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Tomato (Solanum lycopersicum) is a globally important horticultural crop, with Asia contributing 60.45% of total production, followed by the Americas at 13.36%. Tomato productivity is increasingly constrained by southern blight, a destructive disease responsible for yield losses ranging from 30 to 90% and annual economic damage of $10–20 million. The causal pathogen, Sclerotium rolfsii, infects the stem base and induces reddish-brown cankers through secretion of oxalic acid (OA) and cell wall-degrading enzymes, which girdle tissues, impair water transport, and result in rapid plant wilting and death. Its persistence in soil via sclerotia, broad host range, and adaptability make the disease difficult to manage. Recent advances in genomics, transcriptomics, proteomics and other multi-omics approaches have substantially improved understanding of pathogen virulence factors, host defense responses and disease epidemiology. These studies have revealed key roles of OA, carbohydrate-active enzymes, effector proteins, and sclerotial melanization in pathogenesis, while highlighting the activation of salicylic acid (SA)-, jasmonic acid (JA)-, and ethylene (ET)-mediated defense pathways in tomato. Although cultural, biological, and chemical measures are available, these measures often provide inconsistent protection when used alone. Promising strategies include the use of biocontrol agents, hypovirulence-inducing mycoviruses, and chemical fungicides such as carboxamides and quinone outside inhibitors (QoIs), though fungicide resistance remains a risk factor. Integrated Disease Management (IDM) approaches, such as combining biocontrol agents with fungicides, demonstrate enhanced efficacy. This review also evaluates progress in resistance breeding, grafting, RNA interference (HIGS and SIGS), CRISPR-based genome editing, and exploitation of wild genotypes for durable resistance. Furthermore, emerging precision agriculture tools, including hyperspectral imaging, machine learning-assisted disease detection and climate-resilient management strategies, were discussed as new components of sustainable disease management. Full article

The global rise in multidrug-resistant (MDR) fungal pathogens has positioned Candida auris and Candida glabrata as major threats to public health. In recent years, these pathogens have increasingly been reported beyond traditional hospital settings, including neonatal intensive care units, long-term care facilities, oncology wards, and post-pandemic critical care environments. International surveillance bodies, including the Centers for Disease Control and Prevention (CDC), European Centre for Disease Prevention and Control (ECDC), World Health Organization (WHO), and regional monitoring networks, have documented escalating antifungal resistance, complex outbreak dynamics, and persistent gaps in infection control implementation. C. auris has emerged as a major etiological agent of healthcare-associated outbreaks, particularly in intensive care and neonatal units. Surveillance data indicate that a high proportion of C. auris isolates exhibit resistance to azoles, often exceeding 80% in some regions, while echinocandin resistance remains variable. Resistance patterns have evolved from predominantly azole resistance to broader multidrug-resistant phenotypes, including treatment-emergent echinocandin resistance. Six genetically distinct clades (I–VI) have been identified, with Clades I, III, and IV associated with large-scale outbreaks, whereas available data suggests that Clades II, V, and VI are more geographically restricted, although evidence for the recently described clades remains limited. C. glabrata is increasingly recognized as a major cause of invasive candidiasis, with rising resistance reported across multiple regions. While reduced azole susceptibility was historically predominant, emerging evidence highlights rising dual azole–echinocandin resistance, adaptive microevolution during antifungal therapy, and biofilm-associated tolerance mechanisms. Despite these advances, significant gaps persist in global resistance surveillance and in the mechanistic understanding of virulence and antifungal adaptation. Current mitigation strategies include antifungal stewardship programs, expanded resistance testing, and strengthened surveillance systems. Advances in rapid diagnostic technologies such as matrix-assisted laser desorption ionization–time of flight (MALDI-TOF) mass spectrometry, polymerase chain reaction (PCR)-based assays, and genomic surveillance have improved pathogen identification and outbreak detection, although accessibility remains limited in resource-constrained settings. This review examines emerging epidemiological, genomic, and antifungal resistance trends in C. auris and C. glabrata and highlights key priorities for improving diagnosis, surveillance, stewardship, and management of multidrug-resistant Candida infections. Full article

