complex infections are ever on the rise. To curb their increasing evolution, we performed an in-depth study of 43 clinical isolates of cystic fibrosis patients obtained from 2009 to 2020. We identified their subspecies, uncovered their genotypic resistance profiles, characterised their antibiotic-resistant genes, and assessed their phenotypic antibiotic susceptibilities. The phenotypic and genotypic methods showed total agreement in terms of resistance to clarithromycin and amikacin. Of the 43 clinical strains, 28 belonged to subsp. (65.1%), 13 to subsp. (30.2%), and 2 to subsp. (4.6%). The resistant rates for clarithromycin and amikacin, the two main drugs against complex pulmonary infections, were 64.2% and 14.2%, respectively. We found three strains of subsp. that showed heteroresistance in the and genes, and these strains also presented double-resistance since they were macrolide- and aminoglycoside-resistant. subsp. showed a high minimum inhibitory concentration (MIC) and a resistant percentage larger than or equal to 88% to cefoxitin, ciprofloxacin, moxifloxacin, doxycycline, imipenem, and trimethoprim-sulfamethoxazole. These results show a panorama of the high resistance of complex to current drugs for cystic fibrosis patients. Thus, other treatment methods are urgently needed.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10745751 | PMC |
http://dx.doi.org/10.3390/microorganisms11122897 | DOI Listing |
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