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At least 19 recordsLinked to original sources

PubMed2025

Incorporating Epidemiological Data into the Genomic Analysis of Partially Sampled Infectious Disease Outbreaks.

Pathogen genomic data are increasingly being used to investigate transmission dynamics in infectious disease outbreaks. Combining genomic data with epidemiological data should substantially increase our understanding of outbreaks, but this is highly challenging when the outbreak under study is only partially sampled, so that both genomic and epidemiological data are missing for intermediate links in the transmission chains. Here, we present a new dynamic programming algorithm to perform this task efficiently. We implement this methodology into the well-established TransPhylo framework to reconstruct partially sampled outbreaks using a combination of genomic and epidemiological data. We use simulated datasets to show that including epidemiological data can improve the accuracy of the inferred transmission links compared with inference based on genomic data only. This also allows us to estimate parameters specific to the epidemiological data (such as transmission rates between particular groups), which would otherwise not be possible. We then apply these methods to two real-world examples. First, we use genomic data from an outbreak of tuberculosis in Argentina, for which data was also available on the HIV status of sampled individuals, in order to investigate the role of HIV coinfection in the spread of this tuberculosis outbreak. Second, we use genomic and geographical data from the 2003 epidemic of avian influenza H7N7 in the Netherlands to reconstruct its spatial epidemiology. In both cases, we show that incorporating epidemiological data into the genomic analysis allows us to investigate the role of epidemiological properties in the spread of infectious diseases.

Humans↗

PubMed2022

Spatial-temporal and phylogenetic analyses of epidemiologic data to help understand the modes of transmission of endemic typhoid fever in Samoa.

Salmonella enterica serovar Typhi (S. Typhi) is either widely distributed or proximally transmitted via fecally-contaminated food or water to cause typhoid fever. In Samoa, where endemic typhoid fever has persisted over decades despite water quality and sanitation improvements, the local patterns of S. Typhi circulation remain unclear. From April 2018-June 2020, epidemiologic data and GPS coordinates were collected during household investigations of 260 acute cases of typhoid fever, and 27 asymptomatic shedders of S. Typhi were detected among household contacts. Spatial and temporal distributions of cases were examined using Average Nearest Neighbor and space-time hotspot analyses. In rural regions, infections occurred in sporadic, focal clusters contrasting with persistent, less clustered cases in the Apia Urban Area. Restrictions to population movement during nationwide lockdowns in 2019-2020 were associated with marked reductions of cases. Phylogenetic analyses of isolates with whole genome sequences (n = 186) revealed one dominant genotype 3.5.4 (n = 181/186) that contains three Samoa-exclusive sub-lineages: 3.5.4.1, 3.5.4.2, and 3.5.4.3. Variables of patient sex, age, and geographic region were examined by phylogenetic groupings, and significant differences (p<0.05) associated genetically-similar isolates in urban areas with working ages (20-49 year olds), and in rural areas with age groups typically at home (<5, 50+). Isolates from asymptomatic shedders were among all three sub-lineages. Whole genome sequencing provided evidence of bacterial genetic similarity, which corroborated 10/12 putative epidemiologic linkages among cases and asymptomatic shedders, as well as 3/3 repeat positives (presumed relapses), with a median of one single nucleotide polymorphism difference. These findings highlight various patterns of typhoid transmission in Samoa that differ between urban and rural regions as well as genomic subtypes. Asymptomatic shedders, detectable only through household investigations, are likely an important reservoir and mobile agent of infection. This study advances a "Samoan S. Typhi framework" that supports current and future typhoid surveillance and control efforts in Samoa.

Humans↗

PubMed2025

A Digital Tool for Clinical Evidence-Driven Guideline Development by Studying Properties of Trial Eligible and Ineligible Populations: Development and Usability Study.

