Abstract
Abstract Objective: This study aimed to determine prevalence of inducible and constitutive clindamycin resistance among clinical S. aureus isolates and also study their association with methicillin resistance. Methods: A cross-sectional study including 140 non-duplicate isolates of S. aureus was done. Isolates were identified by standard microbiological methods and methicillin resistance was detected by cefoxitin disc diffusion method. Inducible clindamycin resistance was detected by D-test. Results: Prevalence of inducible and constitutive clindamycin resistance was 12.10% and 7.90% respectively. Constitutive and inducible resistance was associated with MRSA. An unusual phenotype, erythromycin sensitive and clindamycin resistance, was detected in 2 MRSA isolates. Conclusions: Inducible and constitutive clindamycin resistance is low in our setting. Constitutive and inducible resistance was associated with MRSA. However the trends in resistance vary in different places. D-test reporting should be done routinely which will allow clinicians to opt for clindamycin judiciously and avoid potential treatment failure. Keywords: Clindamycin resistance, MLSBi, D-test, MRSA, Nepal
Highlights
Antimicrobial resistance in Staphylococcus aureus has become an ever-increasing problem
An unusual phenotype showing erythromycin sensitive and clindamycin resistant was seen in 2 isolates both of which were Methicillin resistant S. aureus (MRSA)
Both MLSBi and MLSBc phenotypes predominated in MRSA strains (P=0.014)
Summary
Antimicrobial resistance in Staphylococcus aureus has become an ever-increasing problem. Methicillin resistant S. aureus (MRSA) which are often multiply resistant to other classes of antibiotics in addition to β–lactams, often presents difficulties in therapy. The macrolide-lincosamide-streptogramin B (MLSB) family of antibiotics is commonly used in the treatment of staphylococcal infections [1]. An erm gene encodes methylation of the 23S rRNAbinding site that is shared by these drugs. Such resistance can be constitutive (MLSBc phenotype) or inducible (MLSBi phenotype) [6]. It is possible for mutations to occur spontaneously that will transform MLSBi strains to MLSBc phenotype without the presence of a macrolide inducer, a concern being that this change might occur in the midst of therapy [7]
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