BACKGROUND:This study describes the clinical profiles, phenotypic and genotypic resistance mechanisms, and outcomes of patients with carbapenem-resistant infections (CRIs) using a registry. METHODS:Hospitalized adults with CRIs in two tertiary institutions were included in this prospective study from January 1, 2023, to December 31, 2025. RESULTS:A total of 411 patients were included. Half were male (207/411, 50.4%), with median age 59 (range 19-98) years. Hypertension (251, 65.5%), diabetes mellitus (150, 39.2%), and cancer (133, 34.7%) were frequent comorbidities. Of 518 CRIs, half were respiratory (n = 284/518, 49.8%) from ventilator-associated pneumonia (VAP) (163/284, 57.4%) or hospital-acquired pneumonia (HAP) (117/284, 41.2%). Carbapanem-resistant Enterobacterales (CRE) (301/518, 58.1%) and carbapenem-resistant Acinetobacter baumannii (CRAB) (154/518, 29.7%) were the most common pathogens. The majority expressed efflux pumps (388/411, 94.4%). Class B metallo β-lactamase (blaNDM) for CRE and Class D blaOXA-51-like for CRAB were frequent. Overall mortality at the end of hospital stay was 46%. CONCLUSION:Most CRIs in this cohort were CRE and CRAB from HAP/VAP. Organisms possessed multiple mechanisms of resistance, with phenotypic expression of efflux pumps and blaNDM and blaOXA-51-like predominating. High mortality rate was independent of the mechanism of resistance. Novel antimicrobials directed against these specific resistance mechanisms are urgently needed. This registry can be expanded to provide a real-world view of clinical practices.
BACKGROUND:Pseudomonas aeruginosa is a major cause of nosocomial infections, with increasing multidrug resistance complicating treatment outcomes. Aminoglycosides remain a cornerstone for managing P. aeruginosa infections, but resistance is escalating globally. This study investigates the prevalence of aminoglycoside resistance and the molecular basis of resistance, focusing on aminoglycoside-modifying enzyme (AME) and 16S rRNA methylase genes in P. aeruginosa clinical isolates from Anhui, China. METHODS:A total of 354 non-duplicate P. aeruginosa isolates were collected from three tertiary hospitals between January 2023 and December 2024. Antimicrobial susceptibility was determined using the agar dilution method. Whole-genome sequencing and polymerase chain reaction (PCR) were employed to identify AMEs and 16S rRNA methylase genes. Statistical analyses assessed resistance profiles and gene-phenotype associations. RESULTS:Aminoglycoside resistance was observed in 63% (222/354) of isolates, with resistance rates highest for streptomycin (60.2%), amikacin (56.1%), kanamycin (55.3%), and tobramycin (45.3%). The most prevalent AME gene was aac(6')-Ib9 (32.3%), followed by aph(3')-IIb (25.5%), aac(6')-IIa (20.8%), and ant(2″)-Ia (11.2%). The 16S rRNA methylase genes rmtB (4.4%) and armA (5.1%) were detected. Resistance genes were often associated with mobile genetic elements, suggesting horizontal gene transfer. CONCLUSION:The high prevalence of aminoglycoside resistance, driven by diverse AMEs and 16S rRNA methylase genes, highlights the urgent need for enhanced antimicrobial stewardship, molecular surveillance, and infection control measures in Chinese hospitals to mitigate the spread of resistant P. aeruginosa.
