[Detection of inducible resistance to clindamycin in cutaneous isolates of Staphylococcus spp. by phenotypic and genotypic methods].
BACKGROUND
Resistance to macrolides, lincosamides and type B streptogramins (MLSB) in Staphylococcus isolates can be due to several mechanisms. The most important are an active efflux mechanism (MSB phenotype) and ribosomal target modification (MLSB phenotype); this latter mechanism confers resistance to all three groups of antimicrobials (MLSB resistance). Expression of MLSB resistance can be constitutive (cMLSB) or inducible (iMLSB).


METHODS
A group of 117 erythromycin-resistant Staphylococcus spp. clinical isolates from cutaneous samples were selected from 536 recent clinical isolates of this microorganism. Resistance phenotypes were determined by the double disk diffusion test. Presence of the ermA, ermC, ermB and msrA genes was detected by real time PCR.


RESULTS
The MSB phenotype was the most common, comprising 11.2% (7.2% in S. aureus and 23% in CoNS) of the erythromycin-resistant strains. The rate of iMLSB resistance was significantly higher, 7.4% (5.2% in S. aureus and 14% in CoNS), than the rate of cMLSB resistance, 3.2% (1.7% in S. aureus and 7.4% in CoNS). The msrA gene was present in all isolates with the MSB phenotype, and the ermC gene was the most common among clindamycin-resistant strains with the MLSB phenotype (constitutive or inducible).


CONCLUSIONS
The good correlation between the phenotypic (disk-diffusion) and genotypic (real time PCR) methods used allows prediction of the mechanisms of erythromycin and clindamycin resistance, provides insight into the epidemiological differences in their distribution, and is an aid to selecting the most appropriate antimicrobial therapy.
Merino-Díaz
Laura
L
Servicio de Microbiología, Hospitales Universitarios Virgen del Rocío, Sevilla, España.
Cantos de la Casa
Angel
A
Torres-Sánchez
María José
MJ
Aznar-Martín
Javier
J
D001426:Bacterial Proteins; D002981:Clindamycin / Q000378:metabolism / Q000494:pharmacology*; D003030:Coagulase / Q000235:genetics; D003199:Computer Systems; D004269:DNA, Bacterial / Q000235:genetics; D004351:Drug Resistance; D024901:Drug Resistance, Multiple, Bacterial / Q000235:genetics; D004790:Enzyme Induction; D004917:Erythromycin / Q000494:pharmacology; D015964:Gene Expression Regulation, Bacterial; D005838:Genotype; D006801:Humans; D016106:Methicillin Resistance; D008780:Methyltransferases; D008826:Microbial Sensitivity Tests / Q000379:methods*; D010641:Phenotype; D016133:Polymerase Chain Reaction / Q000379:methods; D013207:Staphylococcal Skin Infections / Q000382:microbiology; D013211:Staphylococcus aureus / Q000187:drug effects* / Q000201:enzymology / Q000235:genetics / Q000302:isolation & purification
D001426:Bacterial Proteins; D003030:Coagulase; D004269:DNA, Bacterial; D002981:Clindamycin; D004917:Erythromycin; D008780:Methyltransferases; C431709:ErmA protein, Bacteria; C035181:rRNA (adenosine-O-2'-)methyltransferase