ena-STUDY-UNIVERSITY OF LEIPZIG-03-04-2017-20:50:15:204-472
We report the reconstruction of transmission pathways by using WGS and phylogenetics in comparison to descriptive epidemiology in a major outbreak of KPC-2-producing ST258 Klebsiella pneumoniae (Kp). 152 isolates from 89 outbreak patients and 23 Kp strains not linked to the outbreak underwent WGS.
We report the reconstruction of transmission pathways by using WGS and phylogenetics in comparison to descriptive epidemiology in a major outbreak of KPC-2-producing ST258 Klebsiella pneumoniae (Kp). 152 isolates from 89 outbreak patients and 23 Kp strains not linked to the outbreak underwent WGS. Phylogenetic analysis was performed blinded to clinical data and based on the genomic reads. A patient from Greece was confirmed as source of the outbreak. Transmission pathways for 11/89 patients (12.4%) were plausibly explained by descriptive epidemiology, applying strict definitions. For 5/11 patients and additional 15 cases (22.5%) transmissions were proven by phylogenetics. The phylogenetic clarification rate increased significantly from 8/66 (12.1%, time period before) to 12/23 patients (52.2%, time period after; P<0.001) after implementation of systematic screening for KPC-2-Kp (33,623 screening investigations within 11 months). Using descriptive epidemiology, extensive screening showed no significant effect (7/66 patients [10.6%] vs. 4/23 patients [17.4%]; P=0.465). Phylogenetic analysis suggested a contaminated positioning pillow to serve as a reservoir for the persistence of KPC-2-Kp, causing transmission to 8 ICU patients. In conclusion, our study indicates that extensive screening combined with phylogenetic analysis based on WGS should be started as soon as possible in a bacterial outbreak situation.
We report the reconstruction of transmission pathways by using WGS and phylogenetics in comparison to descriptive epidemiology in a major outbreak of KPC-2-producing ST258 Klebsiella pneumoniae (Kp). 152 isolates from 89 outbreak patients and 23 Kp strains not linked to the outbreak underwent WGS. Phylogenetic analysis was performed blinded to clinical data and based on the genomic reads. A patient from Greece was confirmed as source of the outbreak. Transmission pathways for 11/89 patients (12.4%) were plausibly explained by descriptive epidemiology, applying strict definitions. For 5/11 patients and additional 15 cases (22.5%) transmissions were proven by phylogenetics. The phylogenetic clarification rate increased significantly from 8/66 (12.1%, time period before) to 12/23 patients (52.2%, time period after; P<0.001) after implementation of systematic screening for KPC-2-Kp (33,623 screening investigations within 11 months). Using descriptive epidemiology, extensive screening showed no significant effect (7/66 patients [10.6%] vs. 4/23 patients [17.4%]; P=0.465). Phylogenetic analysis suggested a contaminated positioning pillow to serve as a reservoir for the persistence of KPC-2-Kp, causing transmission to 8 ICU patients. In conclusion, our study indicates that extensive screening combined with phylogenetic analysis based on WGS should be started as soon as possible in a bacterial outbreak situation.