Introduction. The spread of carbapenem-resistant Enterobacterales (CRE) is associated with high mortality rates, limited therapeutic options, and the risk of ineffective empirical antibacterial therapy. Cefiderocol retains activity against many producers of serine carbapenemases and metallo-β-lactamases through its utilization of bacterial iron transport systems. However, hyperproduction of β-lactamases, alterations in siderophore receptors and PBP3, as well as heteroresistance, may compromise its efficacy. One potential strategy to enhance the activity of this agent is its combination with sulbactam.

Objective. To summarize and critically appraise the data on the mechanisms of synergy between cefiderocol and sulbactam against carbapenem-resistant Enterobacterales, the available experimental and clinical evidence base, limitations, and prospects for the clinical use of this combination.

Material and Methods. The review was prepared in accordance with the SANRA criteria and PRISMA-S guidelines. A literature search was conducted in PubMed/MEDLINE, SpringerLink, ScienceDirect, eLIBRARY.ru, CyberLeninka, and Google Scholar for the period 2007–2026. Studies on mechanisms of resistance to cefiderocol, inhibitory and PBP-mediated activity of sulbactam, microbiological synergy, heteroresistance, PK/PD characteristics, preclinical efficacy, and clinical use of the agents were analyzed. A total of 92 publications were included in the final analysis.

Results. Potential synergy may be mediated through reduced hydrolysis of cefiderocol by inhibited serine β-lactamases, increased periplasmic exposure of the drug, possible additional action on PBPs, and suppression of certain resistant subpopulations. However, sulbactam does not inhibit metallo-β-lactamases and has limited activity against KPC and OXA-48-like enzymes. It does not compensate for impairments in iron transport, PBP3 alterations, or other non-enzymatic resistance mechanisms. Direct investigation of the combination against CRE included only two isolates of K. pneumoniae. Representative studies on Enterobacterales collections, dynamic PK/PD models, direct in vivo studies, and clinical trials are lacking. Optimal sulbactam exposure, predictors of response, and standardized criteria for laboratory confirmation of synergy have not been established.

Conclusion. The cefiderocol–sulbactam combination has an experimental mechanistic rationale; however, the available evidence is insufficient for its routine use in infections caused by carbapenem-resistant Enterobacterales. The potential therapeutic niche may be limited to laboratory-confirmed salvage therapy in the absence of preferred alternatives. Mechanistically stratified microbiological, PK/PD, preclinical, and clinical studies are required for clinical translation.

Background. Carbapenem-resistant Klebsiella pneumoniae (CRKP) is among the most clinically significant healthcare-associated pathogens. CRKP poses the greatest threat in intensive care units (ICUs), where the combination of severe patient conditions, invasive procedures, and high antimicrobial pressure facilitates colonization, nosocomial transmission, and the development of invasive infections.

Objective. To synthesize data on the epidemiology of CRKP in ICUs, mechanisms of carbapenem resistance, clonal and plasmid dissemination, diagnostic approaches, current therapeutic strategies, and infection control measures.

Material and Methods. A structured narrative review of publications from 2008 to 2026 was performed using PubMed/MEDLINE, SpringerLink, ScienceDirect, eLIBRARY.ru, CyberLeninka, and Google Scholar. A total of 66 sources containing data on ICU patients, epidemiology, molecular resistance mechanisms, diagnosis, treatment, or prevention of CRKP spread were included in the final analysis.

Results. The prevalence of CRKP varies substantially across regions and is determined by a combination of antimicrobial pressure, nosocomial transmission, and circulation of high-risk clones. The primary resistance mechanisms involve the production of KPC, OXA-48-like, and metallo-β-lactamases, frequently combined with ESBL/AmpC, impaired OmpK35/OmpK36 expression, efflux, and heteroresistance. The most epidemiologically significant clones include CG258/ST258, ST11, ST147, and ST307. CRKP infections are associated with increased mortality, prolonged hospitalization, and higher costs. Treatment selection should be based on carbapenemase type, infection site, susceptibility testing results, and drug availability. Containment of spread requires a combination of active epidemiological surveillance, timely isolation, molecular typing, and antimicrobial stewardship programs.

Conclusion. CRKP represents a heterogeneous group of hospital pathogens whose clinical management is impossible without distinguishing colonization from infection and without type-specific determination of the resistance mechanism. Priority areas remain the standardization of diagnostics, acquisition of comparative data on MBL and OXA-48 producers, and integration of genomic surveillance with infection control measures.

Antimicrobial resistance (AMR) is a major medical and social threat because it reduces the clinical effectiveness of antimicrobial therapy, increases the risk of poor infectious disease outcomes and requires coordinated action at the levels of health policy, laboratory services and clinical practice. The aim of this review was to consider AMR control as an integrated system combining national policy, local microbiological monitoring, antimicrobial stewardship and emerging anti-infective technologies, including phage therapy. A narrative analytical review of international and Russian guidance documents, methodological papers and scientific publications addressing AMR surveillance, local susceptibility data, cumulative antibiograms, clinically oriented monitoring and bacteriophage-based treatment of infections caused by resistant Gram-negative pathogens was performed. The clinical value of local monitoring is determined not only by the volume of laboratory data but also by the quality of metadata, separation of diagnostic and screening isolates, deduplication of repeated cultures, expert assessment of results and direct linkage between reports and local empirical treatment protocols. Phage therapy is considered a promising personalised and adjunctive approach for infections caused by Klebsiella pneumoniae, Pseudomonas aeruginosa and Acinetobacter baumannii, particularly when standard antibacterial therapy has limited effectiveness. However, its broader implementation requires standardisation of phage susceptibility testing, development of phage banks, regulatory solutions, quality control of preparations and assessment of clinical efficacy in controlled studies. Integration of surveillance, clinical microbiology, digital platforms, antimicrobial stewardship and phage technologies may be considered a promising model for AMR containment in routine clinical practice.

