| Summary: | We proposed the hypothesis that high-risk clones of colistin-resistant <i>K. pneumoniae</i> (ColR-Kp) possesses a high number of virulence factors and has enhanced survival capacity against the neutrophil activity. We studied virulence genes of ColR-Kp isolates and neutrophil response in 142 patients with invasive ColR-Kp infections. The ST101 and ST395 ColR-Kp infections had higher 30-day mortality (58%, <i>p</i> = 0.005 and 75%, <i>p</i> = 0.003). The presence of yersiniabactin biosynthesis gene (<i>ybtS</i>) and ferric uptake operon associated gene (<i>kfu</i>) were significantly higher in ST101 (99%, <i>p</i> ≤ 0.001) and ST395 (94%, <i>p</i> < 0.012). Being in ICU (OR: 7.9; CI: 1.43–55.98; <i>p</i> = 0.024), <i>kfu</i> (OR:27.0; CI: 5.67–179.65; <i>p</i> < 0.001) and ST101 (OR: 17.2; CI: 2.45–350.40; <i>p</i> = 0.01) were found to be predictors of 30-day mortality. Even the neutrophil uptake of <i>kfu</i>+-<i>ybtS</i>+ ColR-Kp was significantly higher than <i>kfu</i>--<i>ybtS</i>- ColR-Kp (phagocytosis rate: 78% vs. 65%, <i>p</i> < 0.001), and the <i>kfu</i>+-<i>ybtS</i>+ ColR-Kp survived more than <i>kfu</i>--<i>ybtS</i>- ColR-Kp (median survival index: 7.90 vs. 4.22; <i>p</i> = 0.001). The <i>kfu</i>+-<i>ybtS</i>+ ColR-Kp stimulated excessive NET formation. Iron uptake systems in high-risk clones of colistin-resistant <i>K. pneumoniae</i> enhance the success of survival against the neutrophil phagocytic defense and stimulate excessive NET formation. The drugs targeted to iron uptake systems would be a promising approach for the treatment of colistin-resistant high-risk clones of <i>K. pneumoniae</i> infections.
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