
therapeutic range/window
the range of doses that can still achieve a therapeutic benefit without causing adverse side effects or toxicity
therapeutic dose
(index) compare the largest dose of grid that is not toxic to the drugs smallest effective dose (higher index= safer drug)
toxic dose
dose that causes adverse side effects
Outline the possible toxic effects and side effects of the specific antimicrobial agents we
discussed and the organs affected
polymyxin and ahminoglycosides: kidneys
tetracycline: fetal bones and teeth
fluroquinolones: tendon rupture and nerve damage
Explain how microorganisms acquire resistance to chemotherapeutic agents like antibiotics and how humans contribute to this; what can humans do to slow antibiotic resistance?
- cells can mature their won chromosomal genes due to selective pressure
- cells can acquire resistance genes form other bacteria using horizontal gene transfer
we can maintain proper concentration of drug and take when needed; we combat by taking drugs when necessary
Broad-spectrum drugs
- Act on many different kinds of pathogens
- use if you suspect an infection with multiple pathogens at work