BACKGROUND: Clinical guideline development preferentially relies on evidence from randomized controlled trials (RCTs). RCTs are gold-standard methods to evaluate the efficacy of treatments with the highest internal validity but limited external validity, in the sense that their findings may not always be applicable to or generalizable to clinical populations or population characteristics. The external validity of RCTs for the clinical population is constrained by the lack of tailored epidemiological data analysis designed for this purpose due to data governance, consistency of disease or condition definitions, and reduplicated effort in analysis code. OBJECTIVE: This study aims to develop a digital tool that characterizes the overall population and differences between clinical trial eligible and ineligible populations from the clinical populations of a disease or condition regarding demography (eg, age, gender, ethnicity), comorbidity, coprescription, hospitalization, and mortality. Currently, the process is complex, onerous, and time-consuming, whereas a real-time tool may be used to rapidly inform a guideline developer's judgment about the applicability of evidence. METHODS: The National Institute for Health and Care Excellence-particularly the gout guideline development group-and the Scottish Intercollegiate Guidelines Network guideline developers were consulted to gather their requirements and evidential data needs when developing guidelines. An R Shiny (R Foundation for Statistical Computing) tool was designed and developed using electronic primary health care data linked with hospitalization and mortality data built upon an optimized data architecture. Disclosure control mechanisms were built into the tool to ensure data confidentiality. The tool was deployed within a Trusted Research Environment, allowing only trusted preapproved researchers to conduct analysis. RESULTS: The tool supports 128 chronic health conditions as index conditions and 161 conditions as comorbidities (33 in addition to the 128 index conditions). It enables 2 types of analyses via the graphic interface: overall population and stratified by user-defined eligibility criteria. The analyses produce an overview of statistical tables (eg, age, gender) of the index condition population and, within the overview groupings, produce details on, for example, electronic frailty index, comorbidities, and coprescriptions. The disclosure control mechanism is integral to the tool, limiting tabular counts to meet local governance needs. An exemplary result for gout as an index condition is presented to demonstrate the tool's functionality. Guideline developers from the National Institute for Health and Care Excellence and the Scottish Intercollegiate Guidelines Network provided positive feedback on the tool. CONCLUSIONS: The tool is a proof-of-concept, and the user feedback has demonstrated that this is a step toward computer-interpretable guideline development. Using the digital tool can potentially improve evidence-driven guideline development through the availability of real-world data in real time.

Humans↗

PubMed2014

Persistent inflammation, immunosuppression, and catabolism syndrome after severe blunt trauma.

BACKGROUND: We recently proffered that a new syndrome persistent inflammation, immunosuppression, and catabolism syndrome (PICS) has replaced late multiple-organ failure as a predominant phenotype of chronic critical illness. Our goal was to validate this by determining whether severely injured trauma patients with complicated outcomes have evidence of PICS at the genomic level. METHODS: We performed a secondary analysis of the Inflammation and Host Response to Injury database of adults with severe blunt trauma. Patients were classified into complicated, intermediate, and uncomplicated clinical trajectories. Existing genomic microarray data were compared between cohorts using Ingenuity Pathways Analysis. Epidemiologic data and outcomes were also analyzed between cohorts on admission, Day 7, and Day 14. RESULTS: Complicated patients were older, were sicker, and required increased ventilator days compared with the intermediate/uncomplicated patients. They also had persistent leukocytosis as well as low lymphocyte and albumin levels compared with uncomplicated patients. Total white blood cell leukocyte analysis in complicated patients showed that overall genome-wide expression patterns and those patterns on Days 7 and 14 were more aberrant from control subjects than were patterns from uncomplicated patients. Complicated patients also had significant down-regulation of adaptive immunity and up-regulation of inflammatory genes on Days 7 and 14 (vs. magnitude in fold change compared with control and in magnitude compared with uncomplicated patients). On Day 7, complicated patients had significant changes in functional pathways involved in the suppression of myeloid cell differentiation, increased inflammation, decreased chemotaxis, and defective innate immunity compared with uncomplicated patients and controls. Subset analysis of monocyte, neutrophil, and T-cells supported these findings. CONCLUSION: Genomic analysis of patients with complicated clinical outcomes exhibit persistent genomic expression changes consistent with defects in the adaptive immune response and increased inflammation. Clinical data showed persistent inflammation, immunosuppression, and protein depletion. Overall, the data support the hypothesis that patients with complicated clinical outcomes are exhibiting PICS. LEVEL OF EVIDENCE: Epidemiologic study, level III.

Adolescent↗

PubMed2025

ScITree: Scalable Bayesian inference of transmission tree from epidemiological and genomic data.

Phylodynamic models capture joint epidemiological-evolutionary dynamics during an outbreak, providing a powerful tool to enhance understanding and management of disease transmission. Existing phylodynamic approaches, however, mostly rely on various non-mechanistic or semi-mechanistic approximations of the underlying epidemiological-evolutionary process. Previous work by Lau and colleagues has shown that full Bayesian mechanistic models, without relying on these approximations, can enable highly accurate joint inference of the epidemiological-evolutionary dynamics including the unobserved transmission tree. However, the Lau method faces major computational bottlenecks. As the volume of genomic data collected during outbreaks continues to grow, it is crucial to develop scalable yet accurate phylodynamic methods. Here we propose a new Bayesian phylodynamic model, overcoming the major scalability issue in the previous method and enabling a readily deployable, yet accurate, phylodynamic modeling framework. Specifically, we develop a scalable spatio-temporal phylodynamic framework for inferring the transmission tree (ScITree) and other key epidemiological parameters considering the infinite sites assumption in modeling mutation on the sequence level, in contrast to the Lau method in which mutation was modeled explicitly on the nucleotide level. Our approach features full Bayesian implementation utilizing an exact likelihood to mechanistically integrate epidemiological and evolutionary processes. We develop a computationally-efficient data-augmentation Markov Chain Monte Carlo algorithm, inferring key model parameters and unobserved dynamics including the transmission tree. We assess performance of our method using multiple simulated outbreak datasets. Our results indicate that our method can achieve high inference accuracy, comparable to the performance of the Lau method. Additionally, our method scales significantly more efficiently for large outbreaks, with computing time increasing linearly with outbreak size, compared to the exponential scaling of the Lau method. We also demonstrate our method's utility by applying our validated modeling framework to a dataset describing a foot-and-mouth disease outbreak in the UK. Our results show that our method is able to generate estimates of the transmission dynamics consistent with those from the prior method, further demonstrating the robustness of our new approach. In summary, our method provides a computationally-efficient, highly scalable, accurate modeling framework for inferring the joint spatio-temporal dynamics of epidemiological and evolutionary processes, facilitating timely and effective outbreak responses in space and time. Our method is implemented in our R package ScITree.