Background. Antimicrobial resistance (AMR) is shaped by clinical, veterinary, agricultural and environmental processes. Its analysis requires the assessment of resistance genes, experimental models, diagnostic approaches and surveillance systems that track antibiotic resistance genes (ARGs) across human, animal and environmental reservoirs.

Objective. To summarize data on experimental and computational models of ARG dissemination, characterize selected AMR markers and evaluate current methods for their detection.

Material and methods. A narrative review with a transparent search strategy and thematic synthesis was conducted. PubMed/MEDLINE, Scopus, Web of Science and Google Scholar were searched; the last search was performed on May 2, 2026. After full-text assessment, 46 sources were included.

Results. The review discusses blaCTX-M-15, blaNDM, blaKPC, blaOXA-23, floR and intI1, as well as mobile genetic elements involved in their dissemination. It summarizes the strengths and limitations of in vitro models, gut models, mouse models, biofilm systems, mathematical modelling, AST, PCR/qPCR, WGS, mNGS, machine learning and CRISPR-Cas12a diagnostics.

Conclusion. CRISPR-Cas12a platforms may support rapid targeted screening of predefined ARGs but do not replace phenotypic susceptibility testing or genome-scale analysis. The most robust strategy is the integration of AST, WGS/mNGS, targeted molecular diagnostics, machine learning and One Health surveillance.

Antibiotic resistance represents one of the pressing challenges of contemporary clinical practice, as it contributes to increased mortality, prolonged hospitalization, and a growing economic burden on healthcare systems. This problem is of particular significance in infections caused by ESKAPE pathogens, carbapenem-resistant Enterobacteriaceae, Acinetobacter baumannii, and Pseudomonas aeruginosa, for which the timely selection of rational antibacterial therapy directly affects prognosis. The aim of the present review is to synthesize current evidence on the value of rapid methods for pathogen identification and antibiotic resistance mechanism detection in optimizing antibiotic therapy. The literature search was conducted in PubMed/MEDLINE, eLibrary, CyberLeninka, Google Scholar, Springer Link, and ScienceDirect; a total of 70 publications were included in the analysis. The capabilities of multiplex PCR panels, MALDI-TOF MS, rapid phenotypic antimicrobial susceptibility testing methods, metagenomic sequencing, and ancillary biomarkers are examined. It has been demonstrated that rapid diagnostics can shorten the time to appropriate therapy, accelerate escalation upon detection of resistant strains, facilitate de-escalation, and reduce unnecessary antibiotic use. The most pronounced clinical effect is achieved when rapid diagnostic tests are integrated into antimicrobial stewardship programs involving microbiologists, clinical pharmacologists, and infectious disease specialists. At the same time, data on the impact of rapid diagnostics on mortality rates, length of hospital stay, and economic costs remain heterogeneous, which is attributable to local epidemiological indicators, the availability of technologies, the organization of laboratory workflows, and the quality of clinical interpretation of results.

Sepsis remains one of the leading causes of mortality in intensive care units, and its course is frequently complicated by sepsis-induced coagulopathy and disseminated intravascular coagulation, which substantially worsen prognosis. The aim of this review is to systematize current concepts regarding the role of antibacterial therapy in the comprehensive management of patients with sepsis complicated by coagulopathy. Antibacterial therapy is regarded as an essential component of treatment directed at eliminating the infectious trigger of thromboinflammation. The most strongly supported requirement remains early infection control when there is a high probability of bacterial sepsis or septic shock, including adequate empiric therapy and source control. At the same time, the extent to which antibiotics specifically influence the dynamics of coagulopathy remains less well studied, as most investigations do not stratify patients by coagulation status or source of infection. The diagnostic role of biomarkers-namely procalcitonin, presepsin, C-reactive protein, extracellular free DNA, complement markers, antithrombin activity, and fibrinogen-is discussed. Evidence indicates that these may assist in assessing infectious burden, the risk of disseminated intravascular coagulation, and prognosis; however, none should be used as an autonomous criterion for initiating or discontinuing antibiotics and anticoagulants. The organ-specific nature of sepsis-associated disseminated intravascular coagulation further demonstrates that the source of infection influences prognosis, the feasibility of source control, baseline antithrombin activity, and the potential applicability of anticoagulant interventions. A clinical framework is proposed, founded on early adequate antibacterial therapy, concurrent assessment of coagulation status, active source control, individualized antibiotic dosing in the presence of organ dysfunction and extracorporeal support, and the consideration of anticoagulant therapy only after evaluation of the coagulation phenotype, source of infection, and bleeding risk. The need for prospective studies stratified by coagulation status and source of infection is underscored in order to refine optimal therapeutic strategies.