Background: Carbapenem-resistant Klebsiella pneumoniae (CRKP) is a critical public health threat because infections caused by this pathogen are associated with high morbidity, mortality, and limited effective therapeutic options. Whilst the majority of studies have concentrated on inter-patient bacterial transmission, within-host genomic analysis offers unprecedented resolution for tracking dynamic clone predominance, plasmid rearrangements, and microevolution under clinical selection pressures. Methods and Results: Whole-genome sequencing (WGS) of nine isolates recovered from oral and rectal swabs revealed an exceptional case of CRKP clonal turnover in an intensive care unit (ICU) patient. Three distinct high-risk clones were identified during the 18 days of surveillance: an initial ST101 (Clonal Group (CG) 101) strain (days 1–7) followed by concurrent colonization with ST395 (carrying bla_NDM-5) and ST512 lineages (both CG258, days 11–18). Conclusions: This study describes a rare instance of within-host heterogeneity of CRKP, involving three distinct STs spanning two CGs. Whole-genome analysis revealed potential structural rearrangements of resistance- and virulence-associated plasmids between coexisting lineages. These genomic shifts likely reflect rapid adaptation under the intense selective pressure of broad-spectrum antibiotic therapy, culminating in the persistence of a less virulent yet multidrug-resistant ST512 clone and a favorable clinical outcome with patient recovery. Full article

Hantaviruses are emerging rodent-borne pathogens that pose increasing global public health concerns due to their association with hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS), both of which can result in substantial morbidity and mortality. Environmental change, climate variability, urbanization, and land-use transformation are increasingly recognized as critical drivers of hantavirus emergence and transmission. This review summarizes current evidence regarding hantavirus virology, epidemiology, pathogenesis, clinical manifestations, diagnostics, surveillance systems, prevention strategies, and One Health preparedness approaches. Emphasis is placed on the influence of climate change and ecological disruption on rodent reservoir dynamics and spillover risk, as well as major surveillance and diagnostic gaps in tropical and Caribbean regions where hantavirus circulation may be underrecognized. Advances in molecular diagnostics, genomic surveillance, vaccine development, monoclonal antibody therapies, and climate-based early warning systems are also discussed. Existing evidence highlights the importance of integrated One Health surveillance systems that combine human, animal, and environmental monitoring to improve early detection and outbreak preparedness. Strengthening laboratory capacity, ecological surveillance, regional collaboration, and public health infrastructure will be essential for reducing the global burden of hantavirus infections and improving preparedness for future zoonotic disease threats. Full article

In 2025, the Democratic Republic of the Congo (DRC) experienced its 16th Ebola Virus Disease (EVD) outbreak, centered in the Bulape Health Zone of Kasai Province, amid multiple concurrent epidemics and limited health infrastructure. Genomic sequencing revealed a novel zoonotic spillover genetically related to the 1976 Yambuku strain. A Root Cause Analysis (RCA) using the “5 Whys” framework, integrating epidemiological data, genomic analysis, and surveillance reports, identified key contributors to delayed detection and response, with comparative insights drawn from the 2018–2020 North Kivu outbreak. The Mweka outbreak resulted in 28 confirmed, probable, or suspected cases and 15 deaths, including four healthcare workers. Root causes included inadequate ecological surveillance, weak community alert systems, diagnostic delays due to reliance on centralized laboratories, health system overload from concurrent outbreaks, and structural underfunding of preparedness and coordination. Unlike North Kivu, where security issues drove response delays, systemic and ecological vulnerabilities predominated in Mweka. These findings highlight how ecological and structural weaknesses facilitate novel Ebola spillovers and their escalation, emphasizing the need for sustained investment in One Health surveillance, decentralized diagnostics, and resilient public health governance to strengthen outbreak response capacity. Full article

Arboviral diseases are emerging as important public health threats in Saudi Arabia, driven by rapid urbanization, climate variability, the expansion of Aedes aegypti populations, international travel, and large-scale religious mass gatherings. Dengue virus remains the most established arboviral infection in the Kingdom, particularly in the southwestern regions such as Jazan and the western urban centers of Makkah and Jeddah, where ecological and climatic conditions are conducive to sustained vector survival and transmission. This review synthesizes current evidence on the epidemiology, vector ecology, climatic determinants, diagnostics, and prevention strategies of arboviral diseases in Saudi Arabia. Particular attention is paid to the impacts of rising temperatures, changes in rainfall patterns, urban heat island effects, population mobility, and cross-border movement on vector expansion and disease emergence. The review also identifies gaps in surveillance, diagnostics, insecticide resistance monitoring, and integrated vector management programs. Emerging preparedness strategies include climate-informed early warning systems, Geographic Information System-based risk mapping, multiplex molecular diagnostics, genomic surveillance, and community-based vector control. The review emphasizes the importance of implementing a One Health approach that combines data on humans, the environment, entomology, and climate. Currently, sustained endemic transmission of chikungunya and Zika viruses has not been conclusively demonstrated in Saudi Arabia, but increased environmental suitability and connectivity with other areas highlight the need for proactive surveillance and preparedness. Full article