Bayes Theorem↗

PubMed2026

Comparison of phylogenetic metrics of transmission between symptomatic and asymptomatic tuberculosis in individuals who were incarcerated in Brazil in 2008-24: a retrospective genomic epidemiology study.

BACKGROUND: Tuberculosis control efforts have traditionally targeted symptomatic individuals; however, the role of asymptomatic cases in sustaining transmission is increasingly recognised. We aimed to quantify the contribution of asymptomatic tuberculosis to recent transmission using genomic and epidemiological data from a high-transmission setting. METHODS: We conducted a retrospective genomic epidemiology study of Mycobacterium tuberculosis isolates collected in Mato Grosso do Sul, Brazil, between Aug 25, 2008, and March 19, 2024. Available isolates underwent whole-genome sequencing. Demographic, clinical, incarceration history, and laboratory metadata were obtained from surveillance records. From Jan 1, 2017, to March 19, 2024, active case finding was conducted in the state's three largest prisons (all male-only facilities), during which sputum samples were collected from individuals irrespective of symptoms and tested using GeneXpert and culture. Comparisons of transmission between individuals with and without symptoms were restricted to individuals who were incarcerated and were identified through active case finding and for whom high-quality, M tuberculosis lineage 4 genomes were available. Metrics of recent transmission included phylogenetic clustering, time-scaled haplotype density (THD), local branching index (LBI), and transmission probabilities inferred using Bayesian Reconstruction and Evolutionary Analysis of Transmission Histories. FINDINGS: 4448 tuberculosis cases were notified in Mato Grosso do Sul in 2008-24. After excluding cases for which M tuberculosis isolates were not available or had low sequencing quality, who had contaminated cultures or mixed infection, or who were infected with non-lineage 4 M tuberculosis, we included 2362 lineage 4 M tuberculosis isolates with high-quality genome sequences. 1849 (78·3%) of 2362 isolates were part of a genomic cluster. Among 2362 individuals with tuberculosis, 1137 (48·1%) were incarcerated at diagnosis. Of these individuals, 505 were identified through active case finding in three male-only prisons. The median age was 30 years (IQR 25-37); 304 (60·2%) had mixed ethnicity, 90 (17·8%) were White, 56 (11·1%) were Black, 13 (2·6%) were Indigenous, and six (1·2%) were Asian. 277 (54·9%) had symptomatic disease and 228 (45·1%) had asymptomatic tuberculosis. There were no significant differences between symptomatic and asymptomatic individuals in phylogenetic clustering (213 [76·9%] of 277 vs 195 [85·5%] of 228; p=0·37), THD (median 0·39 [IQR 0·06-0·62] vs 0·50 [0·09-0·65]; p=0·12), or LBI (0·00863 [0·00810-0·00988] vs 0·00871 [0·00829-0·01020]; p=0·088). Bayesian transmission trees showed no significant difference in the number of secondary infections inferred from symptomatic compared with asymptomatic individuals (p=0·56). These findings were consistent across genomic clusters and robust to model assumptions. INTERPRETATION: We identified no differences in transmission between individuals who were symptomatic and those who were asymptomatic using multiple genomic measures. In this high-transmission setting, where systematic screening is implemented, our findings indicate that asymptomatic tuberculosis substantially contributes to tuberculosis transmission at the population level. These results suggest that symptom-based case detection alone is likely to be insufficient to interrupt transmission and highlight the importance of expanded screening strategies in high-risk populations. FUNDING: US National Institutes of Health and the Brazilian National Research Council (CNPq).

Humans↗

PubMed2025

Global epidemiology of diabetes and prediabetes in lean or non-obese patients with NAFLD: a systematic review and meta-analysis.

