The researchers evaluated Lacticaseibacillus paracasei LYC1154, Lactiplantibacillus plantarum LYC1322 and Lacticaseibacillus rhamnosus LYC1511. Each strain was successively exposed to sublethal concentrations of ampicillin, minocycline and erythromycin. Antibiotic concentrations were adjusted as minimum inhibitory concentrations increased, and passage-matched wild-type strains served as controls. The resulting variants, identified with the suffix “ame,” showed increased MICs for several drugs, including increases exceeding 1,000-fold for erythromycin and azithromycin in two strains. The study did not test whether resistance persisted after drug withdrawal or examine genomes, so it could not distinguish transient adaptive resistance from stable acquired resistance.

The antimicrobial assay used a co-culture design intended to favor growth of the bacterial pathogens. Each clinical Enterobacterales isolate was added at 10^6 CFU/mL, while lactobacilli were added at 10^7 CFU/mL, producing a 10:1 lactobacilli-to-Enterobacterales ratio. Cultures were incubated at 37 °C under aerobic conditions and sampled after 24 and 48 hours. Parallel cultures containing the pathogen alone established the baseline growth. Recoverable Enterobacterales were measured by plating on MacConkey agar, with cultures containing fewer than 10 CFU/mL classified as below the assay’s limit of detection.

The panel comprised 17 clinical isolates from six species: five Escherichia coli, five Klebsiella pneumoniae, two Citrobacter freundii, one Citrobacter koseri, three Enterobacter cloacae and one Serratia marcescens. It represented five carbapenemase types—KPC-2, NDM, OXA-181, IMP-8 and VIM-1—and included isolates collected from sputum, rectal swabs, blood and urine. At 24 hours, the magnitude of reduction depended on the bacterial species, isolate, lactobacillus strain and whether the strain had undergone resistance induction. Some co-cultures produced counts below 10 CFU/mL, while others showed reductions ranging from more than two to more than four logarithmic units relative to the corresponding pathogen-only controls.

By 48 hours, every combination involving one of the six lactobacilli—three parental strains and three antibiotic-induced variants—had reduced all 17 isolates below 10 CFU/mL. In contrast, the Enterobacterales-only controls maintained viable counts between 10^6 and 10^9 CFU/mL. All three Citrobacter freundii and Citrobacter koseri isolates, all three Enterobacter cloacae isolates and the Serratia marcescens isolate fell below detection at both 24 and 48 hours with every lactobacillus tested. The K. pneumoniae isolates generally reached undetectable counts by 24 hours, while results for E. coli showed greater strain-to-strain variation at that point. These observations establish activity only in the tested laboratory mixture; they do not show that the strains can clear CPE from an infected person or prevent transmission.

The investigators also examined two laboratory proxies for probiotic characteristics: survival under gastrointestinal stress and adhesion to intestinal epithelial cells. Under simulated gastric conditions—PBS at pH 3.0 containing 3 mg/mL pepsin—all six strains remained viable over four hours, with reductions of less than 1.5 log10 relative to their starting counts. The induced variants appeared similar to their parental strains at both the two- and four-hour sampling points. In a separate assay, strains were exposed to 0.3% oxgall to represent physiological bile-salt conditions. Bile tolerance varied substantially by strain rather than showing a consistent advantage or disadvantage after induction.

At 24 hours in the bile assay, viable counts ranged from 5% to 107% of the corresponding bile-free controls for the wild-type strains. L. rhamnosus LYC1511 had the highest value among the parental strains, at 107%, whereas L. plantarum LYC1322 had the lowest, at 5%. The three induced variants ranged from 39% to 68%. Induction increased the relative count for LYC1322ame, from 5% for its parent to 46%, decreased it for LYC1511ame, from 107% to 68%, and produced a similar result for LYC1154ame, at 39% versus 52%. These observations were descriptive rather than inferential, because each assay used only two independent biological replicates.

Adhesion was tested on Caco-2 human colorectal adenocarcinoma cell monolayers. Each wild-type and antibiotic-induced strain was offered bacterial inocula of 10^8 or 10^9 CFU/mL and incubated with the cells for two hours. After non-adherent organisms were washed away and the cells were disrupted, attached lactobacilli were counted. All six strains attached at both inoculum densities, and the induced variants appeared to adhere similarly to their respective parental strains. No obvious loss of epithelial adhesion was therefore detected under these conditions. As with the gastrointestinal assays, the experiment used only two biological replicates, so the findings provide a qualitative comparison rather than a robust estimate of statistical differences.

The results do not establish why the variants continued to suppress CPE. Earlier work by the same research group found that lactic acid was the principal effector of wild-type lactobacilli against carbapenem-resistant Enterobacterales: neutralizing cell-free supernatants to pH 6.5 abolished the activity, whereas catalase and proteinase K treatment did not. The present experiment did not repeat those mechanistic tests on the antibiotic-induced variants. Preserved inhibition therefore does not demonstrate that the same molecular mechanism remained intact; metabolic or transcriptional changes could have altered organic-acid production or introduced other effectors. The possibility that antibiotic induction altered the strains’ physiology was not investigated directly, and no acid production or genomic analysis was reported in the study.

Several design limitations constrain how far the findings can be generalized. The co-cultures used one fixed 10:1 microbial ratio, did not include concurrent antibiotic exposure and did not measure pH. Although the induced variants had been selected with ampicillin, minocycline and erythromycin, these agents are not necessarily those used to treat CPE, and the hypothesis that the variants would remain active during clinical antibiotic therapy therefore remains untested. The isolate panel covered the five major carbapenemase types but included only one or a few isolates for several species and enzyme groups. A single induced lineage was generated for each parental strain, the induced variants were not reconfirmed by molecular species identification, and no animal or human experiments were performed. The work also relied on only two independent biological replicates per assay, limiting the strength of between-strain comparisons and making the results descriptive rather than statistically conclusive.

Safety is an especially important unresolved issue because the study deliberately produced organisms with reduced antibiotic susceptibility. Large MIC increases may reflect stable acquired resistance, yet the absence of reversibility testing, whole-genome sequencing, screening for acquired resistance genes and transfer or conjugation assays leaves the genetic basis and transferability unknown. Those analyses would be essential before the organisms could be considered for administration to patients. The results therefore remain in vitro observations that warrant mechanistic, genomic, animal and clinical investigation. They suggest that reduced susceptibility need not immediately extinguish anti-Enterobacterales activity or the laboratory traits examined, but they do not establish safety, efficacy in people or a clinical strategy for managing CPE colonization or infection.