Healthcare-associated infections (HAIs) and antimicrobial resistance (AMR) are significant problems, especially in intensive care units (ICUs). We evaluated HAI rates, causative pathogens, resistance profiles, and antibiotic consumption retrospectively in a tertiary ICU across three 2-year periods-pre-pandemic period (PreP), pandemic period (PanP), and post-pandemic period (PostP)-to assess the impact of the COVID-19 pandemic. Antibiotic consumption was expressed as defined daily dose (DDD) per 1,000 patient days. The highest infection incidence rate and density were in PanP. Despite lower invasive device use, PanP had a higher rate of catheter-related bloodstream infections (BSIs). The most frequent pathogen across periods was Acinetobacter spp., although its rate declined in PostP. Gram-negative bacteria resistance rates to piperacillin-tazobactam, carbapenem, and aminoglycoside were highest in PanP. Resistant pathogen and resistant infection rates were lower in PostP, and resistant infections were less frequent in PostP than in PanP (OR: 0.371; 95% CI: 0.216-0.637; p < 0.001). Healthcare-associated pneumonia (HAP) was associated with a higher risk of resistance compared with BSI (OR: 3.467; 95% CI: 2.139-5.621; p < 0.001). Total antibiotic consumption remained comparable between PreP and PanP but increased in PostP. During the PanP, carbapenem use increased while piperacillin-tazobactam consumption decreased, whereas glycopeptide use increased and reached its highest level in PostP. Pandemic-related disruptions in the health care system may have contributed to increases in HAI and AMR rates, whereas improvements in the PostP may have supported recovery. Continuous surveillance, infection prevention measures, and antimicrobial stewardship programs are essential to mitigate the impact of future health care crises.
ICESan95 is a serine integrase integrative and conjugative element (ICE) that targets methyltransferase genes for integration. The mosaic ICE ICESag084 contains ICESan95 and partial fragments from two distinct genes (snf2 and hsdM), suggesting a recombination event. This study aimed to experimentally investigate the recombination of multiple ICESan95, leading to the formation of a mosaic ICE resembling ICESag084. Using conjugation assays, we tracked this evolutionary process, confirmed the structures via whole-genome sequencing, and assessed genomic stability through serial passages. Analysis showed that ICESag084 comprises an ICESan95-like ICE, a tyrosine integrase element, and a partial ICESpy009 sequence. The ICESan95-like ICE was flanked by truncated snf2 and hsdM genes, indicating ancestral cointegration of two ICESan95-like ICEs followed by excision and sequence capture. Experiments confirmed that tandem integration of ICESan95 into adjacent snf2 (from an ICESpy009-like element) and hsdM(from the tyrosine integrase element) sites facilitated recombinational excision. This event deleted an ∼36.6-kb intervening fragment, yielding an ∼86.5-kb circularized intermediate and generating an ∼81.0-kb mosaic ICE highly similar to ICESag084. The mosaic ICE was conjugatively transferable and remained stable for ≥60 generations, while the circularized ICE was lost within 20 generations. Thus, tandem integration and recombinational excision drive the emergence and spread of mosaic ICEs. This mechanism facilitates the modular assembly of multiple mobile genetic elements, including ICESpy009, ICESan95, and a tyrosine integrase element. This process creates novel resistance islands with expanded traits, providing a key pathway for long-term adaptive evolution in bacterial pathogens.
The emergence of Escherichia coli sequence type (ST131), especially its H30Rx subclade, has reshaped the epidemiology of urinary tract infections (UTIs) by combining multidrug resistance (MDR), extended-spectrum β-lactamase (ESBL) production, and biofilm formation. Clinical E. coli isolates were genotyped for ST131 and H30Rx using PCR. Antimicrobial susceptibility, ESBL activity, biofilm formation, and plasmid carriage were assessed through standard protocols. Statistical tests were applied to explore associations between clonal types and resistance traits. Nearly half of the isolates (46.3%) were identified as ST131, with 78.9% belonging to H30Rx. Overall, eight isolates (19.5%) were ESBL producers. ESBL production was significantly higher in ST131 (36.8%) compared with non-ST131 (4.5%; p = 0.004). Plasmid carriage was universal in ST131 (100%) and more frequent than in non-ST131 (86.4%; p = 0.029). MDR was observed in almost 90% of ST131 isolates. Biofilm formation was widespread (97.5%), with all ST131 strains positive. Resistance was greatest against fluoroquinolones and third-generation cephalosporins, while fosfomycin, nitrofurantoin, and amikacin retained high activity with low resistance rates. The predominance of ST131, particularly H30Rx, highlights its role as a high-risk clone driving ESBL production, plasmid-mediated resistance, and biofilm-associated persistence in UTIs. Given the rising resistance to commonly used antibiotics, fosfomycin, nitrofurantoin, and amikacin remain promising therapeutic options. Key limitations include a modest sample size ( n = 41 E. coli isolates), the absence of genotypic ESBL characterization, and the use of disk diffusion for fosfomycin and nitrofurantoin without MIC confirmation. Continuous surveillance, molecular characterization, and strengthened antimicrobial stewardship are essential to control the spread of this lineage and preserve treatment efficacy.