BACKGROUND: The presence of diabetes increases the risk of adverse outcomes of patients with non-alcoholic fatty liver disease (NAFLD) even in those with lean or non-obese NAFLD. However, the epidemiological data regarding the prevalence of diabetes and prediabetes in lean or non-obese NAFLD populations remain limited. We assessed the global epidemiology of diabetes and prediabetes in lean or non-obese patients with NAFLD. METHODS: Published studies were searched in PubMed, EMBASE, Cochrane Library, and Web of Science databases from the inception of the databases to October 2024. The pooled global prevalence of diabetes or prediabetes in patients with NAFLD was evaluated using random-effects meta-analysis. Subgroup meta-analysis and meta-regression were used to investigate potential sources of heterogeneity. RESULTS: A total of 54 studies involving 146,714 patients with non-obese or lean NAFLD were included. The pooled global prevalence of diabetes among patients with lean or non-obese NAFLD was 15.6% (95% CI 10.8%-22.7%). Studies from South America reported the highest prevalence (41.3%, CI 39.1%-43.5%). Meta-regression models showed that geographic region and mean age (p < 0.05) were associated with the were associated with the prevalence of diabetes, jointly accounting for 51.61% of the heterogeneity. The global prevalence of prediabetes among patients with lean or non-obese NAFLD was 22.9% (95% CI 12.5%-41.9%) with the highest prevalence reported in studies from Europe (34.4%, CI 23.0%-51.4%). Meta-regression models showed that geographic region and country (p < 0.05) were associated with the prevalence of prediabetes, jointly accounting for 73.65% of the heterogeneity. CONCLUSION: The pooled global prevalence of diabetes and prediabetes were 15.6% and 22.9% in lean or non-obese patients with NAFLD, respectively. These findings suggest the importance of diabetes screening in these patients.

Humans↗

PubMed2026

A Strain of Mycoplasma hominis Causing Pleuropneumonia Infection in an Immunocompetent Patient and Recent Epidemiological Trends: Implications for Clinical Management.

Mycoplasma hominis (M. hominis) is an opportunistic pathogen linked to urogenital and neonatal infections; however, limited genetic and epidemiological data are available. Extragenital infections in healthy adults are rare, and effective antibiotics are species-specific, complicating diagnosis and treatment. Hence, this study aimed to elucidate the clinical process, update the epidemiological characteristics, and investigate the genomic features of a fluoroquinolone-resistant M. hominis isolate from an immunocompetent patient with pleuropneumonia in China. The M. hominis isolate ZY_MH01 was recovered from pleural fluid and was identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) and Whole Genome Sequencing (WGS). The completed genome was annotated using the NCBI Prokaryotic Genome Annotation Pipeline (PGAP). Snippy v4.4.5 was utilized to conduct a core genome single nucleotide polymorphism (cgSNP) analysis between ZY_MH01 and 144 M. hominis strains from the NCBI GenBank database. Subsequently, phylogenies were constructed using IQ-TREE v3.1.2 and visualized by iTOL. Antimicrobial resistance determinants were identified using strict criteria of Comprehensive Antibiotic Resistance Database (CARD) RGI 6.0.5 (Web portal) and broth microdilution test. Virulence genes were screened using Abricate v1.0.1 against the Virulence Factor Database (VFDB). A total of 42 strains (including ZY_MH01) from Genbank with an assembly level of Complete or Chromosome were re-annotated using Prokka v1.2.0 and pangenome analysis was performed using the Roary. The core genome constitutes only 17.1%, which may contribute to the unusually high level of polymorphism observed among M. hominis strains. No antibiotic resistance genes or virulence genes were detected in the genome of ZY_MH01. However, some resistance-associated mutations of gene parC and gyrA in the Quinolone Resistance Determining Region (QRDR) were identified. Phylogenetic analysis indicates that strains originating from the same geographic region typically exhibit reduced genetic distances; this trend is especially pronounced in regions with a higher number of publicly available strain sequences. In specific circumstances, when conventional broad-spectrum antibiotics are ineffective, even immunocompetent patients should consider the possibility of M. hominis infection. This study presents a detailed account of the diagnostic and therapeutic course of a pleuropneumonia infection caused by M. hominis in an immunocompetent patient, and performs an epidemiological analysis of all M. hominis sequences that have been recently made publicly available.

Humans↗

PubMed2024

A novel molecular pathway of lipid accumulation in human hepatocytes caused by PFOA and PFOS.

