Coagulase-Negative Staphylococci Isolated from Human Bloodstream Infections Showed Multidrug Resistance Profile.

Abstract

Coagulase-negative staphylococci (CNS) are important pathogens causing nosocomial infections worldwide with increasing resistance to antimicrobials. The aim of this study was to characterize resistance aspects of CNS isolated from patients with bloodstream infections acquired in hospitals in Belo Horizonte, MG, Brazil. Staphylococcus strains were characterized using repetitive sequence-based polymerase chain reaction (rep-PCR) fingerprinting with (GTG)5 primer. Phenotypic resistance was analyzed using AST-P5085 card (bioMérieuxVitek®). PCR was used to detect mecA, vanA, blaZ, ermA/B/C, aac-aphD, and SCC-mec. For statistical analyses, we used hierarchical cluster, chi-square test (χ2), and correspondence. Several clusters were formed within the same species using (GTG)5 primer, and strains showed resistance to the following antimicrobials: benzylpenicillin (100%); oxacillin (93.1%); gentamicin (36.3%); ciprofloxacin (63.7%); moxifloxacin (32.7%); norfloxacin (81.0%); erythromycin (86.2%); clindamycin (75.8%); linezolid, teicoplanin and vancomycin (1.7%); tigecycline (0%); fusidic acid (10.35%); rifampicin (13.7%); and trimethoprim/sulfamethoxazole (46.5%). Regarding genotypic analyses, 40%, 0%, 78%, 42%, 100%, 24%, and 30% were positive for mecA, vanA, blaZ, ermA, ermB, ermC, and aac-aphD, respectively. Regarding staphylococcal cassette mec (SCCmec) type, 3.4% presented type I; 5.0% type II; 27.1% type III; 20.3% type IIIA; and 32.2% type IIIB. Six clusters were formed and frequency distributions of resistant strains to oxacillin, gentamicin, ciprofloxacin, moxifloxacin, norfloxacin, erythromycin, clindamycin, linezolid, teicoplanin, vancomycin, fusidic acid, rifampicin, and trimethoprim/sulfamethoxazole, and mecA, blaZ, ermC, aac-aphD, and SCCmec type differed (p < 0.001). In conclusion, the strains investigated in this study were multidrug resistant and carried multiple antibiotic resistance genes.