This study evaluated a 6-month, on-farm antimicrobial stewardship model integrating veterinary oversight, appropriate antimicrobial use, enhanced biosecurity, and an all-in/all-out system on five Korean pig farms lacking prior oversight. Antimicrobial usage and resistance of Escherichia coli were compared before and after implementation. The number of antimicrobial prescriptions decreased significantly following the implementation of the model (from 15.2 ± 9.2 to 7.2 ± 4.7). After model implementation, prescriptions for suckling piglets decreased from 2.2 ± 1.6 to 0.4 ± 0.9, and for weaned piglets from 4.4 ± 2.4 to 1.8 ± 1.1. Overall antimicrobial resistance decreased following model implementation, with the largest decreases were observed in ciprofloxacin (from 57.3% to 21.9%), nalidixic acid (from 60.0% to 34.2%), and cefazolin (from 92.0% to 64.4%). The multidrug-resistance rates in eight antimicrobial classes decreased significantly across all stages (from 28.0% to 4.1%), with decreases for suckling piglets (from 33.3% to 7.1%), weaned piglets (from 40.0% to 0.0%), growers (from 26.7% to 0.0%), finishers (from 26.7% to 14.3%), and sows (from 13.3% to 0.0%). The model effectively reduced both antimicrobial use and resistance, supporting its value for antimicrobial stewardship in pig production.
Human infections with non-Helicobacter pylori Helicobacter species (NHPH) are rare. The diagnosis of such infection relies strongly on histological methods, as these bacteria cannot be easily cultured. We describe microbiological analyses that were performed on three cases of infection reported between 2020 and 2023, for which molecular biology was used to identify the species and facilitate the investigation of markers of resistance to macrolides and fluoroquinolones. 16S rRNA sequencing identified two Helicobacter suis strains and one Helicobacter heilmannii sensu strictostrain. Sequencing of 23S rRNA and quinolone resistance determining region of the gyrA gene, classically described as carrying mutations associated with resistance to macrolide and levofloxacin, respectively, did not reveal any mutations. RIDA®GENE H. pylori, the Allplex™ H. pylori and ClariR Assay and Amplidiag® H. pylori+ClariR cross-react with these NHPH strains. Any case of NHPH infection diagnosed by histology should be confirmed by molecular biology in specialized laboratories to identify the species and investigate the resistome.
Since their first identification in Türkiye in 2001, OXA-48-like carbapenemases have posed diagnostic challenges due to variant-specific phenotypic and resistance profiles. We investigated the distribution of OXA-48 variants and their association with antimicrobial susceptibility, carbapenem minimum inhibitory concentrations (MICs), phenotypic detection performance, and single- or dual-carbapenemase production. A total of 703 clinical carbapenem-resistant Enterobacterales isolates recovered over 5 years were included. Identification and antimicrobial susceptibility testing were performed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) and an automated system; carbapenem MICs by broth microdilution; carbapenemase genes by multiplex qPCR; and OXA-48 variants by sequence analysis. CNPt-direct and mCIM were performed for OXA-48 variants. OXA-48-like, NDM, and KPC carbapenemases were detected in 52.3%, 11.7%, and 11.5% of isolates, respectively, with co-production observed in 11.7% of OXA-48-like-positive isolates. The most common OXA-48 variants were OXA-48/245 (39.1%), OXA-232 (36.4%), and OXA-181 (17.6%), while OXA-244, OXA-162, and OXA-1200 were less frequent. This study represents the first report of the OXA-1200 variant from Türkiye. OXA-48/245 was the variant most commonly co-produced with other carbapenemases, whereas OXA-244 predominated among CNPt-direct-negative isolates. Susceptibility to meropenem and imipenem among OXA-48-like producers was 31% and 39.1%, respectively, with higher carbapenem MIC50 values observed for OXA-181, OXA-232, and OXA-48/245 compared to OXA-244. In K. pneumoniae, meropenem resistance rates were higher with OXA-48/245, OXA-232, and OXA-181 than with other variants. MIC50 values of carbapenem were higher in dual carbapenemase producers compared to single carbapenemase producers. Our findings show that OXA-48 variants significantly impact resistance profiles, MIC values, and the sensitivity of phenotypic tests and detection of co-produced carbapenemases. Understanding their regional distribution is crucial for targeted prevention strategies.
