Microbiology Flashcards
How do sulfonomides work? What can we use these guys on?
Bacteriostatic agent
Stops Folic Acid (B9) synthesis
We can use these guys on a broad spectrum
(Another sulfa drug, PAS, we only use on Myco TB, and it specifically targets TB folic acid synthesis)
Trimethoprim function
StopsDHF from turning to THF, so the Folic acid already made by the bacteria can’t be used. Works great when given with sulfa drugs.
However, Trimethoprim Treats Marrow Poorly, be careful.
We can use these on a broad spectrum
Discuss who RNA Pol. Inhibitors work and what we can target with them
RNA Polymerase inhibitors all begin with “Rif-“
Very Narrow window, only with Gram positives, Neisseris and Mycobacter
This is a bacteriacidal agent that binds the beta subunit of prokaryotic RNA polymerase to prevent new transcription.
It can’t break through human mitochondria, so people are safe
How do quinolones work and what can we use them on?
Quinolones that we use are anything that ends in Floxacin, which are broad spectrum with a hankering for pseudomonas, and nalidixic acid, which only works on gram negative UTI infections
These guys care bacteriacidal and inhibit DNA replication through Topoisomerases 2 and 4, leading to defunct DNA gyrase.
Quinolones hurt the bones
Nitroimidazoles work on what and how?
Gram negative anaerobes like H. Pylori
These guys directly damage DNA by having the bacteria directly make the bad product, so humans are safe.
What do we use our membrane inhibitors Daptomycin, polymixins, and -tracins on?
UTI bacteria like Pseudomonas and Acinetobacter.
Bacitracin specifically inhibits cell wall synthesis with peptidoglycan as an added function, they all disrupt cell membranes.
Linezolid affects what? How does it work?
Linezolid is bacteriacidal on Strep and static against staph and enterococcus. It binds to the 50s unit to inhibit the formation of the 70s ribosomal complex
Discuss aminoglycosides, what they target and how they work
Most “-mycins” that are broad spectrum bacteriacidals not too good against intracellular bacteria
They interfere with 30s ribosomal unit function and create an unstable 30 s subunit, stopping protein synthesis initiation.
These guys cause red man syndrome (skin flushing) and NOT many side effects (Nephro, ototoxicity, teratogen)
What are B-lactams and how do they function?
B-lactams are our cillins and bactams, like PCN. They are typically broad spectrum although PCN not so much.
They bind transpeptidases to inhibit cell wall cross-linking.
B-lactamase enzymes made by a bacteria can break these guys down
Our beta lactams target transpeptidases, but making B-lactamase can make a bacteria immune to this type of target. What can we give when this happens?
Give Vancomycin, a glycopeptide that inhibits transglycosylation of cell walls
“2-D-ala’s for vandalism (Binds D-Ala dimer)
Awesome so Vanco should work all the time!
When does it fail…
So if PCN was jacked up due to B-lactamase by the bacteria, and you tried Vanco, you’re probably good until the bacteria get their VanA gene.
Macrolides vs. Ketolides
Macrolides like azithromycin, clarithromycin, and erythromycin don’t work on very many things, just some gram positives. They are bacteriostatic and “macrolides prevent protein slides”, meaning that prevent elongation, tRNA release and transpeptidation, essentially blocking up 50s units.
Ketolides bind 50s very strongly, two of them in fact. Depending on the species, it may be bacteriocidal or static.
How do streptogramins work and what are they similar to?
All drugs that end in “-pristin” are statics, Synercid is bacteriocidal
Narrow scope of effect. Targets staph and strep though which is nice.
Super similar to macrolides and attack the 50s
