Global emergence of the widespread Pseudomonas aeruginosa ST235 clone P. Treepong, V.N. Kos, C. Guyeux, D.S. Blanc, X. Bertrand, B. Valot, D. Hocquet  Clinical Microbiology and Infection  Volume 24, Issue 3, Pages 258-266 (March 2018) DOI: 10.1016/j.cmi.2017.06.018 Copyright © 2017 European Society of Clinical Microbiology and Infectious Diseases Terms and Conditions

Fig. 1 Worldwide distribution of the 79 ST235 isolates of Pseudomonas aeruginosa which genomes were used in this study. The countries of origin of the isolates are shaded in grey. Pie chart diameters are proportional to the number of isolates collected from each country. The area of each slice is proportional to the quantity of isolates of each clade. Clinical Microbiology and Infection 2018 24, 258-266DOI: (10.1016/j.cmi.2017.06.018) Copyright © 2017 European Society of Clinical Microbiology and Infectious Diseases Terms and Conditions

Fig. 2 Phylogenetic network of ST235 Pseudomonas aeruginosa. The clades, labelled from C1 to C14 and shaded with different colours for clarity, formed two groups (Group I and Group II) separated by a dashed line. Clinical Microbiology and Infection 2018 24, 258-266DOI: (10.1016/j.cmi.2017.06.018) Copyright © 2017 European Society of Clinical Microbiology and Infectious Diseases Terms and Conditions

Fig. 3 Time of Most Recent Common Ancestor (MRCA) of Pseudomonas aeruginosa ST235 and chromosomal mutations conferring high-level resistance to fluoroquinolones, extended-spectrum cephalosporinases, and carbapenems. (a) Phylogenetic tree with time scale was calculated from the 69 genomes of isolates with known isolation date with BEAST2 using continent origin as co-variable. The estimated mutation rate was 4.85 × 10−6 (95% CI 4.59 × 10−6 to 5.15 × 10−6) per site per year. The time of MRCA is ∼30 years ago from 2014. The tips are labelled with the isolate name and are coloured by continent of origin (see insert). Names of the isolates are prefixed with the clade to which they belong. (b) Mutations in the quinolone-determining regions (QRDRs) of GyrA, GyrB, ParC and ParE, in the regulators of the cephalosporinase AmpC and in OprD. For the QRDR, the numbers of the corresponding codons in Escherichia coli are in parentheses. Black cells and white cells indicate the presence or absence of a given mutation, respectively. For mutation in each regulator of the cephalosporinase AmpC and in OprD, every single mutation is represented by a single colour. White cells indicate an intact protein. The detail of the mutations is given in the Supplementary material (Table S3). Every protein was compared with its closest homologue born by a β-lactam-susceptible isolate of P. aeruginosa (strain M18 for AmpD, AmpP, DacB; strain PA14 for AmpDh2, AmpG, AmpO, OprD; strain MBT-1 for AmpDh3, AmpR). AmpO polymorphism for all the isolates of the collection: S125T, D256E. AmpP polymorphism for all the isolates of the collection: L74F and L98F. Clinical Microbiology and Infection 2018 24, 258-266DOI: (10.1016/j.cmi.2017.06.018) Copyright © 2017 European Society of Clinical Microbiology and Infectious Diseases Terms and Conditions