The intersection of microbial food safety and antimicrobial resistance (AMR) represents a mounting global threat with profound implications for public health, food safety, and sustainable development. This review explores the complex pathways through which foodborne pathogens—such as Salmonella spp., Escherichia coli (E. coli), Listeria monocytogenes (L. monocytogenes), and Campylobacter spp.—acquire and disseminate resistance within human, animal, and environmental ecosystems. Emphasizing a One Health framework, we examine the drivers of AMR across sectors, including the misuse of antibiotics in agriculture, aquaculture, and clinical settings, and assess the role of environmental reservoirs in sustaining and amplifying resistance genes. We further discuss the evolution of surveillance systems, regulatory policies, and antimicrobial stewardship programs (ASPs) designed to mitigate resistance across the food chain. Innovations in next-generation sequencing, metagenomics, and targeted therapeutics such as bacteriophage therapy, antimicrobial peptides (AMPs), and CRISPR-based interventions offer promising alternatives to conventional antibiotics. However, the translation of these advances into practice remains uneven, particularly in low- and middle-income countries (LMICs) facing significant barriers to diagnostic access, laboratory capacity, and equitable treatment availability. Our analysis underscores the urgent need for integrated, cross-sectoral action—anchored in science, policy, and education—to curb the global spread of AMR. Strengthening surveillance, investing in research, promoting responsible antimicrobial use, and fostering global collaboration are essential to preserving the efficacy of existing treatments and ensuring the microbiological safety of food systems worldwide.

Pseudomonas aeruginosa (P. aeruginosa) forms biofilms that are difficult to eliminate. The matrix protects the cells, efflux pumps reduce intracellular drug levels, and dormant subpopulations survive treatment. Routine minimum inhibitory concentration (MIC) testing does not account for these features, which helps explain why infections often continue even when therapy appears appropriate. This review describes how quorum-sensing (QS) and cyclic di-guanosine monophosphate (c-di-GMP) regulate matrix production, efflux activity, and dormancy within P. aeruginosa biofilms. Important matrix components, including Psl, Pel, alginate, and extracellular DNA, slow the movement of antimicrobial agents. Regulatory proteins such as sagS and brlR increase the activity of the MexAB-OprM and MexEF-OprN efflux systems, further reducing intracellular drug concentrations. Oxygen and nutrient limitation promote persister cells and viable but nonculturable cells, with both having the ability to survive antibiotic levels that would normally be lethal. These defenses explain the gap between MIC values and biofilm-specific measurements, such as the minimum biofilm inhibitory concentration and the minimum biofilm eradication concentration. This review also summarizes emerging antibiofilm strategies. These include QS inhibitors, compounds that lower c-di-GMP, such as nitric oxide donors, nanoparticles, depolymerases, bacteriophages, and therapies that are directed at host targets. Modern diagnostic tools, such as confocal laser scanning microscopy, optical coherence tomography, and Raman spectroscopy, improve detection and guide treatment planning. A staged therapeutic approach is presented that begins with the dispersal or loosening of the matrix, continues with targeted antibiotics, and concludes with support for immune clearance. Viewing these strategies within a One Health framework highlights the role of biofilms in clinical disease and in environmental reservoirs and supports more effective surveillance and prevention.

Helicobacter pylori (H. pylori) is a Gram-negative, spiral-shaped bacterium that colonizes the gastric epithelium and is associated with a range of gastrointestinal disorders, exhibiting a global prevalence of approximately 50%. Despite the availability of treatment options, H. pylori frequently reemerges and demonstrates increasing antibiotic resistance, which diminishes the efficacy of conventional therapies. Consequently, it is imperative to explore non-antibiotic treatment alternatives to mitigate the inappropriate use of antibiotics. This review examines H. pylori infection, encompassing transmission pathways, treatment modalities, antibiotic resistance, and eradication strategies. Additionally, it discusses alternative therapeutic approaches such as probiotics, anti-biofilm agents, phytotherapy, phototherapy, phage therapy, lactoferrin therapy, and vaccine development. These strategies aim to reduce antimicrobial resistance and enhance treatment outcomes for H. pylori infections. While alternative therapies can maintain low bacterial levels, they do not achieve complete eradication of H. pylori. These therapies are designed to bolster the immune response, minimize side effects, and provide gastroprotective benefits, rendering them suitable for adjunctive use alongside conventional treatments. Probiotics may serve as adjunctive therapy for H. pylori; however, their effectiveness as a monotherapy is limited. Photodynamic and phage therapies exhibit potential in targeting H. pylori infections, including those caused by drug-resistant strains, without the use of antibiotics. The development of a reliable vaccine is also critical for the eradication of H. pylori. This review identifies candidate antigens such as VacA, CagA, and HspA, along with various vaccine formulations, including vector-based and subunit vaccines. Some vaccines have demonstrated efficacy in clinical trials, while others have shown robust immune protection in preclinical studies. Nevertheless, each of the aforementioned alternative therapies requires thorough preclinical and clinical evaluation to ascertain their efficacy, side effects, cost-effectiveness, and patient compliance.

