Amikacin sulfate/clarithromycin

Abstract

showed A2058C mutation of the 23S rRNA, which had truncated erm(41) genes. S Amikacin sulfate/clarithromycin Author comment: Only one patient (K) had a last isolate (K2) resistant (MIC >64 μg mL–1) to [amikacin sulfate] . Development of antibiotic resistance in treatment of [I]nitial isolates (E1 and N1) showed inducible clarithromycin Mycobacterium abscessus infection: 5 case reports resistance (susceptible at 3–5 days but resistant by day 14) . In a study of 16 patients conducted between 1 January 2005 Acquired resistance to clarithromycin was observed in the and 28 November 2016, 5 patients [ages and sexes not stated] first and last isolates from patients M and P . were described, who developed acquired resistance to clarithromycin (4 patients) or amikacin sulfate and Daniel-Wayman S, et al. Amikacin exposure and susceptibility of macrolideclarithromycin (1 patients) during treatment of Mycobacterium resistant Mycobacterium abscessus. ERJ Open Research 5: 1-9, No. 2, Apr 2019. Available from: URL: http://doi.org/10.1183/23120541.00154-2018 abscessus infection [not all routes stated, dosages not stated]. USA 803411077 Patient K: The patient, who had Mycobacterium abscessus infection, received amikacin sulfate and clarithromycin for 1.7 years and 5.1 years, respectively. The patient had been receiving other medications concomitantly. The patient had a prior resistant isolate grown from a sample taken 324 days following the initial susceptible isolate (K1). During these 324 days, the patient received inhalation therapy with amikacin sulfate for 241 days. The patient was found to have the last isolate (K2) resistant to amikacin sulfate with MIC >64 μg/mL. Previously, this patient’s first isolate was susceptible to amikacin sulfate with MIC 16 μg/mL. The isolate K2 had an A1408G mutation of the 16S rRNA, which was known to confer aminoglycoside resistance in Mycobacterium abscessus. In the time between isolate K1 and isolate K2, the patient received amikacin sulfate for 611 days, including IV amikacin sulfate for 30 days. Additionally, the isolate K2, which had a full-length erm(41), exhibited an acquired resistance to clarithromycin (A2058G mutation of the 23S rRNA) with MIC >16 μg/mL. Patient E: The patient, who had Mycobacterium abscessus infection, received clarithromycin and amikacin sulfate for 3.3 years and 2.4 years, respectively. The patient had been receiving other medications concomitantly. The patient exhibited inducible clarithromycin resistance. Initially, the patient was susceptible to clarithromycin; however, the patient developed resistance by day 14. The first isolate E1 was identified as Mycobacterium abscessus subsp. abscessus, and the last isolates (E2-1 and E2-2) were identified to be Mycobacterium abscessus subsp. massiliense. Isolate E2-1 and isolate E2-2 were found to be susceptible to clarithromycin after 14 days with MIC ≤2 μg/mL and harboured truncated erm(41) genes. Based on the results of the genetic sequencing of four genes, isolate E1 was noted to be a different strain from isolate E2-1 and isolate E2-2. Also, isolate E2-1 and isolate E2-2 were found to be genetically indistinguishable from each other. Patient N: The patient, who had Mycobacterium abscessus infection, received clarithromycin and amikacin sulfate for 1.8 years and 1.3 years, respectively. The patient had been receiving other medications concomitantly. The patient exhibited inducible clarithromycin resistance. Initially, the patient was susceptible to clarithromycin; however, the patient developed resistance by day 14. The first isolate N1 was identified as Mycobacterium abscessus subsp. abscessus, and the last isolates (N2-1 and N2-2) were identified to be Mycobacterium abscessus subsp. massiliense. Isolate N2-1 and isolate N2-2 were found to be susceptible to clarithromycin after 14 days with MIC ≤2 μg/mL and harboured truncated erm(41) genes. Based on the results of the genetic sequencing of four genes, all the 3 isolates were found to be genetically distinct from each other, and they were classified as different strains. Patient M: The patient, who had Mycobacterium abscessus infection, received clarithromycin and amikacin sulfate. The patient had been receiving other medications concomitantly. The patient acquired resistance to clarithromycin. The first and last isolates showed A2058C mutation of the 23S rRNA, which had truncated erm(41) genes. Patient P: The patient, who had Mycobacterium abscessus infection, received clarithromycin and amikacin sulfate for 1.2 years and 3 years, respectively. The patient had been receiving other medications concomitantly. The patient acquired resistance to clarithromycin. The first and last isolates 1