Background/Objectives: Vancomycin-resistant (VRE) and vancomycin-variable (VVE) Enterococcus spp. represent an increasing clinical challenge due to limited treatment options and the potential for undetected dissemination of such resistance genes. Data on Enterococci genomic epidemiology in healthcare settings remain rather limited. Our study aimed to investigate vancomycin resistance determinants in Enterococcus spp., clonal structure, and occurrence of VVE using whole-genome sequencing (WGS) in Latvia. Methods: Clinical isolates collected from hospitalised patients in two tertiary-level hospitals in Latvia (2021–2024) were analysed using WGS following routine laboratory identification. Vancomycin resistance determinants were identified in silico, along with MLST and cgMLST genotyping. Results: Of 532 sequenced isolates, 482 met the quality and inclusion criteria. E. faecalis (56.64%) and E. faecium (40.25%) predominated. Among 125 isolates carrying vancomycin resistance genes, vanB (54.40%) was the most frequent, followed by vanA (38.20%) and vanC (6.40%); vanC was restricted to E. gallinarum and E. casseliflavus. Vancomycin resistance was more prevalent in E. faecium (51.03%) than in E. faecalis (6.59%). cgMLST identified outbreak clusters among E. faecium ST80 and ST78 with complex type-specific resistance patterns and hospital specificity. E. faecalis showed polyclonal endemicity with the vanB gene present in different clades. Three (0.62%) vancomycin-variable E. faecium (VVE) isolates were identified in one hospital, harbouring vanA-type gene clusters comprising vanHAX but lacking the sensory gene vanS and the regulatory gene vanR. Conclusions: The VanB gene predominated in both hospitals, driven by clonal expansion of hospital-adapted E. faecium ST80/ST78, contrasting with earlier vanA predominance in Europe but aligning with recent regional vanB trends. The detection of VVE highlights clinically relevant genotype–phenotype discordance, underscoring the importance of integrating genomic surveillance with routine phenotypic testing to detect cryptic resistance and guide effective antimicrobial therapy. Full article

Cronobacter spp. are opportunistic foodborne pathogens that can cause neonatal meningitis, necrotizing enterocolitis, and sepsis. This study conducted a systematic contamination survey and whole-genome epidemiological analysis of 562 low-water-activity food samples in Hunan Province of China. The results showed an overall Cronobacter spp. detection rate of 41.99% (236/562), with spices exhibiting the highest contamination rate (60.06%), and with high-level contamination samples (>110 MPN/g) concentrated in this category. The 236 isolates comprised 6 species, 120 sequence types, and 39 clonal complexes, with C. sakazakii being the most frequently isolated species (64.83%) and high-risk clones ST4, ST1, ST148, and ST64 prevailing. Multiple virulence genes (TraJ, fur, rcsAB, rpoS) and antimicrobial resistance genes (qnrS1, blaTEM-1, blaCTX-M-55, blaLAP-2, aac(3)-IId, aadA2, tet(A), floR, mcr-9.1, sul2) were detected. Core genome multilocus sequence typing (cgMLST) identified two clustering patterns: Cluster C, whose genetic clustering was consistent with transmission associated with potential common upstream raw materials across different brands and provinces, and Cluster G, whose clustering suggested potential persistent colonization in the production environment across multiple batches of the same brand. This study elucidates the contamination characteristics of Cronobacter spp. in low-water-activity foods from Hunan Province and provides a basis for WGS-based active surveillance and supply chain traceability. Full article

Background/Objectives: Antimicrobial resistance (AMR), driven by high-risk bacterial pathogens, is a major healthcare threat. This scoping review mapped artificial intelligence/machine learning (AI/ML) and computational approaches integrated with whole-genome sequencing (WGS), genomic surveillance, rapid typing, epidemiological data, or clinical metadata for early warning of AMR outbreak clones. Methods: Following PRISMA-ScR guidance and the Population–Concept–Context (PCC) framework, PubMed/MEDLINE, Scopus, and Web of Science were searched for English-language studies published between 2010 and 2026. Eligible studies addressed AI/ML or computational approaches for AMR outbreak detection, clone surveillance, transmission analysis, or infection prevention and control (IPC). Results: Thirty-eight studies were grouped into five domains: genomic surveillance; rapid typing; resistance, risk-factor, and lineage prediction; transmission reconstruction; and IPC-oriented genomic epidemiology. AI/ML supported automation, isolate prioritization, typing triage, prediction, transmission modelling, and electronic health record (EHR)-linked route identification. Conclusions: AI/ML may enhance WGS-based AMR surveillance, but validation, dataset dependence, heterogeneity, and limited IPC outcome reporting remain key gaps. Full article

