Multiple drugs
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Acquired drug resistance and lack of efficacy: case report A 29-year-old woman acquired resistance to amikacin and ceftazidime, while being treated for Pseudomonas aeruginosa infection. Additionally, she exhibited lack of efficacy with colistin, levofloxacin and meropenem, while being treated for Pseudomonas aeruginosa infection [routes and dosages not stated]. The woman, who had end-stage cystic fibrosis lung disease, underwent bilateral orthotopic lung transplant in 2018. Her pretransplant respiratory cultures were positive for extensively-drug resistant mucoid and non-mucoid Pseudomonas aeruginosa with reduced susceptibility to carbapenems. She had been exposed to unspecified carbapenems approximately 12 months prior to transplant. On day 7 after transplant, she developed a right pleural empyema requiring a thoracic drainage. She started receiving broad-spectrum antimicrobial therapy with amikacin and ceftazidime. Respiratory cultures were collected on the same day (isolate SK76) which revealed presence of extensively-drug resistant mucoid Pseudomonas aeruginosa. SK76 displayed a reduced susceptibility to meropenem but results were negative for carbapenemase production. Thereafter, her condition worsened and infection progressed in the right pleural cavity. Therefore, on day 34, the woman was transferred to the ICU, and was treated with a right pneumonectomy. Lung biopsy cultures were collected on day 34 (isolate SK77). These cultures grew extensively-drug resistant Pseudomonas aeruginosa, resistant to carbapenems. Resistance to carbapenems had been mediated by the production of VIM-type metallo-β-lactamases. She started receiving high-dose colistin, levofloxacin and high-dose extended-infusion meropenem. She required invasive life-support measures with venous-venous extracorporeal membrane oxygenation and continuous renal replacement therapy. However, despite the aggressive antimicrobial treatment, she died on day 56. Whole genome sequencing was performed to analyse genetic variation between isolated SK76 and SK77. Investigation revealed that these two isolates SK76 and SK77 belonged to two different and unrelated Sequence Types ST253 and ST308, respectively. Furthermore, SK76 and SK77 harbored a different resistance genes content. SK76 was characterised by the following resistance determinants: aadA7, aac(6′)-Ib7, blaPDC-9, blaOXA-488, blaOXA- 20, sul1, and gyrA. However, the following resistance genes were detected in SK77: blaVIM-1, aadA7, blaPDC-7, blaPER-1, blaOXA-488, and sul1. Based on these findings and clinical presentation, it was concluded that she acquired resistance to amikacin and ceftazidime. Carugati M, et al. Fatal respiratory infection due to ST308 VIM-1-producing Pseudomonas aeruginosa in a lung transplant recipient: case report and review of the literature. 803508166 [Review]. BMC Infectious Diseases 20: No. 1, 2020. Available from: URL: http://doi.org/10.1186/s12879-020-05338-3
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