Antimicrobial resistance (AMR) represents a critical global health crisis, driving increased mortality, treatment failure, and economic burden. Artificial intelligence (AI) offers transformative potential to counter this threat by enhancing detection, diagnostics, and therapeutic precision. This narrative review synthesizes recent advances in AI-based approaches for AMR prediction, antimicrobial discovery, and clinical decision support, drawing on representative peer-reviewed studies published between January 1, 2015, and April 24, 2026. Models such as Deeparg-LS, XGBoost, and vision transformers achieved remarkable predictive accuracy using genomic, spectroscopic, and clinical data (AUC > 0.90; sensitivity/specificity >95%). AI-driven clinical decision support systems reduced antibiotic mismatches by up to 67%, while generative algorithms accelerated antimicrobial peptide discovery with 76% validation success. Deep learning frameworks improved metagenomic resistance profiling, and microscopy-based diagnostics shortened antimicrobial susceptibility testing by 50-70%. However, major challenges persist, including dataset heterogeneity, computational intensity, limited model transferability, and ethical concerns related to data privacy, bias, and interpretability. Emerging strategies such as explainable AI and federated learning show promise in addressing these issues. Overall, AI stands as a pivotal enabler in the fight against AMR, with future progress hinging on interdisciplinary collaboration, standardized validation, and responsible integration into clinical practice.
BACKGROUND:Nakaseomyces glabratus exhibits intrinsic tolerance to azole antifungals, frequently mediated by gain-of-function (GOF) mutations in the transcription factor CgPDR1. While efflux-mediated resistance is well established, its potential interaction with oxidative stress-dependent cell death pathways in biofilms remains insufficiently characterized. MATERIALS AND METHODS:Fifteen clinical isolates (susceptible, n = 5; resistant, n = 10) were analyzed under planktonic and biofilm conditions. Antifungal susceptibility to itraconazole (0.03-32 µg/mL) was determined, while apoptosis and intracellular reactive oxygen species (ROS) were quantified using Annexin V/PI staining and fluorescence-based assays, respectively. The role of oxidative stress was evaluated using ascorbic acid co-treatment. CgPDR1 mutations were identified by sequencing. RESULTS:Resistant isolates exhibited significantly elevated minimum inhibitory concentration (MIC) values (up to 32 µg/mL) and a high prevalence of CgPDR1 mutations (K274N: 100%; D1082G: 30%; S343F: 10%). Itraconazole induced a marked increase in ROS production and apoptosis in susceptible biofilms (Annexin V+ ≈ 70%), whereas resistant isolates demonstrated attenuated ROS generation and reduced apoptosis (≈10%, p < 0.01). Although ascorbic acid significantly decreased ROS levels in susceptible isolates, it did not alter MIC values or restore antifungal susceptibility. CONCLUSIONS:CgPDR1 GOF mutations are associated with a coordinated resistance phenotype in N. glabratus biofilms, characterized by enhanced drug tolerance and reduced ROS-mediated apoptosis. These findings support a multifactorial resistance model and identify K274N as a potential population-specific biomarker.
