title: Inducible clindamycin resistance and molecular epidemiologic trends of pediatric community-acquired methicillin-resistant Staphylococcus aureus in Dallas, Texas.
abstract: Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) infection occurs commonly in children. Clindamycin resistance may be inducible or constitutive, and the rates of inducible resistance in CA-MRSA that could produce clindamycin treatment failures vary worldwide. The double-disk test was performed in 197 erythromycin-resistant and clindamycin-susceptible CA-MRSA strains from children in Dallas, Texas, from 1999 to 2002 to determine inducible clindamycin resistance. Resistance mechanisms were studied by PCR; epidemiologic trends were studied by pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST). Inducible resistance was demonstrated in 28 (93%+/-6%) of 30 tested isolates in 1999, 21 (64%, +/-11%) of 33 in 2000, 12 (23%+/-7%) of 52 in 2001, and 6 (7%+/-3%) of 82 in 2002. All noninducible strains had the msr(A) gene. Among inducible resistant strains, 31 had erm(B), 24 had erm(C), and 12 had erm(A) genes. Two distinct pulsed types were the most prevalent; one of them was the most common pulsed type in 1999, whereas in 2002 a different pulsed type was prevalent. MLST analyses determined that ST-8 was the most common type, with 76%+/-5% found in 2002. All but one of these clindamycin-susceptible, erythromycin-resistant ST-8 strains showed no induction of clindamycin resistance. We conclude that, among erythromycin-resistant, clindamycin-susceptible CA-MRSA strains isolated from children in Dallas, inducible methylase resistance became less common from 1999 to 2002 (P<0.001). The phenotype of strains was associated with their sequence type. Our results demonstrate a clonal shift in CA-MRSA in Dallas children from 1999 to 2002.
authors.affiliation: University of Texas Southwestern Medical Center of Dallas, and Children's Medical Center of Dallas, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9063, USA. Susana.Chavez-Bueno@UTSouthwestern.edu
authors.forename: Susana
authors.initials: S
authors.lastname: Chavez-Bueno
authors.forename: Bülent
authors.initials: B
authors.lastname: Bozdogan
authors.forename: Kathy
authors.initials: K
authors.lastname: Katz
authors.forename: Karen L
authors.initials: KL
authors.lastname: Bowlware
authors.forename: Nancy
authors.initials: N
authors.lastname: Cushion
authors.forename: Dominick
authors.initials: D
authors.lastname: Cavuoti
authors.forename: Naveed
authors.initials: N
authors.lastname: Ahmad
authors.forename: George H
authors.initials: GH
authors.lastname: McCracken
authors.forename: Peter C
authors.initials: PC
authors.lastname: Appelbaum
mesh_terms: D000293:Adolescent; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D002981:Clindamycin / Q000494:pharmacology*; D017714:Community-Acquired Infections / Q000453:epidemiology* / Q000382:microbiology; D024881:Drug Resistance, Bacterial / Q000235:genetics; D016521:Electrophoresis, Gel, Pulsed-Field; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D016106:Methicillin Resistance; D008826:Microbial Sensitivity Tests; D017720:Molecular Epidemiology; D016133:Polymerase Chain Reaction; D017422:Sequence Analysis, DNA; D013203:Staphylococcal Infections / Q000453:epidemiology* / Q000382:microbiology; D013211:Staphylococcus aureus / Q000187:drug effects* / Q000235:genetics; D013781:Texas / Q000453:epidemiology
chemical_list: D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D002981:Clindamycin