11/20/2022 0 Comments Vcm 2 strainThe phenomenon seems to reveal a weakness of VISA posed by its vancomycin resistance mechanism, which might provide a hint for developing a new strategy in the treatment of VISA infection.J Infect Chemother (2009) 15:274–278 DOI 10.1007/s1015-y Taken together, the results presented here show a curious negative correlation between VCM and LZD susceptibilities in MRSA. Unlike the case with LZD, there was no clear correlation between results for VCM and those for the above antibiotics. We carried out the same experiment using chloramphenicol, clindamycin, azithromycin, and quinupristin-dalfopristin. (Fig.1), 1), indicating that N315LR5-P1 becomes more susceptible to LZD as it acquires VCM resistance. Analysis of resistant subpopulations (population analysis ) of the derivative strains also showed an inverse relationship between VCM and LZD susceptibilities (Fig. Consistent with results of the first two investigations, we found that the derivative strains with higher VCM resistance had greater susceptibility to LZD and vice versa (Table (Table2). This set of isogenic laboratory-derived strains with gradual increments of VCM resistance was subjected to LZD MIC determination. The strain was cultivated in gradual increments of VCM concentrations, and isogenic resistant mutants were selected from ascending VCM concentrations of 1, 2, 3, and 4 mg/liter. The strain is a heterogeneously methicillin-resistant derivative of N315 with its mecI gene inactivated and its penicillinase plasmid eliminated ( 1, 8). Regression analysis with the above 15 triple sets confirmed the existence of a negative correlation between VCM and LZD MICs, with a correlation coefficient of −0.628 ( P < 0.01).īMean result for each strain category ( P < 0.01 ).įinally, to further confirm this negative correlation, we generated another set of isogenic strains from the VCM-susceptible laboratory strain N315LR5-P1 (VCM MIC = 0.75 mg/liter). An inverse relationship between VCM and LZD susceptibilities was again observed in most of these isogenic triple sets of VISA and their derivatives (Table (Table1). To further confirm the phenomenon, we evaluated the VCM and LZD MICs for 15 isogenic sets of clinical VISA strains, their passage-derived VCM-susceptible strains, and VISA phenotypic revertant strains using Etest strips ( 3, 4). The MICs of VCM for VSSA and VISA were 1.65 ± 0.38 and 5.16 ± 1.42 mg/liter, and those of LZD for VSSA and VISA were 2.14 ± 0.81 and 1.46 ± 0.51 mg/liter, respectively (Student's t test P < 0.01 for VISA results versus VSSA results for both VCM and LZD). The test confirmed a significant inverse relationship of VCM and LZD susceptibilities between VSSA and VISA. To evaluate VCM and LZD susceptibilities more precisely, the MICs were also determined using Etest strips (AB Biodisk, Sweden). To confirm this phenomenon, we compared VCM and LZD MICs for clinical VSSA and VISA strains, with a total number of 47 VSSA strains and 43 VISA strains ( 3), including 28 VISA strains from the network on antimicrobial resistance in S. During the susceptibility tests, quite unexpectedly, we noticed that the LZD MIC was relatively low for VISA clinical strains compared to that for VCM-susceptible S. Because VISA tends to exhibit cross-resistance to some anti-MRSA agents, such as teicoplanin and daptomycin ( 4, 9, 11), we evaluated the in vitro activity of LZD toward VISA strains isolated from various countries of the world. Since the first report of a VISA strain in 1997, VISA infection has been reported in many countries ( 2, 7). Linezolid (LZD) has been used for the treatment of nosocomial and community-acquired pneumonia, as well as complicated skin and soft-tissue infection caused by methicillin-resistant Staphylococcus aureus (MRSA), including vancomycin (VCM)-intermediate S.
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