BACKGROUND:Klebsiella pneumoniae is a major etiological agent of pediatric sepsis. The emergence and dissemination of carbapenem-resistant K. pneumoniae (CRKP) and hypervirulent strains (hvKp) represent an escalating global health concern. However, data regarding the coexistence of carbapenem resistance and hypervirulence in pediatric populations, especially in low- and middle-income countries, remain limited. OBJECTIVES:This study aimed to determine the prevalence of carbapenem resistance and hypervirulence-associated genes among pediatric K. pneumoniae bloodstream infections in Egypt and to assess their association. METHODS:A cross-sectional study was conducted involving 100 pediatric patients with culture-confirmed K. pneumoniae sepsis at Mansoura University Children's Hospital between January 2023 and January 2025. Clinical and laboratory data were collected. Antimicrobial susceptibility testing was performed using standard disc diffusion and carbapenemase inhibition assays. Polymerase chain reaction (PCR) was employed to detect carbapenemase genes (including blaNDM for New Delhi metallo-β-lactamase, blaOXA-48 for oxacillinase-48, blaKPC for K. pneumoniae carbapenemase, blaVIM for Verona integron-encoded metallo-β-lactamase, and blaIMP for imipenemase). Hypervirulence genes tested included iucA (aerobactin siderophore synthesis), iroN and iroB (salmochelin siderophore cluster), and peg-344 (putative transporter). Genotypic hvKp was defined as the presence of two or more hypervirulence-associated genes. RESULTS:Carbapenem resistance was identified in 64% of isolates, with blaNDM (New Delhi metallo-β-lactamase) and blaOXA-48-like (oxacillinase-48) genes being the most prevalent carbapenemase determinants. Hypervirulence-associated genes were detected in 86% of isolates, which were classified as genotypic hvKp, most frequently iucA (aerobactin system) and peg-344 (putative transporter). No significant demographic or inflammatory differences were observed between CRKP and carbapenem-susceptible groups. Hypervirulence was present at similarly high frequencies in CRKP (87%) and carbapenem-susceptible K. pneumoniae (84%) isolates, with no significant association between these traits (p = 0.782). Logistic regression analysis did not identify any clinical predictors of hypervirulent infection. CONCLUSION:The detection of multidrug-resistant K. pneumoniae isolates harboring multiple hypervirulence-associated genes highlights the potential convergence of resistance and virulence determinants. However, further phenotypic and functional studies are required to confirm the hypervirulent phenotype and assess its clinical significance.
During whole-genome analysis of 179 Pasteurella multocida isolates from bovine respiratory tract infections collected in the German national resistance monitoring program GE RM -Vet, two isolates carried plasmid-borne bla ROB-1 genes for a small-spectrum β-lactamase. Both plasmids varied slightly in their sizes, 4,320 bp (pHKH171865) and 4,615 bp (pHKH211885), respectively, and carried besides the bla ROB-1 gene, closely related mobilization gene clusters comprising the genes mobA , mobB , and mobC . In vitro intergenus transfer into Escherichia coli confirmed that both plasmids mediated ampicillin resistance. Comparisons with sequences deposited in the National Center for Biotechnology Information (NCBI) database revealed that both plasmids were unique, although similar sized, and structurally closely related plasmids have been identified in a number of other members of the family Pasteurellaceae , including the genera Actinobacillus , Glaesserella , Haemophilus , Histophilus , and Mannheimia , from humans and different animals in North America, Europe, and Australia. These observations suggest in vivo intergenus transfer rather than independent generation of these plasmids in the respective bacterial hosts.
BACKGROUND AND OBJECTIVE:Drug-resistant (DR) mycobacterial infections present escalating threats in Iran, where facility-specific transmission dynamics and demographic disparities remain poorly characterized. This study evaluated the epidemiology of DR Mycobacterium tuberculosis and pulmonary nontuberculous mycobacterial disease over a 9-year period (2016-2024). MATERIALS AND METHODS:This retrospective study analyzed 21,700 molecular and culture-confirmed mycobacterial samples. Species identification used line probe assays and Xpert Mycobacterium tuberculosis/rifampin. Drug susceptibility testing followed World Health Organization standards. Statistical analyses identified associations between resistance patterns, hospital sections, gender, and specimen types. RESULTS:MDR-TB prevalence surged from 0.35% (2017) to 3.27% (2022), peaking during pandemic disruptions. M. simiae dominated nontuberculous mycobacteria (NTM) resistance (55.63% of resistant isolates), with significant increases in 2024 (7.91%). Airborne infection isolation rooms (AIIRs) paradoxically harbored 18.22% of Multidrug-resistant tuberculosis (MDR-TB)isolates (p < 0.0001), while pulmonary medicine units contained zoonotic M. bovis reservoirs (0.27% MDR prevalence). Male patients carried higher burdens of MDR-TB (26.01% vs. 12.45%, p = 0.005) and M. kansasii (2.05% vs. 0.53%, p = 0.012). Diagnostic challenges included 38.14% smear-negative M. abscessus and gastrointestinal NTMs (M. genavense 66.66%). Sample type analysis revealed M. fortuitum in 25.0% of abscesses (p < 0.05) and M. chelonae in 5.55% of synovial fluid (SF) specimens. CONCLUSION:Iran faces converging epidemics of MDR-TB and climate-adapted NTMs concentrated in hospital hotspots, with significant gender disparities. Precision interventions targeting AIIR protocols, water safety regulations, and gender-specific screening are urgently needed.
