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ورود به زیرشاخهبیماریهای مشترک، سلامت حیوانات و رویکرد سلامت واحد
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مقالهها، منابع و پژوهشهای تازه حوزه دامپزشکی
ورود به زیرشاخهمقالهها، منابع و پژوهشهای تازه حوزه بیماریهای مشترک انسان و دام
ورود به زیرشاخهمقالهها، منابع و پژوهشهای تازه حوزه سلامت واحد
ورود به زیرشاخهمقالهها، منابع و پژوهشهای تازه حوزه مدلهای حیوانی
ورود به زیرشاخهمقالهها، منابع و پژوهشهای تازه حوزه بهداشت عمومی دامپزشکی
ورود به زیرشاخهPteropus medius is a major reservoir of Nipah virus (NiV), a zoonotic pathogen responsible for recurrent fatal encephalitis outbreaks in Bangladesh. Human infections are primarily associated with consuming raw date palm sap contaminated with bat excreta. Beyond viral spillover, growing evidence suggests that bat-associated microbiota and guano are potential reservoirs of antimicrobial resistance (AMR), contributing to the environmental dissemination of resistant bacteria and resistance genes. This narrative literature review examined the relationship among NiV spillover, bat microbiota, and AMR within a One Health framework. A structured literature search was conducted using PubMed, Scopus, Web of Science, ScienceDirect, and Google Scholar to identify relevant peer-reviewed studies published between 2006 and 2025. The reviewed evidence indicates that Pteropus medius populations harbor clinically important resistant bacteria, including ESBL-(Extended-Spectrum Beta-Lactamase) producing Escherichia coli, Salmonella spp., and methicillin-resistant Staphylococcus spp. In addition, recent studies indicate that bat roosts near agricultural lands, wastewater discharge sites, and peri-urban settlements may facilitate bidirectional exchange of ARGs among wildlife, livestock, and humans. Habitat fragmentation, wastewater contamination, urbanization, agricultural intensification, and increased human-wildlife interactions were identified as major drivers facilitating both NiV spillover and AMR dissemination. Overall, the literature demonstrates a significant ecological association among anthropogenic environmental disturbance, zoonotic spillover risk, and the emergence of antimicrobial resistance in bat-associated systems. These findings highlight the importance of integrated One Health surveillance and environmental management strategies to mitigate future zoonotic and AMR threats in Bangladesh.
Novel influenza A viruses have cost thousands of lives and billions of dollars of economic losses in the 21st century, and 2 of the past 4 pandemic influenza A viruses likely originated in animal populations on the North American continent. Despite this, the human and veterinary influenza surveillance systems in the United States are poorly connected and have fallen short of congressional mandates for data sharing and interoperability. This places the United States in a reactive posture that is focused on containment of outbreaks that have already occurred rather than proactive surveillance and prevention. The significant investments in surveillance infrastructure and genomic technologies spurred by the COVID-19 pandemic, along with the new National One Health Framework, present a unique opportunity to modernize influenza surveillance with a greater emphasis on the interconnectedness of human and animal health. However, funding for enhanced surveillance is set to decrease significantly as pandemic-era funding sunsets. Continuing investments into novel surveillance technologies have been critical in addressing the recent H5N1 influenza outbreaks and will be critical to prevent future economic losses and losses of both human and animal life. (Am J Public Health. 2026;116(8):1220-1228. https://doi.org/10.2105/AJPH.2026.308445).
Emma Corbett, veterinary surgeon and head of imaging at Pennard Vets, shares what drew her to diagnostic imaging: the skills required, the mentors and the day-to-day reward of clearer answers.
Renal tubular epithelial cells are among the earliest renal parenchymal cells to be injured in the context of acute kidney injury (AKI). Numerous studies have confirmed that fibrinogen-like protein 2 (FGL2) can regulate the occurrence and development of inflammation during disease progression. We found that FGL2 expression is elevated under AKI conditions. However, the role of FGL2 in AKI remains unclear. To elucidate the role of FGL2 in AKI, we employed lentiviral and adeno-associated virus for transfection in cellular and murine models. Furthermore, by leveraging datasets from the gene expression omnibus and gene set enrichment analysis databases, we identified the inflammation-related genes in AKI and predicted their interaction with FGL2. Both in vivo and in vitro studies showed that overexpression of FGL2 markedly increased complement C3a (C3a) levels and exacerbated inflammation and injury. In contrast, knockdown of FGL2 resulted in a marked decline in C3a levels, which not only conferred a substantial protective effect against hypoxia/reoxygenation-induced injury in tubular cells but also effectively alleviated kidney injury in mice. At the molecular level, FGL2 interacts with complement C3, leading to elevated C3a production. This stimulates the inflammatory response of renal tubular epithelial cells, thereby inducing tubular damage. Targeting FGL2 may hold potential prevention and treatment strategy for tubular injury in AKI.
