ArticleBMC research notes2026
The resistance mechanisms and risk factors of carbapenem-resistant Klebsiella pneumoniae to ceftazidime-avibactam.
Article in BMC research notes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
objectiveThis study aimed to investigate the molecular epidemiological characteristics of carbapenem-resistant Klebsiella pneumoniae (CRKP), elucidate the mechanisms underlying ceftazidime-avibactam (CZA) resistance and identify the risk factors associated with the emergence of CZA resistance. Clinical and microbiological data from 292 hospitalized patients with CRKP infections were retrospectively collected at the First Affiliated Hospital of Xi'an Jiaotong University from January 2024 to March 2025. Ptients were categorized into CZA-susceptible (n=228) and CZA-resistant (n=64) CRKP groups based on the findings of CZA susceptibility testing. A total of five carbapenemase genes (blaKPC, blaNDM, blaVIM, blaIMP and blaOXA) were identified by the lateral flow assay and their respective subtypes of the genes was identified by PCR amplification followed by sanger sequencing. The relative expression of blaKPC was quantified using real-time quantitative PCR (RT-qPCR). Independent risk factors for CZA-resistant CRKP infections were identified using multivariate logistic regression analysis.
resultsAmong the 292 CRKP isolates, a total of 64 were CZA-resistant CRKP strains. Among these, isolates co-producing KPC and NDM accounted for 42.18%; those producing NDM alone accounted for 35.94%, those producing KPC alone accounted for 15.63%, isolates co-expressing NDM and IMP accounted for 1.56%, and carbapenemase-negative isolates accounted for 4.69%. Among the 10 KPC-only producing isolates, 8 were KPC mutants, including five harboring blaKPC-33, two harboring blaKPC-90 and one harboring blaKPC-78. Additionally, the relative gene expression levels of two blaKPC-2 isolates increased by 2.80- and 3.07-fold, respectively. This study demonstrates that, alongside MBLs, mutated KPC variants serve as the predominant mechanism underlying high-level CZA resistance. The multivariate logistic regression analysis showed that the patients receiving renal replacement therapy (OR = 2.611, 95 % CI: 1.192 - 5.721) and those with previous exposure to CZA (OR = 2.749, 95 % CI: 1.269 5.953) were independent risk factors for CZA-resistant CRKP infections.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.