Mechanisms of antibiotic resistance? Also, spleen w/bacterial clearance?

[bomgd3]

Hey everyone, my test is Friday and I've realized that I keep getting antibiotic resistance questions wrong because FA does not list all of them.

Can you guys please suggest some very simple, high-yield ways to learn the resistance mechanisms? UWorld asks about many more mechanisms of resistance than the paltry few in FA, but I've yet to find anything better.

Another question: How exactly does the spleen clear encapsulated bacteria? I haven't found anywhere that is explicit. Since the capsule is supposed to help escape phagocytosis, how does c3b opsonization + phagocytosis clear the SHiNs?

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[Phloston]

Hey everyone, my test is Friday and I've realized that I keep getting antibiotic resistance questions wrong because FA does not list all of them.

Can you guys please suggest some very simple, high-yield ways to learn the resistance mechanisms? UWorld asks about many more mechanisms of resistance than the paltry few in FA, but I've yet to find anything better.

I haven't come across any particularly awesome way to memorize these. I've just bit the bullet and memorized them.

Somewhat drug-unique mechanisms:

Aminoglycosides: phosphorylation, acetylation, adenylation (perhaps PAPA)
Macrolides: decreased influx
Tetracyclines: increased efflux
Chloramphenicol: plasmid-encoded acetyltransferase that inhibits drug

Shared mechanisms:

Modified ribosomal binding site (23S rRNA): macrolides, chloramphenicol

I'm actually over-simplifying it (going off the top of my head here). There are a few more, if someone else wants to fill in the gaps.

However I also remember that all antibiotic resistance is plasmid-encoded, except for fluoroquinolones (mutated gyrase), which is chromosome-encoded.

Another question: How exactly does the spleen clear encapsulated bacteria? I haven't found anywhere that is explicit. Since the capsule is supposed to help escape phagocytosis, are we left assuming that immunoglobulins clear the SHiN+salmonella bugs?

As far as encapsulated bacteria are concerned, it has been my understanding that they require opsonization for eradication, which necessitates IgM/G binding to the capsule using the Fab fragment; complement then binds to the Fc regions of these same Igs, enabling macrophages to phagocytose. Because the cords of Billroth of the spleen house ~50% of the body's reservoir of cells of monocytic lineage and the spleen itself is such a prominent secondary lymphoid organ, hypo- or asplenia results in decreased phagocytosis of opsonized pathogens.

I'm fairly sure Klebisella also falls into this category.

Someone please add to that if I'm missing something.

 

[bomgd3]

Thanks phloston, your posts are always very helpful! However, FA says macrolide resistance is due to 23s binding site methylation.