Subject of Research: In vitro antimicrobial and probiotic characteristics of antibiotic-induced resistant lactobacilli tested against carbapenemase-producing Enterobacterales

Article Title: Antimicrobial activity of antibiotic-induced resistant lactobacilli against carbapenemase-producing Enterobacterales

Article References: Chen, S.-C., Chen, C.-C., Lai, C.-C., & Tang, H.-J. (2026). Antimicrobial activity of antibiotic-induced resistant lactobacilli against carbapenemase-producing Enterobacterales. Frontiers in Microbiology, 17, Article 1931966. https://doi.org/10.3389/fmicb.2026.1931966

Image Credits: AI Generated

DOI: 10.3389/fmicb.2026.1931966

Keywords: antibiotic-induced resistance, lactobacilli, Enterobacterales, carbapenemase, antimicrobial activity, in vitro co-culture, probiotics, gastrointestinal tolerance, Caco-2 adhesion, genomic safety testing, Antimicrobial, activity

The research team, led by Rameen Parvez and Mohsin Khurshid of the Institute of Microbiology at Government College University Faisalabad, with collaborators including James Jacob Sasanya of the International Atomic Energy Agency in Vienna, sampled three distinct tiers of the poultry economy between September 2024 and April 2025. By including commercial broiler operations, small-scale backyard flocks and retail markets, the design captured the full trajectory of poultry production from intensive rearing to point of sale. This matters because each tier represents a different interface between bacteria and humans, from farm workers exposed directly to birds and litter, to consumers handling raw meat in their kitchens.

Identification of the isolates was rigorous. The team combined conventional biochemical testing with API 20E strips, matrix-assisted laser desorption ionization time-of-flight mass spectrometry, a proteomic technique that fingerprints bacterial species by their protein profiles, and amplification of the rpoB gene, a molecular marker widely used to confirm species identity. This layered approach guards against the misidentification that has plagued some earlier surveys, since K. pneumoniae and its close relative K. oxytoca can be difficult to distinguish phenotypically. Of the 900 samples, 303, or 33.7 percent, yielded K. pneumoniae, a prevalence figure that underscores how thoroughly this organism has colonized the poultry environment.

The resistance picture that emerged was grim. Among the 303 isolates, 199, or 65.7 percent, qualified as multidrug-resistant under internationally accepted definitions, meaning they were nonsusceptible to at least one agent in three or more antibiotic classes. A further 48 isolates, 15.8 percent, were extensively drug-resistant, a category reserved for bacteria that have lost susceptibility to agents in all but one or two classes. Perhaps most tellingly, isolates from commercial broiler farms carried a heavier resistance burden than those recovered from backyard flocks or retail markets, a gradient consistent with the intensive antimicrobial use documented on industrial poultry operations in the region.

At the molecular level, polymerase chain reaction screening revealed a familiar but troubling cast of resistance genes. The dominant extended-spectrum beta-lactamase determinants were blaCTX-M-15 and blaTEM, enzymes that hydrolyze third-generation cephalosporins, workhorse antibiotics in both human and veterinary medicine. CTX-M-15 in particular is a global success story for the bacterium, having spread explosively through human clinical populations over the past two decades. Its prominence in poultry-associated isolates suggests that the farm environment is not merely a passive reservoir but an active participant in the circulation of the very genes that compromise treatment of urinary tract infections, bloodstream infections and hospital-acquired pneumonia.

More alarming still was the detection of carbapenemase genes among carbapenem-resistant isolates. The team identified blaNDM, blaKPC and blaOXA-48, three of the most clinically consequential carbapenemase families known. Carbapenems are often described as last-line antibiotics for infections caused by gram-negative bacteria, and the World Health Organization lists carbapenem-resistant K. pneumoniae as a critical-priority pathogen. The presence of NDM-type enzymes, which originated on the Indian subcontinent and have since spread worldwide, in bacteria recovered from poultry points to a plausible environmental bridge by which these determinants could move between animal, food and human compartments.

Colistin, a polymyxin antibiotic revived as a treatment of last resort when carbapenems fail, fared no better. Resistance to colistin was detected in 5.9 percent of the isolates, and the plasmid-mediated mcr-1 gene was identified among the resistant strains. The mcr-1 gene is of particular concern because, unlike chromosomal mutations that confer colistin resistance, it sits on mobile genetic elements that can hop between bacterial species and genera with relative ease. First described in Chinese pigs and pork in 2015, mcr-1 has since been reported on every inhabited continent, and its presence in poultry systems in Pakistan adds another node to its global distribution network.

One of the study’s most striking findings is the sheer combinatorial diversity of the resistance determinants. The researchers identified twenty-one distinct resistance gene combinations, including combinations that unite ESBL genes, carbapenemase genes and colistin resistance determinants within the same isolates. Co-occurrence of this kind is the molecular nightmare scenario for antimicrobial resistance control, because a single plasmid carrying multiple determinants can simultaneously confer resistance to front-line, last-line and reserve antibiotics. Such plasmids can be transferred laterally to other Enterobacteriaceae, including Escherichia coli and Salmonella, multiplying the number of pathogenic species that can acquire the resistance package in a single horizontal gene transfer event.

The authors frame their findings within a One Health perspective, the recognition that human, animal and environmental health are inextricably linked. Poultry production is a recognized amplifier of resistance: antimicrobials are used for growth promotion, prophylaxis and treatment in many low- and middle-income settings, selective pressure favors resistant clones, and resistant bacteria and their genes disperse through litter, wastewater, workers, carcasses and meat. Prior studies have documented intermingled K. pneumoniae populations between retail meats and human urinary tract infections, and the persistence of multidrug-resistant strains long after colistin withdrawal in poultry production, suggesting that contamination events can leave durable legacies in the food chain.

The study’s conclusions point toward concrete interventions: strengthened antimicrobial stewardship to curb unnecessary drug use, improved farm-level biosecurity to reduce the infection pressure that drives treatment, and integrated molecular surveillance that tracks resistance genes across the production chain rather than in isolated snapshots. The work was funded under an International Atomic Energy Agency Coordinated Research Project, and the authors report no competing interests. As resistance genes continue to accumulate in the animals that feed billions of people, the Faisalabad survey serves as a quantitative warning that the poultry sector, if left unmonitored, can function as both a reservoir and a launchpad for some of medicine’s most feared resistance determinants.