Exposed to ubiquitously perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) has been associated with non-alcoholic fatty liver disease (NAFLD), yet the underlying molecular mechanism remains elusive. The extrapolation of empirical studies correlating per- and polyfluoroalkyl substance (PFAS) exposure with NAFLD occurrence to real-life exposure was hindered by the limited availability of mechanistic data at environmentally relevant concentrations. Herein, a novel pathway mediating hepatocyte lipid accumulation by PFOA and PFOS at human-relevant dose (<10 μM) was identified by integrating CRISPR-Cas9 genome screening, concentration-dependent transcriptional assay in HepG2 cell and epidemiological data mining. 1) At genetic level, nudt7 showed the highest enriched potency among 569 NAFLD-related genes, and the transcription of nudt7 was significantly downregulated by PFOA and PFOS exposure (<7 μM). 2) At molecular pathway, upon exposure to ≤10-4 μM PFOA and PFOS, the downregulation of nudt7 transcriptional expression triggered the reduction of Ace-CoA hydrolase activity. 3) At cellular level, increased lipids were measured in HepG2 cells with PFOA and PFOS (<2 μM). Overall, we identified a novel mechanism mediated by transcriptional downregulation of nudt7 gene in hepatocellular lipid increase treated with PFOA and PFOS, which could potentially explain the NAFLD occurrence associated with exposure to PFASs in humans.

Humans↗

PubMed2026

Genomic Features Do Not Account for Differences in Multiple Myeloma Risk by Ancestry.

UNLABELLED: Studies have reported conflicting findings regarding the contribution of germline variants or somatic genomic drivers to racial disparities in multiple myeloma. To comprehensively investigate somatic drivers in relation to inherited genetics in multiple myeloma, we combined newly sequenced whole-genome sequencing data with publicly available datasets (total n = 1,286). Overall, we did not identify germline or somatic genomic differences that explain the different risk of developing multiple myeloma between patients with genetic similarity to African (AFR) or European (EUR) reference populations. A difference in the detectability and timing of APOBEC-associated and germinal center mutational activity was observed. Integrating epidemiologic data and mutational signature-based temporal estimates, we challenge the assumption that individuals in the AFR group develop multiple myeloma at a younger age. Finally, we demonstrate that, with equal access to efficacious therapies, patients in the AFR and EUR groups have equivalent clinical outcomes. SIGNIFICANCE: Multiple myeloma is reported to occur at higher rates in individuals who self-identify as non-Hispanic Black. In this large dataset, genomic drivers occur at the same rate among ancestry groups, except for APOBEC mutagenesis. With equivalent therapy, clinical outcomes did not differ for patients grouped by genetic ancestry similarity.

Humans↗

PubMed2026

Detection of feline kobuvirus in filtered fecal inocula and molecular epidemiological characterization of feline kobuvirus in Japan.

Feline kobuvirus (FKoV) is an enteric virus detected in cats in several countries, but its prevalence and genomic characteristics in Japan remain unclear. Here, we report the detection of FKoV in specific-pathogen-free (SPF) cats inoculated with filtered fecal material that had tested negative for FKoV by an initial RT-PCR assay. The inoculum was derived from a shelter-housed cat positive for a feline norovirus (FNoV) strain (KU22; GVI.1; GenBank accession no. LC935948), which shared 99% VP1 nucleotide identity with the Japanese strain M49-1. FKoV RNA was undetectable in all four inoculated cats at day 0 using a degenerate universal kobuvirus primer set, but was detected in all four cats at days 5, 20, and 30 post inoculation. FKoV RNA in the inoculum was negative by the initial RT-PCR assay but positive by the degenerate universal kobuvirus primer set, indicating that FKoV was present in the inoculum but was missed by the initial assay; FKoV RNA was subsequently detected in the inoculated cats, consistent with inoculum-associated introduction of FKoV. Near-complete genome sequencing confirmed that the Japanese strain belonged to the feline kobuvirus lineage, representing the first near-complete FKoV genome sequence from Japan. In a field survey of 83 domestic cats, FKoV RNA was detected in 10 samples (12.0%), with higher prevalence in cats with gastroenteritis than in apparently healthy cats (40.0% vs. 8.2%; Bonferroni-adjusted p = 0.049), and exclusively in cats younger than 1 year. These findings provide genomic and epidemiological data on FKoV in Japan and highlight the need for broad-spectrum screening of biological inocula used in experimental infection studies.

Animals↗

PubMed2026

Bacteriocin-mediated intraspecies competition driven by acquired Bac41 operon in epidemic Enterococcus faecalis ST179.

Enterococcus faecalis is a common gut commensal and an opportunistic pathogen causing hospital-acquired infections. Despite its clinical importance, comprehensive global genomic and epidemiological data remain limited. Here, we analyzed 5,895 E. faecalis genomes collected between 2000 and 2020 and identified ST179, a human-derived single-operon variant of the high-risk CC16 clonal complex, as an emerging epidemic clone in China. Spot-killing assays revealed that ST179 strongly inhibited other clinical E. faecalis sequence types. Biochemical purification and proteomic analyses identified BacL1 as a key effector associated with this species-specific antibacterial activity. Functional assays confirmed its inhibitory phenotype, providing ST179 with a lineage-specific, bacteriocin-mediated competitive advantage. The high prevalence of the Bac41 operon likely contributed to the epidemiological success and ecological fitness of ST179. These findings highlight the role of bacteriocin-mediated intraspecies competition in shaping E. faecalis population dynamics and suggest that ST179 might become an emerging high-risk lineage in China.IMPORTANCEEnterococcus faecalis is a common gut bacterium and an opportunistic pathogen. We identify ST179 as an emerging epidemic clone in China and show that it outcompetes other strains via the bacteriocin Bac41. This competitive advantage helps explain its rapid spread. Our findings highlight how bacterial competition shapes population dynamics and provide insights into the emergence of high-risk E. faecalis lineages, informing strategies for monitoring and infection control.