We conducted whole-genome sequencing to investigate serotypes, virulence-associated genes, antimicrobial resistance determinants, and genetic relationships among Glaesserella parasuis isolates from diseased pigs in Japan, focusing on underrecognized aspects of disease epidemiology and control. Although Glässer’s disease is well recognized in swine production, its epidemiology remains incompletely understood, particularly regarding the relationship between serotype, genotype, and pathogenicity. Serotypes 5 or 12 (5/12) (28.9%) were predominant, followed by serotype 7 (10.8%). Phylogenetic analysis based on core-genome single nucleotide polymorphisms and cluster analysis classified the isolates into three genetic groups, with no clear association between serotype and genetic grouping. One genetic group tended to exhibit a lower proportion of severe clinical cases compared with the others, with a statistically significant difference observed in one comparison but not in the other. These findings provide evidence suggesting genotype-associated differences in disease severity, indicating that pathogenic potential may be more closely linked to genetic background than to serotype. These findings suggest a potential limitation of serotype-based vaccine strategies. Although 86.7% of isolates lacked antimicrobial resistance genes, resistance determinants were identified on contigs predicted to be of plasmid origin. These results indicate that antimicrobial resistance, while not widespread, may be underestimated and could disseminate. Overall, our findings highlight underexplored aspects of Glässer’s disease relevant to improving control and prevention. Full article

The cryopreservation of pre-implantation embryos has become routine in medically assisted reproduction (MAR), and the proportion of frozen embryo transfers has steadily increased in recent years. Because cryopreservation through either slow-cooling protocols or ultra-rapid vitrification requires potentially cytotoxic cryoprotective agents to prevent uncontrolled and detrimental ice crystal formation, the safety of these procedures must be carefully considered. Evidence from human epidemiological studies, including retrospective and prospective controlled studies, and data from national patient registries indicate that children born after frozen embryo transfer have a higher birth weight than those born after spontaneous conception and have an increased risk of rare genomic imprinting disorders, such as Beckwith–Wiedemann, Silver–Russell, or Prader–Willi syndrome. Encompassing not only reversible DNA methylation patterns established during gametogenesis, but also the timed abundance and availability of transcripts and proteins required to establish or maintain epigenetic marks throughout development and differentiation, as well as persistent or transient post-translational histone modifications and non-coding RNAs, the epigenome may be particularly sensitive to cryopreservation. Importantly, epigenetic regulation is highly complex. Alterations of the epigenome at any developmental stage are often not monocausal, do not necessarily result in immediate disturbances in the pre-implantation embryo, and are unlikely to operate through simple all-or-nothing mechanisms; however, they may have long-lasting effects at later developmental stages. To make matters even more complex, differences between species in terms of epigenetic regulation or lineage differentiation are well known and translation from animal model systems to humans must be considered with caution. More recently, epigenetic regulation by non-coding RNAs has also come into focus, as these molecules are crucial, either directly or indirectly, for gene expression, translation, and protein biosynthesis during development. Therefore, assessing potential adverse effects of cryopreservation on the entire epigenome remains a major challenge, particularly because little is known about indirect factors, such as post-translational histone modifications and non-coding RNAs. In this review, we focus on the potential influence of the cryopreservation of pre-implantation embryos on the epigenetic profile in humans and animals. Specifically, we consider DNA methylation of imprinted genes and global DNA methylation; post-translational histone modifications; the abundance and availability of transcripts and proteins required to establish, maintain, or protect epigenetic patterns; and the presence of non-coding RNAs involved in epigenetic control. Full article

Epilepsy is a heritable neurological disorder that is frequently comorbid with sleeping difficulties, including short/long sleep duration and insomnia. Although epidemiological studies have consistently reported the comorbidity between sleep disturbances and epilepsy, the shared genetic architecture and molecular mechanisms underlying this relationship remain poorly characterized, hindering therapeutic development. In this study, we integrated large-scale genome-wide association study (GWAS) summary statistics of European ancestry to dissect the genetic and molecular links between sleep traits and epilepsy. Using LDSC and GWAS-pw, we identified modest but statistically significant (Bonferroni-corrected) global and local genetic correlations between sleep behaviors and epilepsy. Subsequent CPASSOC cross-trait meta-analysis and transcriptome-wide association studies (TWAS) pinpointed specific pleiotropic loci and shared candidate genes, including SPAG7, VRK2, and LINC00925, which are functionally associated with neuroimmune signaling. While preliminary Phenome-Wide Association Study (PheWAS) profiling of these candidate targets did not identify major adverse associations in current databases, we emphasize that rigorous in vitro and in vivo experimental validations are required before considering them for therapeutic strategies. Finally, pleiotropy-robust bidirectional Mendelian Randomization (MR) analyses suggested unidirectional causal liability from epilepsy to short sleep duration. Although the estimated causal effect size was minimal, it reflects lifelong polygenic architecture rather than acute clinical magnitude. In conclusion, our multi-omics approach unveils the shared genetic architecture of the sleep-epilepsy axis and highlights potential biomarkers for future functional investigation. Full article

