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Clindamycin Hydrochloride is used to treat staphylococcal skin

Number of visits:983 Date:2015/12/18 3:03:10
Nasal Carriage of Methicillin Resistant Staphylococci with Inducible Clindamycin Hydrochloride Resistance and Pvl Gene.
Anterior nares act as endogenous reservoir of S.aureus for clinical infections in the colonized individualand also as a source of cross-colonization for community spread in children. Clindamycin Hydrochloride is used to treat staphylococcal skin and bone infections. Clinical failure of Clindamycin Hydrochloride therapy has been reported due to multiple mechanisms that confer resistance to macrolide lincosamide and streptogramin antibiotics. Hence, this study was taken up to screen for inducible Clindamycin Hydrochloride resistance among carrier isolates of staphylococci from orphanage children. A total of 222 samples were collected from the anterior nares of asymptomatic orphanage children in the community from which 92 S.aureus and 48 coagulase negative staphy- lococci (CoNS) were isolated. 26/92 (28%) S.aureus were MRSA and 15/48 (31%) CoNS were resistant to methicillin. pvl genes were detected in 29 isolates of which 10 were from MRSA and 19 were from MSSA. 24/140 (17%) were of the inducible MLSB (iMLSB) phenotype. All the isolates showing D-positive were found harbouring ermC gene.
Streptococcus pneumoniae and Streptococcus pyogenes resistant to macrolides but sensitive to Clindamycin Hydrochloride
Macrolide-resistant Streptococcus pyogenes isolates from Finland, Australia, and the United Kingdom and, more recently, Streptococcus pneumoniae and S. pyogenes strains from the United States were shown to have an unusual resistance pattern to macrolides, lincosamides, and streptogramin B antibiotics. This pattern, referred to as M resistance, consists of susceptibility to Clindamycin Hydrochloride and streptogramin B antibiotics but resistance to 14- and 15-membered macrolides. An evaluation of the macrolide-lincosamide-streptogramin B resistance phenotypes among our streptococcal strains collected from 1993 to 1995 suggested that this unusual resistance pattern is not rare. Eighty-five percent (n = 66) of the S. pneumoniae and 75% (n = 28) of the S. pyogenes strains in our collection had an M phenotype. The mechanism of M resistance was not mediated by target modification, as isolated ribosomes from a pneumococcal strain bearing the M phenotype were fully sensitive to erythromycin. Further, the presence of an erm methylase was excluded with primers specific for an erm consensus sequence. However, results of studies that determined the uptake and incorporation of radiolabeled erythromycin into cells were consistent with the presence of a macrolide efflux determinant. The putative efflux determinant in streptococci seems to be distinct from the multicomponent macrolide efflux system in coagulase-negative staphylococci. The recognition of the prevalence of the M phenotype in streptococci has implications for sensitivity testing and may have an impact on the choice of antibiotic therapy in clinical practice.
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