Enterococcus faecalis↗

PubMed2026

Molecular Epidemiology of Non-Polio Enterovirus: Insights From L20B Cell Line Adaptation From Children With Acute Flaccid Paralysis in Pakistan.

BACKGROUND: Non-polio enteroviruses (NPEVs) are increasingly implicated in acute flaccid paralysis (AFP), often resembling poliomyelitis and complicating eradication efforts. In Pakistan, limited molecular surveillance has hindered comprehensive characterization. The L20B cell line, designed for poliovirus detection, occasionally supports NPEV replication, challenging AFP case interpretation. METHODS: Between January 2021 and December 2022, 4615 stool samples from AFP cases in children ≤15 years were analyzed. Of these, 435 were identified as NPEVs via L20B cytopathic effects and intertypic differentiation reverse transcription-polymerase chain reaction. VP1 sequencing was performed on 218 representative isolates, yielding 153 high-quality sequences (70.2%). The 224/222 primer set showed superior amplification. Phylogenetic analysis used MUSCLE alignment and the Neighbor-Joining method in MEGA X, with statistical evaluation of epidemiological data. RESULTS: NPEVs were frequently found in L20B-positive AFP cases, highlighting the cell line's limited specificity. Most cases involved children under 5, with a slight male bias. Enterovirus B was predominant (98.0%), especially Echovirus 7 (20.3%) and Echovirus 11 (10.5%), followed by Coxsackievirus B1 and Echovirus 33 (5.9% each). Geographic clustering was noted in Punjab (45.1%), Khyber Pakhtunkhwa (30.7%) and Sindh (20.3%), with seasonal peaks in late summer and early autumn. Phylogenetic data revealed localized Enterovirus B circulation with minimal genetic variation. CONCLUSIONS: The detection of diverse NPEVs in L20B-positive AFP cases emphasizes their relevance in post-polio surveillance. Incorporating routine VP1 sequencing, optimized primer use, and targeted seasonal and regional monitoring is vital to reduce diagnostic uncertainty and inform public health strategies.

Humans↗

PubMed2026

Investigation of Mycobacterium abscessus Cluster in Hospital, Maryland, USA, 2024.

Mycobacterium abscessus infections are frequently drug resistant and can cause severe disease, particularly among vulnerable populations in healthcare settings. In June 2024, a cluster of M. abscessus infection cases was reported at a hospital in Maryland, USA. An investigation involving hospital infection prevention staff, the Maryland Department of Health, the Centers for Disease Control and Prevention, and the Wadsworth Laboratory of the New York State Department of Health included initiation of mitigation efforts such as tap water use restrictions, point-of-use water filters, hospitalwide water flushing, and staff education regarding sink safety. Whole-genome sequencing of patient and environmental isolates, coupled with epidemiologic data, revealed a strong association (0-24 single-nucleotide polymorphism differences) between environmental and patient samples, indicating that infections were likely a result of patient exposure to M. abscessus. Ensuring initiation of mitigation initiatives likely prevented additional patient infections. Although effective in this investigation, not all mitigation strategies are equal or sustainable.

Humans↗

PubMed2025

Inferring the sensitivity of wastewater metagenomic sequencing for early detection of viruses: a statistical modelling study.

