Abstract
Spiramycin, a macrolide antibiotic consisting of a 16-membered lactone ring with three sugar moieties, stimulates the dissociation of peptidyl-tRNA from ribosomes during the protein elongation cycle and induces rapid polyribosomal breakdown. Spiramycin is close to erythromycin in the spectrum of effects; their higher minimal inhibitory concentrations in some microbial species are mostly compensated by the identical minimal bactericidal concentrations of both antibiotics.
Spiramycin reduces the capability of staphylococci and streptococci to adhere to cells of the human buccal cavity and has a twice as long postantibiotic effect compared to erythromycin. Resistance to spiramycin, as well as to other macrolides, is most commonly due to ribosomal methylation or due to another mechanism.
The active efflux pump that inhibits the effect of 14- and 15-membered macrolides does not cause resistance to spiramycinu and other 16-membered macrolides and lincosamides. Oral spiramycin is readily absorbed; its bioavailability is 33-39 % (range 10-69 %), but is reduced by about 50 % when the drug is given with meals.
Spiramycin has been in use for years and is highly effective: it concentrates in cells to be slowly released over a long period of time. It has a probiotic effect by stimulating protective mechanisms against pathogens and an important postantibiotic effect.
An added advantage is its low toxicity that makes it suitable for pediatric use.