There are two main mechanism
of resistance to macrolides: i) modification by methylation, ii) reduced
intracellular accumulation due to decreasedinflux or increased efflux of the
drug

 

Pneumococci and
staphylococci have an enzyme that can methylates a specific adenine
residue(A2058)..After methlyation with A2058, bacteria can not bind macrolides
and bacteria resistant to these agents.

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Methylation of A2058 reasons resistance to
clindamycin, a lincosamide, and to streptogramin type B antibiotics (e.g.,
quinupristin) Methylation or substitution of A2058 changes the major contact
site for

the drugs. The erythromycin- resistance
methylase genes (erm genes) codes methylase. Lots of of bacteria such as
pneumococci and staphylococci describes methylase genes . The erm genes are
expressed both constitutively and by induction. If it is expressed
constitutively, the bac- teria test positive in terms of MLSB resistance. Otherwise,
the isolates test positive in terms of resistance to macrolides. The resistance
of MLSB is showed by using a disk approximation test. In pneumococci  erm gene usually expressed constitutively.

 

Reduced intracellular
accumulation due to decreased in flux or increased efflux of the drug is the
other common mechanism of macrolide resistance in pneumococci. Strains that
have this resistance mechanism have the macrolide efflux pump, that uses energy
to remove macrolides from the inside of the bacteria. Therefore, the macrolide
could not reach inside the cell (the ribosome).

 Macrolide efflux gene (meJ) codes the efflux
pump.The mechanism of macrolide resistance  consist mutations that influence ribosomal
proteins or RNA . For instance, the strains that include point mutations of
A2059 have  resistance because macrolides
can not bind to their ribosomes. Some mutations or amino acid insertions
influence ribosomal proteins and can produce macrolide resistance .