BACKGROUND: Metagenomic sequencing of wastewater (W-MGS) can in principle detect any known or novel pathogen in a population. We aimed to quantify the sensitivity and cost of W-MGS for viral pathogen detection by jointly analysing W-MGS and epidemiological data for a range of human-infecting viruses. METHODS: In this statistical modelling study, we analysed sequencing data from four studies of untargeted W-MGS to estimate the relative abundance of 11 human-infecting viruses. Corresponding prevalence and incidence estimates were obtained or calculated from academic and public health reports. We combined these estimates using a hierarchical Bayesian model to predict relative abundance at set prevalence or incidence values, allowing comparison across studies and viruses. These predictions were then used to estimate the sequencing depth and concomitant cost required for pathogen detection using W-MGS with or without use of a hybridisation capture enrichment panel. FINDINGS: After controlling for variation in local infection rates, relative abundance varied by orders of magnitude across studies for a given virus. For instance, a local SARS-CoV-2 weekly incidence of 1% corresponded to a predicted SARS-CoV-2 relative abundance ranging from 3·8 × 10-10 to 2·4 × 10-7 across studies, translating to orders-of-magnitude variation in the cost of operating a system able to detect a SARS-CoV-2-like pathogen at a given sensitivity. Use of a respiratory virus enrichment panel in two studies greatly increased predicted relative abundance of SARS-CoV-2, lowering yearly costs by 27-fold (from US$7·87 million to $287 000) and 29-fold (from $1·98 million to $69 100) for a system able to detect a SARS-CoV-2-like pathogen before reaching 0·01% cumulative incidence. INTERPRETATION: The large variation in viral relative abundance after controlling for epidemiological factors indicates that other sources of inter-study variation, such as differences in sewershed hydrology and laboratory protocols, have a substantial impact on the sensitivity and cost of W-MGS. Well chosen hybridisation capture panels can greatly increase sensitivity and reduce cost for viruses in the panel, but might reduce sensitivity to unknown or unexpected pathogens. FUNDING: The Wellcome Trust, Open Philanthropy, and Musk Foundation.

Humans↗

PubMed2026

Molecular epidemiology of levofloxacin-resistant Klebsiella pneumoniae and the association of plasmid-mediated quinolone resistance genes with key biological phenotypes.

UNLABELLED: Klebsiella pneumoniae is a major opportunistic pathogen in China, yet the molecular epidemiology of quinolone resistance remains poorly characterized. This study analyzed 2,433 clinical isolates from 37 Chinese hospitals (2018-2022). The overall levofloxacin-non-susceptible (NS) rate was 53.60%, with urinary tract isolates showing higher resistance. Whole-genome sequencing identified 12 plasmid-mediated quinolone resistance (PMQR) genes. Among 1,304 NS strains, 74.54% carried at least one PMQR gene (mainly qnrS, qnrB, and aac(6')-Ib-cr), and 60.20% also had quinolone resistance-determining region (QRDR) mutations. Functional studies revealed diverse phenotypic impacts. Most PMQR genes conferred low-level resistance (minimum inhibitory concentration [MIC] = 1 mg/L), while qnrB52 and qnrB91 caused high-level resistance (MIC = 8-16 mg/L). Notably, qnrB91 reduced biofilm formation, indicating a trade-off between resistance and colonization. Growth assays showed that qnrB52, qnrB91, and qnrS1 inhibited normal growth, whereas qepA1 and qnrS1 enhanced growth under ethanol stress. Most PMQR genes (except qnrB6) attenuated bacterial adhesion. qepA1 promoted intracellular survival in macrophages, suggesting a role in chronic infection. Animal models confirmed that qnrB6, qnrB7, qnrVC6, and aac(6')-Ib-cr significantly enhanced virulence. This study is the first in China to report qnrVC6 and novel gyrA mutations (Ser83Ala/Val, Asp87Phe/His) in K. pneumoniae. It systematically reveals how PMQR genes influence infection by modulating resistance, immune evasion, and pathogenicity. These findings highlight that PMQR genes contribute not only to antibiotic resistance but also to virulence, suggesting that treatment strategies should consider specific PMQR genotypes. This research provides the largest-scale molecular epidemiological data and a theoretical basis for controlling quinolone-resistant K. pneumoniae in China. IMPORTANCE: Quinolone-resistant Klebsiella pneumoniae poses a serious threat to public health, yet the role of plasmid-mediated quinolone resistance (PMQR) genes beyond antibiotic resistance remains underexplored. In this largest-scale multicenter study in China, we analyzed 2,433 clinical isolates and discovered that PMQR genes do more than just confer drug resistance-they also influence bacterial growth, stress survival, biofilm formation, and the ability to evade or persist within host immune cells. Some PMQR genes even enhance virulence in an animal model. These findings challenge the traditional view of resistance genes as mere contributors to drug failure, revealing that they can also shape infection outcomes by altering bacterial behavior. Understanding these dual roles may guide more precise treatment strategies targeting specific PMQR genotypes.

Klebsiella pneumoniae↗

PubMed2026

Genomic Characterisation of Carbapenem-Resistant Klebsiella pneumoniae and Enterobacter hormaechei Clinical Isolates from Nigeria: Evidence of Resistance, Virulence, and Putative Plasmid-Mediated Gene Sharing.