Subject of Research: Molecular characterization of antimicrobial resistance genes in Klebsiella pneumoniae from poultry production systems in Pakistan

Article Title: Molecular characterization and co-occurrence of ESBL, carbapenemase and mcr-1 genes in Klebsiella pneumoniae from poultry production systems in Pakistan

Article References: Parvez, R., Khurshid, M., Rasool, M. H., Aslam, B., & Sasanya, J. J. (2026). Molecular characterization and co-occurrence of ESBL, carbapenemase and mcr-1 genes in Klebsiella pneumoniae from poultry production systems in Pakistan. Molecular Biology Reports, 53(1), Article 1538. https://doi.org/10.1007/s11033-026-12718-6

Image Credits: AI Generated

DOI: 10.1007/s11033-026-12718-6

Keywords: Klebsiella pneumoniae, antimicrobial resistance, ESBL, carbapenemase, mcr-1, colistin resistance, poultry, One Health, Pakistan, multidrug resistance, food chain, molecular surveillance

The research team worked with strains of Enterococcus and Lactobacillus originally isolated from traditional fermented dairy products, including Enterococcus faecium KE5, Enterococcus durans KE6, Lactobacillus rhamnosus 2012, and Lactobacillus helveticus KG5. These strains were cultivated in a specialized curd whey medium under anaerobic conditions, and their cell-free supernatants were concentrated five-fold before the active compounds were separated. Bacteriocins—ribosomally synthesized antimicrobial peptides classified as Generally Regarded As Safe—were purified by gel filtration on Sephadex columns, while exopolysaccharides, high-molecular-weight carbohydrate polymers, were precipitated with ethanol and likewise purified chromatographically. High-performance liquid chromatography confirmed that the exopolysaccharide fractions were heteropolysaccharides composed primarily of glucose and galactose.

To benchmark the postbiotics against clinical reality, the team assembled a demanding test panel drawn from internationally recognized culture collections, including the American Type Culture Collection and the UK’s National Collection of Type Cultures. The panel deliberately included both susceptible control strains and notorious resistant phenotypes: an ESBL- and AmpC-producing Klebsiella pneumoniae, a multidrug-resistant Pseudomonas aeruginosa, an OXA-48 carbapenemase-producing Acinetobacter baumannii, methicillin-resistant Staphylococcus aureus, and resistant strains of Streptococcus pneumoniae and Enterococcus faecalis. Resistance mechanisms were confirmed phenotypically through double-disk synergy and modified Hodge tests, and carbapenemase genes including KPC, NDM, and OXA were verified by polymerase chain reaction.

The initial screening established a standardized effective dose of 5 milligrams per milliliter against the model organism Salmonella typhimurium G-38, determined by the serial dilution method. This concentration was then applied across the broader pathogen panel using agar diffusion assays, allowing direct comparison with standard antibiotic discs interpreted according to EUCAST clinical breakpoints. The stepwise design meant that every postbiotic preparation and every antibiotic faced the same targets under the same conditions, a comparison the authors argue is rarely attempted at this scale for both Gram-positive and Gram-negative resistant strains.

Concentration-dependence emerged as a defining theme. All exopolysaccharide preparations achieved nearly complete growth inhibition at 100 milligrams per milliliter, but their activity fell away steeply at lower doses, with the exception of the preparation from E. faecium KE5, which retained measurable effects down to 1 milligram per milliliter. Bacteriocins told a similar but sharper story: all preparations inhibited 95 to 100 percent of growth at 10 to 50 milligrams per milliliter, yet only the bacteriocin from E. faecium KE5 sustained substantial activity at 5 milligrams per milliliter, a property the researchers describe as dose sustainability. L. rhamnosus 2012 stood apart for producing two distinct bacteriocins of different molecular weights, 1.42 and 0.60 kilodaltons, which broadened its inhibitory spectrum.

The comparative results against antibiotics revealed what the authors call an erosion of susceptibility among resistant isolates. The ESBL- and AmpC-producing K. pneumoniae strain showed complete resistance to beta-lactams and only 5 percent susceptibility to carbapenems, while remaining fully susceptible to fluoroquinolones and aminoglycosides. Among the non-fermenting Gram-negatives, the resistant P. aeruginosa strain and the OXA-48-positive A. baumannii resisted most antibiotic classes, with the Pseudomonas control strain itself showing only 10 percent susceptibility to beta-lactams and none to fluoroquinolones. Resistant Gram-positive cocci fared little better, with the resistant S. pneumoniae strain showing just 28.5 percent susceptibility to beta-lactams and complete resistance to fluoroquinolones and aminoglycosides.

Against this backdrop of patchy antibiotic performance, the purified bacteriocins from L. rhamnosus 2012 and E. faecium KE5 delivered the study’s most striking result: 100 percent inhibitory activity against every tested reference strain, regardless of resistance phenotype. Whether a pathogen carried ESBL enzymes, carbapenemase genes, or methicillin resistance made no difference to the bacteriocins’ performance under the experimental conditions. The exopolysaccharides, by contrast, showed far weaker and more variable effects, with most Enterobacteriaceae isolates classified as resistant to them. The authors attribute the disparity to fundamental biochemical differences: bacteriocins are thought to kill directly by permeabilizing bacterial membranes and forming pores, whereas exopolysaccharides act more indirectly, potentially by interfering with adhesion or biofilm formation.

That mechanistic interpretation comes with important caveats. The researchers acknowledge that the proposed membrane-disruption pathways remain hypotheses, since no direct membrane permeability assays or electron microscopy imaging were performed. Diffusion-based assays also carry inherent limitations for large molecules, and the exopolysaccharides, at molecular weights of 10 to 44 kilodaltons, may simply diffuse poorly through agar, understating their true activity. The authors also stress that the narrower spectrum of the postbiotics, while potentially advantageous for preserving the host microbiome, means they cannot simply replace broad-spectrum antibiotics across the board.

Even so, the case for bacteriocins as complementary agents is compelling on several fronts. Unlike antibiotics that suppress bacterial metabolism and synthesis, bacteriocins tend to damage target cell structures directly, which the authors argue reduces the likelihood of resistance emerging. They are active at very low concentrations, are completely metabolized in the human body, and generally show low toxicity. Previous work by the same group indicated that bacteriocins and exopolysaccharides from these strains can inhibit pneumonia-causing pathogens, and the current data open the possibility of combination preparations—bacteriocins paired with exopolysaccharides or with conventional drugs—that could enhance efficacy while lowering antibiotic doses and resistance pressure.

