Comparative evaluation of the effect of different growth media on in vitro sensitivity to azithromycin in multi-drug res
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SHORT REPORT
Comparative evaluation of the effect of different growth media on in vitro sensitivity to azithromycin in multi-drug resistant Pseudomonas aeruginosa isolated from cystic fibrosis patients Michael Sörensen1,2*, Bakhodur Khakimov1, Dennis Nurjadi1, Sébastien Boutin1, Buqing Yi3, Alexander H. Dalpke1,3* and Tatjana Eigenbrod1,4*
Abstract Long-term treatment with azithromycin is a therapeutic option in Cystic Fibrosis (CF) patients chronically infected with P. aeruginosa. It was recently shown that azithromycin has direct antimicrobial activity when P. aeruginosa isolates are tested in Roswell Park Memorial Institute medium supplemented with fetal calf serum (RPMI 1640/FCS) by broth microdilution. We now investigated whether (i) azithromycin might also be active against multidrug resistant (MDR) P. aeruginosa isolated from CF patients and (ii) how in vitro sensitivity assays perform in synthetic cystic fibrosis sputum medium (SCFM), a medium that mimics the particular CF airway environment.In 17 (59%) out of 29 MDR P. aeruginosa CF isolates MICs for azithromycin ranged between 0.25 and 8 μg/ml and 12 isolates (41%) showed a MIC ≥512 μg/ ml when measured in RPMI/FCS. In contrast, MICs were ≥ 256 μg/ml for all P. aeruginosa MDR isolates when tested in either SCFM or in conventional cation-adjusted Mueller Hinton Broth. High MIC values observed in CF adapted medium SCFM for both PAO1 and MDR P. aeruginosa CF isolates, as opposed to findings in RPMI, argue against routine azithromycin MIC testing of CF isolates. Keywords: Cystic fibrosis, Pseudomonas aeruginosa, Multidrug resistance, Broth microdilution, Azithromycin, SCFM Background Cystic fibrosis (CF) is a chronic disorder caused by autosomal-recessive mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Airway infections with Pseudomonas aeruginosa (P. aeruginosa) *Correspondence: m.soerensen@labor‑enders.de; [email protected]; tatjana.eigenbrod@slk‑kliniken.de 1 Department of Infectious Diseases, Medical Microbiology and Hygiene, Heidelberg University Hospital, 69120 Heidelberg, Germany 2 Laboratory Enders and Partners, 70193 Stuttgart, Germany 3 Institute of Medical Microbiology and Hygiene, Medical Faculty, Technische Universität Dresden, Fetscherstraße 74, 01307 Dresden, Germany Full list of author information is available at the end of the article
are common in CF patients. They are associated with a decline in lung function, thereby contributing to increased mortality [1]. Current therapeutic strategies aim at eradicating initial or first infection with P. aeruginosa. When eradication fails, chronic infection can develop and then therapy tries to suppress P. aeruginosa load [2, 3]. Yet, antibiotic targeting of P. aeruginosa can be challenging as approximately 20% of P. aeruginosa positive patients have been reported by the North American CF registry to carry multidrug resistant (MDR) strains, as defined by resistance to all routinely tested antibiotics in two or more of the following classes: β-lac
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