Klebsiella pneumoniae remains a major cause of invasive infections and is highly capable of acquiring antimicrobial resistance. This exploratory study investigated the antimicrobial resistance profiles and virulence determinants of Klebsiella pneumoniae isolates collected between January and December 2022 at a tertiary-care hospital in Panama City, Panama. A subset of 27 K. pneumoniae isolates was phenotypically and genetically characterized using antimicrobial susceptibility testing. (VITEK® system), 16S rRNA gene sequencing, multilocus sequence typing (MLST), and virulence gene screening. Our results indicated multidrug resistance (MDR) in 52% (14/27) of these isolates. Virulence gene analysis revealed a high prevalence of genes associated with fimbriae 96% (26/27), capsule formation 96% (26/27), lipopolysaccharide synthesis 59% (15/27), and siderophore production 48% (13/27). The MLST of 14 isolates harboring MDR, resistant, and susceptible phenotypes identified known sequence types (ST348, ST111, ST1104, ST6394, ST806, ST45, and ST163), as well as seven novel sequence types (ST6917-ST6923). Phylogenetic analysis based on 16S rRNA sequences confirmed Klebsiella genus identity and proved close genetic relatedness among isolates. No clear association between MDR profiles and sequence types was observed. These findings suggest the uncontrolled widespread of MDR K. pneumoniae strains containing multiple virulence determinants in a high-complexity health care setting in Panama. We urge the need to strengthen antimicrobial stewardship programs and reinforce infection prevention strategies to limit the spread of high-risk clones and preserve antimicrobial efficacy.
BACKGROUND:The increasing prevalence of multidrug-resistant Pseudomonas aeruginosa limits treatment options and highlights the need for new antimicrobials. Although agents such as ceftazidime-avibactam (CZA), ceftolozane-tazobactam, imipenem-relebactam, and cefiderocol have expanded therapeutic choices, resistance to these antibiotics is also emerging. Combination therapies therefore remain an important strategy. This study evaluated the in vitro synergistic activity of the CZA-colistin (COL) combination in carbapenem-resistant P. aeruginosa (CRPA) isolates. METHODS:Twelve clinical CRPA isolates obtained from Kocaeli University Hospital (2021-2022) were included. Minimum inhibitory concentration values were determined by broth microdilution, and synergy was assessed using the checkerboard method. Synergy categories were defined as follows fractional inhibitory concentrations index (FICI) ≤ 0.5 synergism, 0.5 < FICI ≤ 1.0 partial synergism, 1.0 < FICI ≤ 4.0 indifference, and >4.0 antagonism. RESULTS:All isolates were susceptible to colistin, whereas four were resistant to CZA. Checkerboard analysis showed partial synergy in nine of 12 isolates (75.0%), with no antagonism detected. Partial synergy was more frequent in CZA-resistant isolates (100%) than in CZA-susceptible ones (62.5%) and was notably associated with isolates carrying blaNDM and blaOXA-48. CONCLUSIONS:CZA-COL combination may offer partial synergy, especially in CZA-resistant CRPA strains; however, broader in vivo and prospective studies are needed to support clinical use.