The study’s authors frame their endemic Armenian strains as a valuable reservoir for next-generation antimicrobials, with potential applications spanning nutrition, prevention, and eventually therapy. They are careful, however, to position the findings as preliminary in vitro observations. Before any clinical translation, in vivo efficacy and toxicological studies will be required to establish whether the dose sustainability and uniform activity seen on agar plates survive the far harsher conditions of a living host. For now, the message is that the microscopic inhabitants of traditional fermented foods may hold molecules that drug-resistant bacteria have not yet learned to defeat.

Subject of Research: Antimicrobial activity of bacteriocins and exopolysaccharides from lactic acid bacteria against multidrug-resistant human pathogens

Article Title: Antimicrobial properties of postbiotics of different LAB against multidrug resistance bacteria

Article References: Tkhruni, F., Danova, S., Melik-Andreasyan, G., Aleksanyan, N., & Israyelyan, A. (2026). Antimicrobial properties of postbiotics of different LAB against multidrug resistance bacteria. Pharmacia, 73, Article e189800. https://doi.org/10.3897/pharmacia.73.e189800

Image Credits: AI Generated

DOI: 10.3897/pharmacia.73.e189800

Keywords: antimicrobial resistance, postbiotics, bacteriocins, exopolysaccharides, lactic acid bacteria, multidrug-resistant bacteria, probiotics, Enterococcus faecium, Lactobacillus rhamnosus, ESBL, carbapenemase, fermented milk

Carbapenems have long been considered the most reliable last line of defense against severe Gram-negative bacterial infections. Yet the growing prevalence of carbapenemase-producing organisms, particularly among Enterobacteriaceae and non-fermenting Gram-negative bacilli, has severely restricted treatment options and is associated with alarming mortality rates exceeding 50% in some regions. Carbapenem resistance is primarily mediated by carbapenemase enzymes encoded by genes such as blaKPC, blaNDM, blaIMP, blaVIM, and blaOXA-48. These resistance determinants are frequently located on mobile genetic elements like plasmids, transposons, and integrons, facilitating horizontal gene transfer among diverse bacterial species. While the co-occurrence of multiple carbapenemase genes within individual bacterial isolates represents an escalating global concern, the simultaneous detection of multiple carbapenemase genes within a single clinical specimen remains rare.

To characterize the pathogens and resistance genes present in the lavage fluid, the team employed metagenomic next-generation sequencing (mNGS), a culture-independent approach that enables identification of pathogens and resistance genes directly from clinical samples. The BALF sample was processed within 24 hours of collection, with DNA extracted using a magnetic bead-based kit and libraries sequenced on the MGI200 platform using DNA Nanoball technology, generating over 10 million single-end 50-bp raw reads. After quality filtering and removal of human sequences, the remaining reads were aligned to reference databases containing genomes of viruses, bacteria, fungi, and parasites. Microbial identification required at least three non-overlapping reads per organism that were either undetected in negative controls or present at counts at least 10 times higher than in controls.

The metagenomic analysis detected Pseudomonas stutzeri, Klebsiella pneumoniae, Shewanella algae, and Elizabethkingia anophelis in the sample. Beyond the four carbapenemase genes, the specimen contained a diverse array of antimicrobial resistance genes spanning multiple categories, including beta-lactamase genes such as blaCTX-M-65, blaSHV-66, blaOXA-55, and blaOXA-246; aminoglycoside-modifying enzymes; sulfamethoxazole resistance genes sul1 and sul2; trimethoprim resistance determinants dfrA27, dfrA6, and dfrB3; tetracycline, chloramphenicol, rifampicin, fluoroquinolone, and macrolide resistance genes. Various virulence-associated genes were also detected, including those involved in iron acquisition, fimbriae formation, and outer membrane protein synthesis, suggesting a virulence-associated genetic profile within the polymicrobial community.

Using selective culturing techniques with LB agar plates containing 0.5 µg/mL of imipenem, three carbapenemase-producing strains were isolated from the same specimen. Klebsiella pneumoniae strain CQPMC-KpYD carried blaKPC-2, Shewanella algae strain CQPMC-SheW1 harbored blaNDM-1, and Pseudomonas stutzeri strain CQPMC-PStu co-harbored both blaIMP-1 and blaAFM-1. Targeted reanalysis of the BALF sequencing data yielded 148, 477, 232, and 325 reads compatible with blaKPC-2, blaNDM-1, blaAFM-1, and blaIMP-1, respectively, with corresponding coverage breadths exceeding 99% and mean depths ranging from 8.39× to 29.34×. All three isolates showed minimum inhibitory concentrations of ≥16 µg/mL for imipenem, meropenem, and ertapenem, confirming high-level carbapenem resistance across distinct bacterial species.

Whole-genome sequencing using Oxford Nanopore Technologies on the MinION platform revealed the genetic architecture underlying these resistance determinants. The K. pneumoniae isolate was identified as an ST11 strain, a predominant clone associated with carbapenem resistance and linked to hospital outbreaks and high mortality rates across multiple continents. The blaKPC-2 gene was located on a 132,742 bp plasmid designated pCQPMC-KpYD1, which harbors 172 predicted open reading frames and contains IncFII(pHN7A8) and IncR replicons. BLAST database comparisons showed that this plasmid shares 100% coverage and 99.99% identity with the K. pneumoniae plasmid pCRKP-35_KPC, isolated from a patient’s blood sample in China in 2019. Further searches identified 45 plasmids with over 99% identity and coverage, all from K. pneumoniae isolates across various regions in China—43 from hospital patients and 2 from animals—suggesting that related plasmid backbones may contribute to blaKPC-2 dissemination.

The K. pneumoniae isolate also harbored virulence genes including iucABCD, iutA, rmpA, rmpD, and rmpC, located on a 200,970 bp IncHI1B-IncFIB hybrid plasmid lacking additional antibiotic resistance genes. Genetic analysis revealed that the core structure of the blaKPC-2 gene region, termed variable region 1, comprises IS26-ΔTn3-ISKpn27-blaKPC-2-ISKpn6-korC-orf-klcA-ΔrepB. Two additional resistance gene clusters adjacent to blaKPC-2 were identified: a mercury resistance gene cluster flanked by IS5057 and TnpA, and a cluster containing blaSHV-12 enclosed by TnAs1 and IS26. These genetic contexts suggest potential roles for transposition and recombination in the genetic diversity and mobility of blaKPC-2-carrying plasmids.

