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Life sciences · Journal article
Annals of Hematology · October 15, 2026
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Abstract We evaluated the 13-year (2012–2025) evolution of infectious epidemiology in a Polish acute myeloid leukemia (AML) induction cohort, contextualizing these findings within shifting antimicrobial resistance (AMR), the SARS-CoV-2 pandemic, changing prophylaxis protocols (including fluoroquinolone cessation), and evolving diagnostic methodologies. Secondarily, we compared historical standard induction therapy (SIT) and novel targeted induction (NIT) regimens. This exploratory, retrospective, single-center study assessed induction-related infections in 219 newly diagnosed AML adults. We observationally evaluated temporal shifts in etiology and AMR, utilizing an interrupted time series approach to assess the 2018 cessation of universal fluoroquinolone prophylaxis, alongside a secondary comparison of SIT (n=189) and NIT (n=30) cohorts. The evolving infectious etiology in AML is driven by temporal, diagnostic, and ecological transitions rather than novel agents. Halting fluoroquinolone prophylaxis was clinically safe. Integrating contemporary therapies requires continuously adapting supportive frameworks to local epidemiology.Overall 30-day mortality was 8.2%. Comparing the pre-2018 (active fluoroquinolone) and post-2018 (discontinued) eras, proportional bloodstream infections (BSI; 40.6% vs. 34.7%) and multidrug-resistant organism (MDRO) rates (77.2% vs. 68.6%) decreased, without a compensatory Gram-negative surge. Concurrently, 30-day mortality dropped from 11.9% to 5.1%. Between NIT and SIT, incidences of microbiologically documented infections (53.3% vs. 51.3%), invasive fungal diseases (6.7% vs. 13.2%), and BSI (33.3% vs. 38.1%) were comparable. The higher incidence of VIM-producing Pseudomonas aeruginosa (30.8% vs. 3.3%; p=0.005) and SARS-CoV-2 (53.3% vs. 33.3%; p=0.034) in NIT was confounded by total overlap with the pandemic era and advanced molecular diagnostics. The evolving infectious etiology in AML is driven by temporal, diagnostic, and ecological transitions rather than novel agents. Halting fluoroquinolone prophylaxis was clinically safe. Integrating contemporary therapies requires continuously adapting supportive frameworks to local epidemiology.