OBJECTIVE:To characterize the clinical and genomic features of vancomycin-resistant enterococci (VRE) in a tertiary hospital in Huizhou and identify risk factors to inform local infection control. METHODS:A retrospective study included 58 VRE and 25 vancomycin-susceptible Enterococci (VSE) strains (August 2023-May 2025). Clinical data and antimicrobial susceptibility were analyzed; whole-genome sequencing (WGS) was performed on 54 VRE strains. RESULTS:Midstream urine was the primary VRE-positive specimen. ICU admission, polyantibiotic use (≥3 agents), and urinary catheterization were key risk factors for VRE. All VRE isolates were Enterococcus faecium and showed a predominantly clonal population structure, dominated by CC17/ST80 (68.8%) and CC2/ST106 (64.6%) under the two multilocus sequence typing schemes; five novel STs were ultimately identified in the latter scheme. VRE was universally resistant to ampicillin, with high resistance to penicillin, levofloxacin, and teicoplanin, while linezolid and tigecycline remained effective. Genotypically, 94.8% carried vanA, 100% carried virulence gene esp, and aminoglycoside and macrolide resistance genes were prevalent. A unique VRE strain (VRE48) showed resistance without canonical van genes, harboring a Ddl Ser210Tyr mutation.
BACKGROUND:This study aimed to determine the prevalence of carbapenem-resistant Enterobacterales (CRE), to characterize their molecular resistance mechanisms, and to assess associated clinical outcomes among intensive care unit (ICU) patients in Tunisia. METHODS:A cross-sectional study was conducted from January to March 2025 in the ICU of Habib Thameur Hospital and included all patients with clinically significant CRE infections. Resistance determinants were identified using multiplex polymerase chain reaction with reverse dot blot hybridization. RESULTS:Among 95 ICU admissions, 17 patients developed CRE infections, corresponding to an incidence density of 21.6 cases per 1,000 patient-days. All infections were hospital-acquired. The most frequent risk factors were the presence of central venous and urinary catheters (16 patients each) and mechanical ventilation (15 patients). Klebsiella pneumoniae predominated, accounting for 26 of 27 isolates, all of which were multidrug-resistant (MDR), with a median antibiotic resistance index of 1.00. The blaNDM and blaOXA-48 genes were detected in 81.5% and 77.8% of isolates, respectively, with 70.4% co-producing both carbapenemases. All K. pneumoniae isolates harbored blaSHV and/or blaCTX-M, while a single Escherichia coli isolate carried blaOXA-48. Cluster analysis revealed strong associations between β-lactamase production and resistance to aminoglycosides and fluoroquinolones, suggesting co-selection of MDR strains. Empirical antimicrobial therapy was appropriate in only 47% of cases, and ICU mortality reached 82.4%. CONCLUSION:These findings highlight an alarmingly high burden of CRE infections in this ICU, driven mainly by K. pneumoniae co-producing NDM and OXA-48, and underscore the urgent need for strengthened infection control and antimicrobial stewardship strategies.
The current study was conducted to determine the antibiotic resistance profile and prevalence of extended-spectrum β-lactamases (ESBLs)-producing Escherichia coli among the uropathogenic E. coli (UPEC) strains (n = 100), isolated from patients with urinary tract infection (UTI) in Hamedan, western Iran. In addition, the molecular prevalence of antibiotic resistance genes (ARGs) and ESBL genes among these strains was investigated using polymerase chain reaction. Out of 100 UPEC isolates, 46 (46%) and 40 (40%) isolates were phenotypically identified as multidrug-resistance (MDR) strains and ESBLs producer strains, respectively. UPEC isolates showed the highest resistance to trimethoprim/sulfamethoxazole (55%), followed by amoxicillin (51%) and ampicillin (45%). The most prevalent ARG in UPEC strains was tetA (10%), followed by aadA1 (9%), sul1 (9%), qnrs (7%), and dfrA1-like (3%). Among the 40 UPEC isolates that phenotypically confirmed as ESBL producers, 19 (475%) isolates harbored blaCTX-M gene, 9 (22.5%) harbored blaTEM gene, 8 (20%) harbored blaOXA gene, and 4 (10%) harbored blaCIT-M. The ESBL gene blaCTX-M displayed a significant association with ESBL phenotypic isolates at p value <0.05. Due to the relatively high prevalence of MDR-UPEC strains and ESBLs producer UPEC isolates among patients with UTI reported herein and also regarding incidence of ARGs and β-lactamase gene among these isolates, applying precise antibiotic stewardship, continuous surveillance to use appropriate antibiotics, and the control of UTI infections seem necessary to decrease ESBLs producer UPEC and MDR-UPEC strains.