The Shewanella algae strain CQPMC-SheW1 presented an equally striking genomic picture. Its 4,891,834 bp chromosome assembly contained two blaNDM-1 copies in the same orientation, with start positions separated by 6,399 bp in repeated ISCR1-associated contexts. The related context was ISCR1-partial trpF-bleMBL-blaNDM-1-ΔISAba125-catB3-arr-3-qacEΔ1-sul1. Remarkably, a similar ISCR1-NDM-1 structure is observed in E. coli strain Y5, which shares 100% homology with the chromosomal ISCR1-NDM-1 element in CQPMC-SheW1. Downstream of blaNDM-1, an IntI1 integron with a cassette of six resistance genes was identified. Comparative analysis indicates that the blaNDM-1 gene and its surrounding resistance cluster share up to 99% homology with plasmid p6061604-KPC from E. coli strain 2016061604, highlighting potential cross-species transmission. While that plasmid contains only one complete ISCR1-NDM-1 element, CQPMC-SheW1 exhibits a more complex composition with two same-orientation blaNDM-1 copies, possibly resulting from recombination or transposition events.

The Pseudomonas stutzeri strain CQPMC-PStu, with a 5,242,803 bp genome and 62.2% GC content, co-harbored blaAFM-1 and blaIMP-1, genes encoding metallo-β-lactamases that confer high-level resistance to carbapenems. The blaAFM-1 gene is located within an approximately 12 kb multidrug-resistant region primarily composed of an ISCR29 element and two class 1 integrons. Comparative genomic analysis revealed that this region is highly similar to the chromosome of clinically isolated Pseudomonas qingdaonensis strain L1712hy, exhibiting 99.9% nucleotide identity. The blaIMP-1 gene is located within a truncated class 1 integron arranged as IntI1-blaIMP-1-aac(6′)-IIa-aph(3′)-VIa, a structure closely resembling integron In86. Notably, this multidrug-resistant region exhibits high homology with the chromosome of P. putida strain AHSWHJXPP1, demonstrating 100% coverage and 99% identity, and that strain also carries both blaAFM-1 and blaIMP-1. Similar genomic compositions have been discovered in plasmids of three P. aeruginosa strains, revealing related resistance-associated regions across several bacterial species and suggesting potential mobility of the associated determinants.

The coexistence of four carbapenemase genes within one clinical sample highlights the complexity of polymicrobial carbapenem resistance and underscores the importance of genomic surveillance. The authors note important limitations: the absence of direct transfer experiments and longitudinal evidence limits inference of horizontal gene transfer within the patient, the contribution of each organism and its resistance determinants to the fatal outcome could not be established, and BALF short reads do not establish isolate origin or copy-specific coverage, with independent long-read validation across the SheW1 repeat junctions not established. Nevertheless, the mobile-element-associated genetic contexts of these co-occurring genes suggest their potential mobility, and the findings emphasize the value of comprehensive genomic surveillance networks to detect and monitor the spread of highly resistant organisms, informing international infection control measures and guiding effective therapeutic strategies against the growing global threat of antibiotic resistance.

Subject of Research: Co-occurrence and genetic contexts of four carbapenemase genes in a single clinical specimen from a critically ill patient

Article Title: Co-occurrence and genetic contexts of NDM-1, KPC-2, IMP-1, and AFM-1 carbapenemase genes in a critically ill patient

Article References: Zhang, Y., Zhang, Z., Ying, S., Wang, S., & Xiang, R. (2026). Co-occurrence and genetic contexts of NDM-1, KPC-2, IMP-1, and AFM-1 carbapenemase genes in a critically ill patient. Frontiers in Cellular and Infection Microbiology, 16, Article 1973471. https://doi.org/10.3389/fcimb.2026.1973471

Image Credits: AI Generated

DOI: 10.3389/fcimb.2026.1973471

Keywords: carbapenemase, antimicrobial resistance, NDM-1, KPC-2, IMP-1, AFM-1, metagenomic sequencing, whole-genome sequencing, Klebsiella pneumoniae, Pseudomonas stutzeri, Shewanella algae, genomic surveillance

The numbers alone are striking. Twenty-eight of the 30 isolates—93 percent—were classified as multidrug-resistant, meaning they were resistant to three or more antibiotic classes. Seven of those, or a quarter of the MDR isolates, were extensively drug-resistant, showing non-susceptibility across eight antibiotic classes including the carbapenems, drugs typically reserved as last-line therapies for serious Gram-negative infections. Only amikacin, an aminoglycoside, retained activity against the XDR strains. Six of the seven XDR isolates came from a single institution, UTH, which serves as Zambia’s national referral hospital, while one originated from NUTH. Non-susceptibility was pervasive across the broader panel: 90 percent of isolates resisted ceftriaxone and cefepime, 87 percent resisted ceftazidime, and 90 percent resisted trimethoprim-sulfamethoxazole.

To understand what was driving this resistance, the team turned to whole-genome sequencing on an Illumina NextSeq 2000 platform, generating 150-base-pair paired-end reads that were quality-trimmed, de novo assembled, and mined with tools including the Comprehensive Antibiotic Resistance Database and PlasmidFinder. Multilocus sequence typing based on seven housekeeping genes assigned the isolates to sequence types, the standard shorthand for tracking bacterial lineages. The result was remarkable diversity: 18 distinct sequence types among 29 confirmed K. pneumoniae isolates, including two novel types never before designated. One isolate initially presumed to be K. pneumoniae turned out to be K. oxytoca, a related species, underscoring the value of genomic species confirmation in clinical microbiology.

Within that diversity, the researchers identified a roster of internationally notorious high-risk clones: ST11, ST15, ST101, ST307, ST377, and ST607. These lineages have been implicated in hospital outbreaks on multiple continents and are strongly associated with extended-spectrum beta-lactamases and carbapenemases. UTH hosted all five of the dominant hospital-associated types detected in the study, and several types—ST15, ST307, ST377, and ST607—appeared at more than one hospital, suggesting circulation through patient referral networks or regional dissemination rather than independent emergence. Notably, ST607 has only been reported twice before in Africa, in Malawi and Kenya, where it emerged as a major ESBL-producing clone carrying IncFIB plasmids and the blaCTX-M-15 gene—precisely the profile of the Zambian isolates.

