<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Fraile-Ribot PA</submitter><funding>Ministerio de Economía, Industria y Competitividad, Gobierno de España</funding><pagination>e0098621</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8370190</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>65(9)</volume><pubmed_abstract>The mechanisms underlying an &lt;i>in vivo&lt;/i> switch in the resistance phenotype of P. aeruginosa after ceftazidime-avibactam treatment was investigated. The initial isolate (a blood culture) was resistant to meropenem but remained susceptible to antipseudomonal cephalosporins and combinations with β-lactamase inhibitors. One week after ceftazidime-avibactam therapy, a subsequent isolate (a rectal swab) recovered from the same patient showed the opposite phenotype. Whole-genome sequence analysis revealed a single SNP difference between both (ST235) isolates, leading to a P162S change in &lt;i>bla&lt;/i>&lt;sub>GES-5&lt;/sub>, creating &lt;i>bla&lt;/i>&lt;sub>GES-15&lt;/sub>. Thus, &lt;i>bla&lt;/i>&lt;sub>GES-1&lt;/sub>, &lt;i>bla&lt;/i>&lt;sub>GES-5&lt;/sub>, and &lt;i>bla&lt;/i>&lt;sub>GES-15&lt;/sub> were cloned and expressed in the wild-type strai</pubmed_abstract><journal>Antimicrobial agents and chemotherapy</journal><pubmed_title>&lt;i>In Vivo&lt;/i> Evolution of GES β-Lactamases Driven by Ceftazidime/Avibactam Treatment of Pseudomonas aeruginosa Infections.</pubmed_title><pmcid>PMC8370190</pmcid><funding_grant_id>RD16/0016</funding_grant_id><funding_grant_id>PI18/00076</funding_grant_id><funding_grant_id>PI21/00017</funding_grant_id><pubmed_authors>Oliver A</pubmed_authors><pubmed_authors>Mulet X</pubmed_authors><pubmed_authors>Fernandez J</pubmed_authors><pubmed_authors>Gomis-Font MA</pubmed_authors><pubmed_authors>Forcelledo L</pubmed_authors><pubmed_authors>Lopez-Causape C</pubmed_authors><pubmed_authors>Fraile-Ribot PA</pubmed_authors></additional><is_claimable>false</is_claimable><name>&lt;i>In Vivo&lt;/i> Evolution of GES β-Lactamases Driven by Ceftazidime/Avibactam Treatment of Pseudomonas aeruginosa Infections.</name><description>The mechanisms underlying an &lt;i>in vivo&lt;/i> switch in the resistance phenotype of P. aeruginosa after ceftazidime-avibactam treatment was investigated. The initial isolate (a blood culture) was resistant to meropenem but remained susceptible to antipseudomonal cephalosporins and combinations with β-lactamase inhibitors. One week after ceftazidime-avibactam therapy, a subsequent isolate (a rectal swab) recovered from the same patient showed the opposite phenotype. Whole-genome sequence analysis revealed a single SNP difference between both (ST235) isolates, leading to a P162S change in &lt;i>bla&lt;/i>&lt;sub>GES-5&lt;/sub>, creating &lt;i>bla&lt;/i>&lt;sub>GES-15&lt;/sub>. Thus, &lt;i>bla&lt;/i>&lt;sub>GES-1&lt;/sub>, &lt;i>bla&lt;/i>&lt;sub>GES-5&lt;/sub>, and &lt;i>bla&lt;/i>&lt;sub>GES-15&lt;/sub> were cloned and expressed in the wild-type strai</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Aug</publication><modification>2025-04-22T09:57:23.19Z</modification><creation>2025-04-05T23:23:17.013Z</creation></dates><accession>S-EPMC8370190</accession><cross_references><pubmed>34125593</pubmed><doi>10.1128/aac.00986-21</doi><doi>10.1128/AAC.00986-21</doi></cross_references></HashMap>