4.2 Article

Inducible clindamycin resistance in clinical isolates of staphylococcus aureus in Suez Canal University Hospital, Ismailia, Egypt

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JOURNAL OF INFECTION IN DEVELOPING COUNTRIES
卷 14, 期 11, 页码 1281-1287

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J INFECTION DEVELOPING COUNTRIES
DOI: 10.3855/jidc.12250

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Clindamycin resistance; inducible; constitutive; MRSA; MLSB; erm genes

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Introduction: The increasing incidence of methicillin resistance among Staphylococci has led to renewed interest in the usage of macrolidelincosamide-streptogramin B (MLSB) antibiotics to treat S. aureus infections, with clindamycin being the preferable agent owing to its excellent pharmacokinetic properties. Inducible clindamycin resistance my lead to therapeutic failure. Aim: Detection of the prevalence of constitutive and inducible clindamycin resistance in clinical isolates of S. aureus to improve the clinical outcomes in patients. Methodology: A total of 176 non-duplicate staphylococcal isolates were isolated from different clinical samples. Methicillin resistance was detected using Cefoxitin disk diffusion (CDD) method. Phenotypic clindamycin resistance was performed for all isolates by D test. Polymerase Chain Reaction (PCR) assay were done for detection of erm resistance genes (ermA, ermB and ermC). Results: Out of 176 strains of S. aureus, 108 isolates (61.3%) were identified as MRSA. Erythromycin and clindamycin resistance was detected in 96 isolates (54.5%) and 68 isolates (38.6%) respectively. Clindamycin resistance (cMLSB) was significantly higher (p value < 0.001) in MRSA strains (56 isolates) compared to MSSA (12 isolates). Resistant genes were detected in 160 isolates (91%). The ermA gene was detected in 28 isolates (16%), the ermB gene was detected in 80 isolates (45.5%) (p < 0.001). Conclusions and recommendations: The frequency of constitutive and inducible clindamycin resistance in MRSA isolates emphasizes the need to use D test in routine antimicrobial susceptibility testing to detect the susceptibility to clindamycin as the inducible resistance phenotype can inhibit the action of clindamycin and affect the treatment efficacy.

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