Increasing evidence shows that CD8+ T cells are the pathogenic mediators of tissue injury in systemic lupus erythematosus (SLE), sustaining the chronic inflammation through the accumulation of long-lived cytotoxic memory populations. However, the transcriptional mechanisms that prevent the aberrant differentiation of pathogenic CD8+ T cells remain poorly understood. Here, the transcription factor E4BP4 (NFIL3) was identified as a critical restraint of cytotoxic effector-memory CD8+ T cells in lupus. E4BP4 expression was reduced in CD8+ T cells from SLE patients and inversely correlated with disease activity. Using a lupus-like disease model, we found that E4BP4 deficiency accelerated disease progression, resulting in heightened autoantibody production, immune complex deposition, and renal pathology. This phenotype was associated with the systemic accumulation of cytotoxic effector-memory CD8+ T cells. Depletion of CD8+ T cells significantly ameliorated the disease phenotype, confirming the functional contribution of CD8+ T cells to lupus-like immunopathology. Competitive adoptive transfer experiments revealed that E4BP4 functions cell-intrinsically to limit the cytotoxicity and proliferation of CD8+ T cells in autoimmunity. Beyond autoimmunity, E4BP4 deficiency also resulted in an exuberant CD8+ effector-memory T cell response to Listeria monocytogenes infection, indicating a broader role for E4BP4 in limiting CD8+ T cell effector-memory responses. Collectively, these findings establish E4BP4 as a transcriptional checkpoint that restricts pathogenic CD8+ effector-memory T cell responses to maintain immune homeostasis in autoimmunity and infection.
Although opioids are effective analgesics, they can lead to problematic drug use behaviors that underlie opioid use disorder (OUD). Opioids also cause gut microbiota dysbiosis, which is linked to altered opioid responses. We used a longitudinal paradigm of voluntary oral morphine self-administration to capture multiple facets of drug seeking and preserve both individual behavioral responses and individual gut microbiota variation to investigate the role of the gut microbiota in a mouse model of OUD. Although all the mice consumed morphine, only a subset of the mice that transitioned to a state we defined statistically as compulsive. In compulsive mice, morphine constricted natural variability and fragmented the microbiota community networks, which convergently reorganized to form robust novel connections post-morphine. In contrast, the more variable communities of non-compulsive mice were highly interconnected during morphine disturbance and displayed more continuity post-morphine, suggesting greater flexibility and adaptability. Compulsive mice displayed a greater loss of functional diversity and a shift in favor of potential pathobionts, whereas non-compulsive mice better preserved genera associated with gut health and broader functional diversity. These findings highlight the potential role of persistent and stable opioid-induced microbiota dysbiosis in long-term behavioral changes underlying OUD and contributing to vulnerability to relapse.
INTRODUCTION: Brucellosis remains a severe zoonotic threat in the Inner Mongolia Autonomous Region of China. METHODOLOGY: This study integrates a comprehensive epidemiological trend analysis with a novel methodological comparison of forecasting techniques to inform control strategies. RESULTS: Using reported human brucellosis surveillance data from Inner Mongolia for 2004-2024, joinpoint regression analysis revealed a persistently increasing yet fluctuating long-term trend (AAPC = 5.13%, P < 0.001), characterized by significant epidemic surges in 2004-2010 (APC = 22.43%, P < 0.001) and 2016-2021 (APC = 29.83%, P < 0.001), interrupted by a decline phase in 2010-2016 (APC = -17.17%, P < 0.001) and 2021-2024 (APC = -12.15). The disease demonstrated strong seasonality with June-August peaks, and predominance among farmers and herdsmen aged 30-60 years. Building on this epidemiological foundation, we rigorously compared the predictive performance of the standard Seasonal Autoregressive Integrated Moving Average (SARIMA) model against its Bootstrap-enhanced version for 24-month-ahead forecasting (2023-2024 validation). This finding offers a novel perspective on enhancing the predictive performance of brucellosis models. While the Bootstrap approach achieved superior point forecast accuracy by reducing Mean Absolute Error by 39.95% and Median Absolute Percentage Error by 33.55% compared to SARIMA, it produced severely overconfident prediction intervals, with only 33.33% empirical coverage compared to SARIMA's 91.67%. This study validates the SARIMA model as a robust baseline for brucellosis forecasting and introduces a Bootstrap ensemble method as a powerful tool for significantly enhancing point prediction accuracy. CONCLUSION: The findings provide novel epidemiological insights that offer a scientific basis for disease control measures and decision-making. Future work should aim to develop hybrid models that bridge this gap, and delivering high accuracy in both point and interval forecasts.