The rising incidence of early-onset colorectal cancer (CRC) remains incompletely explained despite extensive investigation into genetic, environmental and metabolic factors. Emerging evidence suggests that infectious agents may contribute to colorectal carcinogenesis. A recent study by Tehrani et al. demonstrated the presence of Mycobacterium avium subspecies paratuberculosis (MAP) in a majority of colorectal cancer lesions and in approximately half of precancerous lesions, providing a critical epidemiologic anchor. MAP, a zoonotic intracellular pathogen long associated with Crohn’s disease, exhibits biological features consistent with inflammation-driven carcinogenesis, including persistence, immune modulation and systemic dissemination. Mechanistically, MAP infection may promote tumorigenesis through chronic mucosal inflammation, epithelial barrier disruption and activation of human endogenous retroviruses (HERVs) linking persistent infection to genomic instability. Detection of MAP in early lesions argues against secondary colonization and supports a potential initiating or promoting role. Within a One Health framework, MAP represents a plausible, pleiotropic and potentially modifiable contributor to CRC. While causality remains unproven, the convergence of epidemiologic association, mechanistic plausibility and early lesion involvement warrants rigorous investigation. Full article

Background: Hearing loss is a widespread sensory disorder affecting over 1.5 billion people worldwide, with the number projected to exceed 700 million by 2050. It imposes social and economic burdens across all ages and regions. Approximately half of adult cases are preventable, but the underlying causes are complex, with 75–80% due to autosomal recessive genetic factors and key roles for mutations in genes such as GJB2. Advances in sequencing technologies have accelerated gene discovery, but challenges remain in interpreting variants. Epigenetic mechanisms such as DNA methylation and histone modifications are increasingly recognized as crucial in auditory biology and could offer new biomarkers and therapeutic targets. Integrating epidemiological, genetic, and epigenomic data is essential to developing targeted prevention and treatment strategies to reduce the global burden of hearing loss. Methods: This narrative review examines recent genomic and epigenomic advances in hearing loss, with particular emphasis on molecular mechanisms, emerging diagnostic applications, and translational therapeutic opportunities. A comprehensive review of current epidemiological data, genetic studies, and epigenomic research was conducted using the peer-reviewed literature from international databases. Key areas of interest include inheritance patterns, molecular pathways, and recent advances in omics technologies. Results: Epigenetic mechanisms, including DNA methylation and histone modifications, are increasingly recognized as important regulators of cochlear development and hair cell survival, although much of the current evidence remains preclinical. Studies suggest that peripheral epigenetic signatures may serve as biomarkers for early diagnosis and risk stratification. Conclusions: Integrating established screening pathways with epidemiological trends and molecular knowledge offers a promising path toward precision medicine in hearing care. Connecting these domains is essential to developing equitable and effective interventions and addressing persistent global disparities in hearing health. This review highlights the evolving landscape of auditory genetics and epigenetics and outlines future directions for translational research and personalized therapy. Full article

Begomoviruses are among the most destructive plant viruses, causing substantial yield losses across diverse cropping systems. Their epidemiological success is driven by high genetic plasticity, broad host range, and efficient transmission by the whitefly vector Bemisia tabaci. Traditional epidemiological models based on the classical disease triangle (virus–host–vector) fail to fully capture the ecological and evolutionary complexity of begomovirus pathosystems. Increasing evidence highlights the critical role of non-cultivated plants, particularly weeds, as persistent reservoirs that maintain viral populations during off seasons, facilitate recombination, and act as primary inoculum sources for subsequent outbreaks. Here, we propose the Begomovirus Disease Tetrahedron, an integrative framework that expands the disease triangle by incorporating weeds as a fourth essential component. We synthesize current knowledge on begomovirus adaptive evolution, including genome plasticity, noncanonical protein functions, and virus–vector mutualism, alongside key ecological drivers such as seasonal dynamics, agricultural intensification, and landscape connectivity. By integrating molecular, ecological, and epidemiological perspectives, this framework provides a comprehensive understanding of begomovirus emergence and persistence, offering new insights for the development of sustainable and ecologically informed disease management strategies. Full article