Evidence map›Paper›PMID 39514175›Full record

ArticleInfection2025

In vivo divergent evolution of cross-resistance to new β-lactam/β-lactamase inhibitor combinations in Pseudomonas aeruginosa following ceftazidime/avibactam treatment.

Heng Cai, Minhua Chen, Yue Li, Nanfei Wang, Hanming Ni, Piaopiao Zhang, Xiaoting Hua, Yunsong Yu

Abstract read
PubMed Publisher
In one paragraph

Article in Infection, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Heng Cai *Department of Infectious Diseases, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Minhua Chen *Department of Infectious Diseases, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Yue LiDepartment of Infectious Diseases, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Nanfei WangDepartment of Infectious Diseases, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Hanming NiDepartment of Infectious Diseases, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Piaopiao ZhangDepartment of Infectious Diseases, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xiaoting HuaDepartment of Infectious Diseases, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China. XiaotingHua@zju.edu.cn.
Yunsong YuDepartment of Infectious Diseases, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China. yvys119@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo describe and characterize the evolutionary process of cross-resistance to ceftazidime/avibactam, ceftolozane/tazobactam and imipenem/relebactam of a carbapenem-resistant Pseudomonas aeruginosa (CRPA) lineage isolated from a patient receiving two courses of ceftazidime/avibactam treatment.

methodsThe minimum inhibitory concentrations (MICs) of strains were determined by broth microdilution methods. The mutant genes were identified by the whole genome sequencing results. Cloning, knockout and complementation experiments were used to evaluate the impact of the resistance relative genes on the MICs. Reverse transcription-quantitative PCR was used to evaluate the relative expression of ampC and mexA. The fitness cost was measured by growth curve tests.

resultsA total of 24 CRPA strains were isolated encompassing the whole ceftazidime/avibactam treatment. The CRPA strains developed high-level resistance to ceftazidime/avibactam and cross-resistance to ceftolozane/tazobactam or imipenem/relebactam, clustering into clade A and clade B, respectively. In both clades, the overexpression of AmpC was crucial to ceftazidime/avibactam resistance, which was driven by AmpD deficiency in clade A and dacB mutation in clade B, respectively. In clade A, mraY mutation and a new allele of AmpC (bla

conclusionDivergent resistance evolution resulted in a complex phenotype in the CRPA lineage, posing significant challenge to clinical treatment. The resistance surveillance needs to be prioritized, and new therapeutic strategies are urgently required.

Indexed as

Anti-Bacterial AgentsAzabicyclo Compoundsbeta-Lactamase InhibitorsCeftazidimeDrug Resistance, Multiple, BacterialPseudomonas aeruginosaPseudomonas InfectionsBacterial Proteinsbeta-LactamasesDrug CombinationsHumansImipenemMicrobial Sensitivity TestsTazobactamAnti-Bacterial Agentsavibactam, ceftazidime drug combinationAzabicyclo CompoundsBacterial Proteinsbeta-Lactamase Inhibitorsbeta-LactamasesCeftazidimeDrug CombinationsImipenemTazobactamCeftazidime/avibactamCeftolozane/tazobactamCross-resistanceImipenem/relebactamPseudomonas aeruginosaResistance evolution

Identifiers

PMID39514175

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.