The global proliferation of carbapenem-resistant Enterobacterales (CRE) constitutes one of the most urgent public health threats, yet high-resolution genomic data from sub-Saharan Africa remain critically scarce. We applied whole-genome sequencing (WGS) and comparative phylogenomics to characterise antimicrobial resistance determinants, virulence genes, and mobile genetic elements (MGEs) in three carbapenem-resistant clinical isolates originating from three tertiary hospitals (selected from a broader surveillance collection spanning four facilities) in Osun State, southwestern Nigeria. We purposively selected three isolates, two Klebsiella pneumoniae subsp. pneumoniae (K22, ST411; K31, ST17) and one Enterobacter hormaechei subsp. steigerwaltii (K32, ST45) from a broader surveillance collection of 27 carbapenem-non-susceptible Enterobacterales, to represent phenotypically and genotypically divergent lineages. Resistome analysis revealed extensive plasmid-associated β-lactam and aminoglycoside resistance in K31 (including blaCTX-M-15, blaOXA-1, and blaTEM-1). K32 harboured an intrinsic chromosomal blaACT-17 AmpC gene, while IS26 and ISEcp1 insertion sequences, consistent with transposon-mediated mobilisation, flanked its acquired aminoglycoside and sulfonamide resistance cassettes. K22 lacked detected acquired carbapenemase, ESBL, or plasmid-mediated AmpC genes, indicating that its carbapenem-resistant phenotype may involve non-carbapenemase mechanisms such as porin alteration or efflux-mediated reduced susceptibility; however, this mechanism requires confirmation by direct ompK35/ompK36 sequence analysis and/or phenotypic outer membrane protein profiling. Virulome profiling identified a broader repertoire of siderophore, adhesion, and biofilm genes in both K. pneumoniae isolates than in E. hormaechei. Phylogenomic analysis demonstrated that K22 and K31 cluster within the broader K. pneumoniae population framework but represent distinct high-risk lineages (ST411 and ST17) rather than a single clonal outbreak. Analysis also identified a shared plasmid backbone between K31 and K32, supporting interspecies horizontal gene transfer. These descriptive genomic findings identify clinically relevant resistance and virulence determinants in three purposively selected carbapenem-resistant Enterobacterales from Nigerian tertiary-care hospitals. The detection of shared resistance elements between K. pneumoniae and E. hormaechei suggests possible plasmid-mediated gene sharing. Still, larger WGS studies with long-read sequencing and patient-level epidemiological data are required to define transmission and dissemination patterns.

Nigeria↗

PubMed2026

Epidemiological and phylogenetic analysis of anthrax in Kazakhstan in 2024.

BACKGROUND: Anthrax remains an important zoonotic disease in Kazakhstan due to the persistence of environmental reservoirs and long-standing endemic foci. Despite ongoing surveillance, the epidemiological characteristics and genetic diversity of circulating Bacillus anthracis strains in the country remain incompletely understood. METHODS: A retrospective epidemiological and phylogenetic investigation of anthrax outbreaks reported in Kazakhstan during 2024 was conducted. Epidemiological data were collected for all laboratory-confirmed human cases and associated outbreak foci. Confirmation of infection was performed by PCR, and B. anthracis isolates were obtained from clinical, environmental and animal-associated samples. Whole-genome sequencing and core-genome single nucleotide polymorphism (cgSNP) analysis were used to characterize the genetic relationships among isolates and to determine their phylogenetic placement. RESULTS: Nine anthrax outbreaks were identified across four regions of Kazakhstan (Almaty, Zhambyl, Atyrau, and West Kazakhstan), resulting in 20 confirmed human cases. All patients were male, with the highest proportion occurring among individuals aged 36-55 years (45%). The mean patient age was 43.9 years (range: 16-64 years). Most infections were associated with slaughtering infected livestock (65%), followed by handling contaminated meat (15%). PCR confirmed infection in all 20 human cases. Culture yielded 17 human-derived B. anthracis isolates from 14 patients and 17 environmental/animal-derived isolates, resulting in 34 isolates in total. Of these, 22 representative isolates underwent whole-genome sequencing. Phylogenetic analysis revealed the circulation of two major lineages. Isolates from Atyrau and West Kazakhstan clustered within the Trans-Eurasian (TEA/STI) lineage. Atyrau isolates formed a tight cluster differing by only 21-32 cgSNPs, consistent with a shared epidemiolocal source, whereas the West Kazakhstan isolate was highly divergent. Zhambyl and Almaty region belonged to the A.Br.Ames lineage but diverged into two distinct sublineages. Zhambyl region isolates demonstrated minimal divergence from the global reference genome Ames Ancestor, differing by only 16-31 SNPs. Almaty region isolates formed an endemic subclone, separated from the reference group by approximately 114 SNPs. Comparison with the Ames Ancestor and Sterne reference strains demonstrated substantial genetic divergence. CONCLUSION: Anthrax outbreaks in Kazakhstan during 2024 were primarily associated with livestock exposure and occurred within established endemic regions. Whole-genome sequencing revealed the coexistence of distinct TEA and Ames lineages, including evidence of persistent local transmission and long-term evolutionary stability of endemic B. anthracis populations. These findings enhance understanding of anthrax epidemiology in Central Asia and support the integration of genomic surveillance into national outbreak investigation programs.

Anthrax↗