Among the seven XDR isolates, five belonged to clinically dominant clones: two ST377 isolates plus single representatives of ST101, ST307, and ST607. The remaining two belonged to ST13 and ST831, lineages that had not previously been reported with XDR profiles, hinting that resistance is spreading into clones not traditionally considered high-risk. Hierarchical clustering of susceptibility and resistance gene data grouped the isolates into five clusters, Kp1 through Kp5, with the most resistant cluster, Kp5, concentrated at UTH. The authors suggest that the national referral hospital may act as a central hub that accumulates diverse MDR lineages and seeds regional facilities through inter-facility patient transfers.

The resistance determinants themselves were dominated by plasmid-borne beta-lactamase genes. blaCTX-M-15, the quintessential ESBL gene of the modern era, was present in 93 percent of isolates, while blaTEM variants appeared in 70 percent. The carbapenemase gene blaNDM-5, which encodes an enzyme capable of destroying even last-resort carbapenem antibiotics, was detected in 13 percent of isolates. Aminoglycoside-modifying enzymes were widespread, led by aac(6′)-Ib-cr5 at 77 percent and aac(3)-IIe at 64 percent, and every single isolate carried emrD, a multidrug efflux pump gene. Genes conferring resistance to sulfonamides, fosfomycin, and quinolones, including oqxA at 83 percent, rounded out a resistance repertoire of 40 distinct genes detected across the collection.

Plasmid analysis revealed the likely engine of this dissemination. Nine plasmid replicon types were identified, but one stood out: IncFIB(K)_1_Kpn3, found in 26 of 30 isolates, or roughly 86 percent. This replicon is known to be associated with dozens of resistance profiles, including ESBLs and carbapenemases. Its presence across phylogenetically distinct lineages—dominant high-risk clones and minor types alike—points to horizontal gene transfer as a critical force sustaining multidrug resistance in these hospitals. Several sequence types, including ST39, ST86, ST101, ST5133, and ST831, co-harboured both IncFIB(K)_1_Kpn3 and IncHI1B_1_pNDM-MAR, the latter a replicon strongly linked to NDM-mediated carbapenem resistance. Such plasmid promiscuity means that even if a dominant resistant clone is eliminated, the resistance genes themselves can persist and jump into new bacterial backgrounds.

Virulence profiling added a further dimension of concern. All isolates carried genes for enterobactin iron acquisition, adherence, and immune evasion, and complete yersiniabactin loci were found in 18 isolates spanning multiple sequence types, including high-risk MDR lineages. One ST86 isolate, ZLU0042372, carried complete aerobactin and salmochelin loci—a siderophore combination characteristic of hypervirulent K. pneumoniae—making it the leading candidate hypervirulent isolate in the study, although the authors caution that definitive classification would require functional validation. Encouragingly, classic hypervirulence markers such as rmpA and peg-344 were absent from all isolates. Phylogenetically, the Zambian isolates did not form hospital-specific lineages; instead, they dispersed across the tree and several clustered with non-Zambian reference genomes, situating local strains within global genetic backgrounds.

The study has limitations that the authors acknowledge. Short-read sequencing cannot reliably resolve whether resistance genes sit on plasmids or the chromosome, and the relatively small sample—just three isolates from Livingstone and six from Ndola—constrains conclusions about diversity at those sites. The restriction to bloodstream isolates may also bias findings toward strains adapted to invasive disease. Even so, as the first genomic characterisation of K. pneumoniae in Zambia, the work establishes a baseline that was previously missing from sub-Saharan Africa, a region where genomic surveillance of this pathogen has lagged despite its recognised priority in Zambia’s National Action Plan on antimicrobial resistance.

The implications are clear. With XDR strains already circulating in referral hospitals and mobile plasmids shuttling resistance genes across clonal boundaries, the window for containment is narrowing. The authors call for strengthened laboratory surveillance across all tertiary hospitals in Zambia, coordinated genomic monitoring between facilities, and reinforced infection prevention and control alongside antimicrobial stewardship programmes. Without such interventions, they warn, these clones could disseminate from tertiary centres into secondary hospitals and the wider community, turning a hospital problem into a national public health crisis.

Subject of Research: Genomic surveillance of multidrug-resistant and extensively drug-resistant Klebsiella pneumoniae bloodstream infections in Zambian tertiary hospitals

Article Title: Genomic insights into multidrug and extensively drug-resistant Klebsiella pneumoniae from bloodstream infections at three Zambian tertiary hospitals

Article References: Chizimu, J. Y., Kamboyi, H. K., Kasanga, M., Sinyawa, T., Shawa, M., Nakazwe, R., Mudenda, S., Njung’e, J., Kiiru, S., Chuluun, M., Lukwesa, C., Muhimba, Z., Daka, V., Tibatemwa, D., Wesangula, E., Shikanga, O.-T., Mwadetsa, S. D., Machila, N., Chuchu, V., … Chilengi, R. (2026). Genomic insights into multidrug and extensively drug-resistant Klebsiella pneumoniae from bloodstream infections at three Zambian tertiary hospitals. Frontiers in Antibiotics, 5, Article 1933211. https://doi.org/10.3389/frabi.2026.1933211

Image Credits: AI Generated

DOI: 10.3389/frabi.2026.1933211

Keywords: Klebsiella pneumoniae, antimicrobial resistance, genomic surveillance, Zambia, XDR, high-risk clones, carbapenemase, NDM-5, ESBL, plasmids, bloodstream infections, whole-genome sequencing

Klebsiella pneumoniae is a common inhabitant of the human gut and an opportunistic pathogen that can cause pneumonia, bloodstream infections, urinary tract infections, and wound infections, particularly in hospitalized and immunocompromised patients. When the bacterium acquires carbapenemases, enzymes that hydrolyze carbapenems, a class of last-resort beta-lactam antibiotics, treatment options collapse to a handful of toxic or expensive drugs. The World Health Organization classifies carbapenem-resistant K. pneumoniae as a critical priority pathogen, and the burden falls disproportionately on South Asia, where resistance genes circulate widely in hospitals and communities alike.

The enzymes involved are mechanistically distinct. The bla_NDM gene encodes New Delhi metallo-beta-lactamase, a metallo-enzyme that destroys nearly all beta-lactam antibiotics including carbapenems. The bla_OXA-48-like family encodes oxacillinases that are less potent against broad-spectrum cephalosporins but are highly efficient carbapenem hydrolyzers and are notoriously difficult to detect in routine phenotypic testing. When a single isolate carries both genes, the bacterium effectively deploys two independent biochemical strategies against the same class of drugs, and laboratory susceptibility testing can understate the true resistance arsenal. The new study set out to determine whether this molecular redundancy translates into worse outcomes at the bedside.

