Dd - Antibiotic Resistance Mechanisms

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o Resistance transfer factors (RTFs):

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plasmids that can self-replicate and transfer themselves to nearby bacteria (ie conjugation).

carry oriR genes for own replication

tra genes for own transfer one bacterium to another

RTFs may or may not carry genes encoding antibiotic resistance

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o Integrons:

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DNA sequences that allow the capture and integration of genes from external DNA sources.

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chloramphenicol's influence on humans

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can induce aplastic anemia in humans.

still used in animal feed lots

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IS elemetns

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pieces of DNA that carry genes encoding proteins (transposases) for their own transmission from one replicon to another

hop from one DNA source to antoher (plasmid, chromosome, etc)

CANNOT replicated themselves autonomously

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Transposon

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one or more genes (which can convey antimicrobial resistance) flanked by insertion sequences. This means that the entire IS-gene-IS complex can jump between DNA sources. They cannot replicate by themselves either.

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o Conjugative transposons:

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can't replicate by themselves, but these are transposons whose genes encode the RTF-like ability to jump from microorganism to microorganism.


require another replicon (plasmid, bacteriophage, chromosome) for survival

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beta lactam

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penicillins, cephalosporins, carbapenems and monobactams have beta lactam rings

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beta lactamase

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bacteria express beta lactamase to resist beta lactam antibiotics (PCN, CEPH, carbapenems, monobactams)

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augmentin

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amox and clavulanic acid

amox is a beta lactam antibiotic

clav is a beta lactamase inhibitor

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biochemical and physiological mechanisms of resistance

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i) alter defensive fxns of bacteria by changing target of drug

ii) detoxifying the drug enzymatically

iii) ejecting the antibiotic

iv) routing metaboic pathways around the point disrupted by the antibiotic

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biofilms

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resistant structure produced by bacteria

e.g. beta lactams cannot kill organisms that are not growing yet are still viable so biofilms block these antibiotics

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mutatino in ribosomal protein can result in resistance to what type of antibiotic

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aminoglycoside

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mutaiton in cell wall structure can lead to what type of antibiotic resistance

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beta lactam

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examples of enzymatic alteration of the antibiotic target

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vancomycin resistance - series of enzymes that alter the peptidoglycan precursor of vancomycin

erythromycin - methylation of the antibiotic target, a ribosomal lprotein - the gene encoding the enzyme is regulated by erythromycin

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what do aminoglycoside modifying enzymes do

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phosphorylate,
adenylate, or
acetylate aminoglycosides


can lead to AG resistance

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efflux pumps

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transport antibiotic out of the cell

e.g. tetracycline resistance

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what mechanism is mainly seen in tetracycline resistance and pseudomonas aeruginosa

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efflux pump

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examples of alteration in the expression of endogenous genes that lead to antimicrobial resistance

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-mutation in promotoer of a gene encoding a porin thats requried for uptake of antibiotic

-mutation in promoter of an inducible gene (e.g. encoding beta lactamase) --> expression of enzyme that inactivates antibiotic

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sulfonamides

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inhibit enzyme dihydrofolate reductase

--> interferes folic acid and pyrimidine synthesis in bacteria cells


organisms may develop resistance to antimicrobial agents by mutation leading to overproduction of PABA or structural changes in the metabolic enzyme dihydrofolate reducatase.

lower affinity for drug

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Intrinsic resistance

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Gram-negative bacteria are intrinsically penicillin-resistant due to outer membrane buffer

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acquired resistance

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mutation or acquired DNA produces resistance

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Innate resistance:

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many bacteria produce biofilms-- a matrix coating the bacteria that keeps it mainly in a quiescent (nondividing) state. Since most antibiotics work only on actively dividing bacteria, this matrix provides some resistance. Notice that bacteria don't have to divide to secrete toxin.

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Mutational alteration of the antibiotic target:

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for example, a tandem repeat region expansion of the transpeptidase where beta-lactam binds can reduce or eliminate penicillin efficacy. This mechanism is less likely to be clinically significant, but there are exceptions (eg. M. tuberculosis).