Bloodstream infections and sepsis necessitate rapid, sensitive, and clinically relevant diagnostics to minimize treatment delays and improve clinical outcomes. Next-generation sequencing enables culture-independent pathogen detection, antimicrobial resistance profiling, and genome-informed epidemiology. This narrative review integrates clinical evidence with practical workflows across three complementary approaches. We describe the use of plasma microbial cell-free DNA for broad organism detection and burden monitoring, as well as metagenomic next-generation sequencing of blood or plasma for unbiased pathogen discovery, including culture-negative and polymicrobial infections. Same-day Oxford Nanopore Technologies sequencing of positive blood culture broth is also discussed as a way to accelerate species identification, targeted resistance reporting, and infection-prevention decisions. We outline the sample-to-result steps, typical turnaround time (TAT), and stewardship-aligned decision points. Analytical reliability depends on effective reduction in human DNA background, stringent control of background and reagent-derived nucleic acids in low-biomass samples, and documented and validated bioinformatics workflows that are supported by curated taxonomic and resistance databases. Quantitative reports should adhere to validated thresholds and should be interpreted in the context of internal controls and clinical pretest probability. Ongoing challenges include variable correlation between genotype and phenotype for specific pathogen and antibiotic pairs, interpretation of low-level signals, and inconsistent regulatory and reimbursement environments. Advances in portable sequencing, faster laboratory and analytical workflows, and scaled liquid biopsy strategies may further reduce the TAT and expand access. Integrating these tools within One Health frameworks and global genomic surveillance programs could support early resistance detection and coordinated public health action, which could help to advance sepsis care toward more precise treatment and real-time infection control insights.

Helicobacter pylori (H. pylori) infection is one of the major causes of gastric cancer and remains an important global health concern. However, the biological processes linking chronic infection to malignant transformation are still not fully understood. Unlike previous reviews that mainly emphasized oxidative injury or individual virulence factors, this review synthesizes current evidence into an integrated redox-centered framework for gastric carcinogenesis. This framework links signaling pathways, epithelial adaptation, diagnostic interpretation, and therapeutic stratification. Current evidence indicates that persistent redox imbalance interacts with inflammatory signaling, mitochondrial dysfunction, metabolic reprogramming, epigenetic alteration, microbiome disruption, and oncogenic pathway activation throughout disease progression. Particular attention is given to the coordinated roles of NF-κB, STAT3, PI3K/AKT, HIF-1α, β-catenin, and Hippo-YAP signaling pathways. These pathways contribute to epithelial survival, chronic inflammation, genomic instability, and malignant transformation. This review additionally introduces a conceptual threshold model describing the progression from early epithelial stress to increasingly stable oncogenic reprogramming during long-standing infection. In addition, the limitations of conventional infection-centered diagnostics and non-selective antioxidant therapies are critically discussed. Emerging diagnostic approaches include oxidative injury biomarkers, transcriptomic and epigenetic profiling, artificial intelligence-assisted pathology, and multi-parameter predictive models. These approaches may improve risk stratification and facilitate earlier identification of high-risk gastric states. The translational implications further emphasize the importance of stage-specific and compartment-directed therapeutic strategies, particularly selective redox modulation and precision-guided targeting. Overall, this review provides a multidimensional perspective on H. pylori-associated gastric carcinogenesis and highlights future directions for predictive diagnostics, mechanistic stratification, and precision-based therapeutic development.

Drug-resistant biofilm infections remain a major challenge for medical devices and implants. Biofilm formation can reduce antimicrobial effectiveness through physiological heterogeneity, tolerance, persistence, and interactions with the host and biomaterial surface. Antimicrobial biomaterials have been developed to prevent colonization, detect infection, provide antimicrobial activity, control established biofilms, and support tissue recovery. However, their performance depends on the biological context in which they function. This review examines these strategies through interactions among the host, microbe, and material, using carbapenem-resistant Acinetobacter baumannii, methicillin-resistant Staphylococcus aureus, and carbapenem-resistant Pseudomonas aeruginosa as selected biological stress-test examples for evaluating biomaterial performance. It also considers the limitations in current evaluation, including planktonic testing, biological conditioning, microbial adaptation, effects on non-target microorganisms, material stability, manufacturing, and clinical translation. Antimicrobial activity alone does not establish effective performance in infection. Material function must match the microbial state, host environment, and intended clinical use while maintaining host compatibility and function during use. We propose infection resilience as a design framework organized around Prevent, Detect, Respond, Resolve, and Regenerate. Infection resilience refers to coordinated material performance under changing microbial and host conditions rather than the number of functions incorporated into a material. This framework offers a practical basis for more biologically relevant evaluation and purposeful design of antimicrobial biomaterials for drug-resistant biofilm infections.