Researchers led by Pravalika Sathyanarayana, Sharadadevi Y Mannur, and Mahadevamma Lingaiah conducted a prospective observational study at a tertiary care hospital in South India between January 2024 and January 2025. They enrolled ICU patients with culture-confirmed carbapenem-resistant K. pneumoniae infections and used real-time polymerase chain reaction to detect five carbapenemase genes: bla_NDM, bla_OXA-48-like, bla_IMP, bla_VIM, and bla_KPC. Patients were stratified into four genotypic groups, those carrying bla_NDM alone, those carrying bla_OXA-48-like alone, co-producers carrying both, and non-producers, and the primary outcome was 28-day all-cause in-hospital mortality. Written informed consent was obtained from patients or their legally authorized representatives, and the study was approved by the institutional ethics committee and conducted under the Declaration of Helsinki.

The molecular findings were striking. Of the 106 patients, 30, or 28.3 percent, harbored isolates that co-produced both carbapenemases, while 16 patients, or 15.1 percent, died within 28 days of infection. Mortality varied significantly across genotypes, and the highest proportion of deaths occurred among patients infected with co-producing isolates, with 9 of 30 such patients, or 30 percent, dying within the follow-up window. That is roughly double the overall cohort mortality rate and suggests that the dual-enzyme phenotype marks a subset of infections that behave differently in critically ill hosts.

To quantify these associations, the team used Firth penalized logistic regression, a statistical approach designed for situations where outcome events are sparse and conventional maximum-likelihood models can fail or produce unstable estimates. In univariable analysis, mechanical ventilation was associated with a 12.47-fold increase in the odds of 28-day mortality, septic shock with a 25.11-fold increase, and each point increase on the APACHE II illness-severity score with a 29 percent increase in odds. Co-producer status itself carried an unadjusted odds ratio of 4.09, meaning patients with dual-carbapenemase isolates had roughly four times the odds of death compared with the rest of the cohort, a statistically significant association.

The exploratory multivariable model, which adjusted for these competing risk factors, retained three independent predictors: higher APACHE II score with an adjusted odds ratio of 1.24, septic shock with an adjusted odds ratio of 12.23, and carbapenemase co-production with an adjusted odds ratio of 7.50. In other words, even after accounting for how sick patients were on admission and whether they had progressed to septic shock, carrying a dual-carbapenemase strain was associated with more than a sevenfold increase in the odds of dying within 28 days. Model diagnostics showed no problematic multicollinearity, with variance inflation factors ranging from 1.12 to 1.28, and the apparent area under the receiver operating characteristic curve reached 0.975, indicating strong discrimination within this dataset.

The authors are careful to frame these numbers with appropriate scientific caution. The adjusted odds ratio for co-production of 7.50 came with a 95 percent confidence interval stretching from 1.50 to 51.67, an extraordinarily wide range that reflects the limited number of mortality events in the cohort. With only 16 deaths distributed across four genotypic groups, the point estimate is statistically significant but the true magnitude of the effect could plausibly be anywhere from a modest doubling of risk to a fifty-fold increase. The adjusted analysis was therefore explicitly labeled exploratory, and the apparent AUC of 0.975 was not internally validated, meaning its impressive value may partly reflect overfitting to this particular sample.

Residual confounding also looms over the findings. The study did not capture detailed data on antimicrobial management or source control, the surgical or procedural measures used to eliminate the focus of infection, and both are powerful determinants of survival in severe bacterial sepsis. It is conceivable that patients with co-producing strains received less effective empiric therapy, or that their infections were harder to eradicate for reasons unrelated to the resistance genes themselves. The single-center design further limits generalizability, since gene prevalence, prescribing patterns, and ICU case mix vary widely across institutions and regions. The authors call for larger multicenter studies incorporating detailed treatment and source-control data to determine whether the association is reproducible.

Even with those caveats, the study carries a pointed message for clinicians and laboratories. Rapid molecular detection of carbapenemase genes, rather than reliance on phenotypic susceptibility panels alone, can identify high-risk co-producing strains early enough to inform therapy, infection control measures, and conversations with families about prognosis. It also reinforces the urgency of stewardship programs designed to slow the horizontal spread of these plasmid-borne genes, because every co-producing isolate that circulates in an ICU represents a patient population at elevated risk. As antimicrobial resistance continues to outpace the development of new antibiotics, studies like this one demonstrate that the genetic composition of a pathogen is not just an epidemiological detail but a clinical variable that can mean the difference between recovery and death.

Subject of Research: Clinical impact of dual carbapenemase co-production on 28-day mortality in ICU patients with carbapenem-resistant Klebsiella pneumoniae: a prospective study from South India

Article Title: Clinical impact of dual carbapenemase co-production on 28-day mortality in ICU patients with carbapenem-resistant Klebsiella pneumoniae: a prospective study from South India

Article References: Sathyanarayana, P., Mannur, S. Y., & Lingaiah, M. (2026). Clinical impact of dual carbapenemase co-production on 28-day mortality in ICU patients with carbapenem-resistant Klebsiella pneumoniae: a prospective study from South India. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14539-1

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14539-1

Keywords: Clinical, impact, dual, carbapenemase, co-production, mortality, patients, carbapenem-resistant, Klebsiella, pneumoniae, prospective, South

The research team, led by Shahida Kashif of Liaquat College of Medicine and Dentistry together with Muhammad Sohail of the University of Karachi and collaborators at several Karachi institutions and Taif University in Saudi Arabia, analyzed 308 Gram-negative bacterial isolates recovered from urine samples of patients with catheter-associated urinary tract infections. The samples were collected between June and December 2024, and the work received ethical approval from the Institutional Review Board of Darul Sehat Hospital in Karachi, with written informed consent obtained from all participants or their legal representatives. The study was designed to answer three linked questions: how common carbapenem resistance is in this setting, which carbapenemase-encoding genes are responsible, and what patient characteristics are associated with carrying those genes.

Species identification revealed a familiar hierarchy of uropathogens. Escherichia coli was the dominant organism, accounting for 134 of the 308 isolates, or 43.5 percent, followed by Klebsiella pneumoniae with 96 isolates, or 31.2 percent. The remaining isolates included other Gram-negative species, among them Pseudomonas aeruginosa. This distribution mirrors global patterns of catheter-associated infection, in which Enterobacterales, the family of gut-dwelling bacteria that includes both E. coli and K. pneumoniae, colonize the urinary tract and catheter surfaces with ease. The ubiquity of these organisms in hospital plumbing, on catheter biofilms, and in patients’ own gut flora makes them persistent adversaries in intensive care units and general wards alike.

Antimicrobial susceptibility testing exposed a stark pattern of resistance to the older, cheaper, and more widely used drugs. Resistance to ceftriaxone, a third-generation cephalosporin, was found in 244 of 308 isolates, a rate of 79.2 percent, while resistance to ciprofloxacin, a fluoroquinolone, appeared in 238 isolates, or 77.3 percent. By contrast, resistance to the carbapenems remained lower but far from negligible: 104 isolates, or 33.8 percent, were resistant to meropenem, and 96 isolates, or 31.2 percent, were resistant to imipenem. That roughly one in three Gram-negative uropathogens from catheter-associated infections could shrug off carbapenems underscores how far these last-line drugs have been eroded in this clinical setting, leaving clinicians with progressively fewer options for seriously ill patients.

The molecular core of the study focused on five carbapenemase-encoding genes detected by polymerase chain reaction: bla_NDM, bla_OXA-48, bla_KPC, bla_IMP, and bla_VIM. These genes encode enzymes that hydrolyze carbapenems and most other beta-lactam antibiotics, rendering them ineffective. Among the 104 carbapenem-resistant isolates, bla_NDM, which encodes the New Delhi metallo-beta-lactamase, was by far the most prevalent, detected in 66 isolates, or 63.5 percent. bla_OXA-48, encoding the oxacillinase-48 beta-lactamase, came second at 40 isolates, or 38.5 percent. Notably, bla_KPC, bla_IMP, and bla_VIM were not reported as significant contributors in this collection, marking NDM and OXA-48 as the dominant resistance determinants in these Karachi hospitals.

The distribution of genes across species was not uniform, and this species-specific pattern carries practical implications for diagnostics and treatment. bla_NDM was particularly concentrated in K. pneumoniae, appearing in 31 of 48 carbapenem-resistant K. pneumoniae isolates, or 64.6 percent. bla_OXA-48, by contrast, was more predominant in carbapenem-resistant P. aeruginosa, detected in 4 of 10 such isolates, or 40 percent. The study also documented co-carriage of both bla_NDM and bla_OXA-48 in 12 of the 104 carbapenem-resistant isolates, or 11.5 percent. Dual carriage is especially concerning because enzymes from these two classes, a metallo-beta-lactamase and a class D carbapenemase, together dismantle a broader spectrum of beta-lactam drugs and can complicate the interpretation of phenotypic susceptibility tests, which may fail to flag resistance when multiple mechanisms interact.

Beyond cataloguing genes, the investigators used chi-square tests and binary logistic regression to identify independent predictors of carbapenemase gene carriage, with a p-value of 0.05 or less considered statistically significant. Three clinical factors emerged as independent predictors of gene positivity: admission to the intensive care unit, previous exposure to antibiotics, and catheterization lasting longer than seven days. Each of these factors fits a coherent biological and epidemiological narrative. ICU patients are exposed to the highest densities of resistant organisms and the most intensive antimicrobial use. Prior antibiotic exposure selectively eliminates susceptible strains, clearing the way for resistant ones to colonize. And prolonged catheterization gives bacteria time to form biofilms on the device surface, where they are shielded from both immune defenses and antibiotics and can freely exchange resistance genes on plasmids and other mobile elements.

The public health significance of these findings extends well beyond a single city. Carbapenemase genes, particularly bla_NDM, are notorious for their mobility, hitchhiking on plasmids that move readily between bacterial species and genera. A patient colonized with an NDM-producing E. coli strain can serve as a silent reservoir, disseminating the gene into hospital environments, water systems, and community settings. Because catheter-associated infections are so common, the urinary tract represents one of the largest and most underappreciated reservoirs for these genes in healthcare facilities. The identification of modifiable risk factors, especially catheter duration, provides concrete targets for intervention: strict catheter stewardship, daily assessment of the ongoing need for a catheter, and early removal are inexpensive measures that directly shorten the window in which resistance can emerge and spread.

The study also highlights the importance of molecular surveillance in an era where phenotypic testing alone may not capture the full resistance picture. Rapid PCR-based detection of bla_NDM and bla_OXA-48 in carbapenem-resistant isolates allows infection control teams to isolate carriers promptly, adjust antibiotic therapy, and interrupt transmission chains before outbreaks take hold. The authors note that the co-existence of multiple carbapenemase genes in a meaningful fraction of isolates further argues for comprehensive molecular panels rather than single-gene assays, since treatment decisions and infection control responses may differ depending on which enzymes are present. For laboratories in resource-limited settings, the study’s straightforward PCR approach offers a practical template for building such surveillance capacity.

Published open access in BMC Infectious Diseases with a permanent DOI, the study arrives as the global health community intensifies efforts against antimicrobial resistance, a threat the WHO has identified as one of the top challenges facing public health. The Karachi data, showing E. coli as the predominant uropathogen, bla_NDM as the leading carbapenemase in resistant Enterobacterales, and bla_OXA-48 as the more prevalent mechanism in resistant P. aeruginosa, add a valuable regional data point to the global map of resistance. More importantly, the clear linkage of gene carriage to ICU admission, prior antibiotic exposure, and extended catheterization converts an abstract molecular threat into a set of actionable clinical priorities. If hospitals act on these predictors, limiting unnecessary catheter days and curbing indiscriminate antibiotic use, the study suggests that the spread of carbapenemase genes in catheter-associated infections can be slowed, preserving the effectiveness of last-line antibiotics for the patients who need them most.

Subject of Research: Carbapenemase gene prevalence and risk factors in Gram-negative uropathogens causing catheter-associated urinary tract infections

Article Title: Molecular detection and risk factors of carbapenemase -encoding gene among the Gram-negative uropathogens associated with catheter-associated urinary tract infection

Article References: Kashif, S., Sohail, M., Uddin, F., Ansari, A., Alorabi, M., Khan, R. N., & Husain, S. (2026). Molecular detection and risk factors of carbapenemase -encoding gene among the Gram-negative uropathogens associated with catheter-associated urinary tract infection. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14568-w

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14568-w

Keywords: carbapenemase, bla_NDM, bla_OXA-48, catheter-associated urinary tract infection, antimicrobial resistance, Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, carbapenem-resistant Enterobacterales, risk factors, PCR detection, hospital infection control