The gut-skin axis plays a pivotal role in psoriasis pathogenesis, yet the precise metabolic crosstalk by which intestinal commensals regulate cutaneous immunity remains elusive. Here, we identify a functional "microbe-enzyme-metabolite-immune" axis that orchestrates skin homeostasis. Through multi-omics analyses of psoriatic patients and imiquimod-induced murine models, we reveal a significant depletion of the gut commensal Parabacteroides distasonis (P. distasonis) and its metabolite, genistein. We demonstrate that P. distasonis utilizes its inherent β-glucosidase activity to convert dietary genistin into bioactive genistein, a process we validated using an engineered β-glucosidase-expressing E. coli strain. Therapeutically, supplementation with P. distasonis or genistein significantly ameliorates psoriatic phenotypes, restores skin barrier integrity (filaggrin/loricrin), and suppresses IL-23/IL-17-mediated inflammation. Mechanistically, we uncovered that genistein enhanced CD200-CD200R signaling and suppressed macrophage activation. It effectively reactivates CD200 expression, thereby inhibiting the canonical NF-κB signaling pathway and blunting macrophage-driven inflammation. Notably, the therapeutic efficacy of this axis was abrogated by CD200 blockade, confirming its indispensability. Collectively, our findings elucidate a causal mechanism linking gut microbial enzyme activity to host skin immunity, highlighting P. distasonis-derived genistein as a promising precision intervention for psoriasis management.
While interferon regulatory factor 1 (IRF1) has been implicated in reactive oxygen species (ROS)-dependent neutrophil extracellular trap (NET) release during acute lung injury, its regulatory role in mitochondrial dysfunction-driven NETosis specific to pediatric pneumonia remains unexplored. Neutrophils were isolated from the bronchoalveolar lavage fluid (BALF) of pediatric pneumonia patients and the bone marrow of mice. IRF1 expression was quantified via qRT-PCR and Western blotting. Mitochondrial ROS (mtROS) and total ROS were measured by flow cytometry. Mitochondrial dysfunction was assessed by ATP quantification. NETosis was evaluated through immunofluorescence staining and ELISA quantification of neutrophil elastase (NE), myeloperoxidase-DNA (MPO-DNA), and citrullinated histone H3 (Cit-H3) levels. For in vivo studies, pneumonia-related lung injury was induced by intratracheal LPS instillation in mice, with pathological severity graded by H&E staining, pulmonary edema quantified via the wet/dry weight ratio, and inflammation assessed by the BALF protein concentration. Mechanistically, the IRF1/MMP9 interaction was predicted by bioinformatics (STRING database) and validated by co-immunoprecipitation (Co-IP) and immunofluorescence staining, while MMP9 overexpression was achieved via lentivirus transduction to delineate pathway regulation. IRF1 was significantly upregulated in BALF neutrophils from patients and correlated with elevated ROS production and mitochondrial dysfunction, as well as NETs release. IRF1 knockdown attenuated ROS-driven NETosis in vitro. Matrix metalloproteinase 9 (MMP9) was predicted to interact with IRF1, and MMP9 overexpression effectively reversed the beneficial effects of IRF1 deficiency on ROS release, mitochondrial dysfunction, neutrophil apoptosis, and NETosis. Consistently, in mouse models, MMP9 overexpression abolished the protective effects of IRF1 deficiency, exacerbating acute lung injury and restoring NETs levels in BALF.
In an interview with Samantha Nelson, a scientific editor of Cell Chemical Biology, the authors of the minireview entitled "Pyroptosis across species and its potential impact on host defense against zoonotic pathogens" share their perspectives on their field and life as scientists.
Nipah virus continues to pose a recurrent zoonotic threat in Bangladesh. The sporadic spillover events are associated with high case fatality and limited opportunities for clinical intervention. Despite nearly two decades of surveillance response, early warning systems remain reactive, relying heavily on laboratory confirmation and case accumulation. This Perspective argues that early warning has been conceptually misframed as outbreak detection, rather than risk anticipation. Drawing on the epidemiological characteristics of Nipah virus and Bangladesh's current surveillance architecture, this study highlights key structural constraints delaying signal recognition. These include community-level blind spots, diagnostic uncertainty, and fragmented cross-sectoral surveillance. This article also outlines priority shifts that emphasize anticipatory risk assessment, operational One Health integration, context-sensitive alert thresholds, and a direct linkage between early signals and preparedness actions. Reframing early warning in this way is essential to improve readiness for the Nipah virus and other rare, high-impact zoonotic threats.
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease, and currently, there are no effective means to reverse its progression. Cuproptosis is a newly discovered copper-dependent programmed cell death mechanism, but its role in IPF remains unknown. This study aimed to investigate whether Cuproptosis is involved in the pathogenesis of IPF and to evaluate its potential as a therapeutic target. METHODS: In vitro, a fibrosis model was induced in human lung epithelial cells by bleomycin treatment. In vivo, a C57BL/6J mouse IPF model was established by intratracheal instillation of bleomycin. The effects on fibrosis progression were observed using the Cuproptosis inhibitor ammonium tetrathiomolybdate and siRNA knockdown of the copper ion transporter Slc31a1. RESULTS: Significant Cuproptosis was observed in both BLM-induced lung epithelial cells and mouse lung tissue. Gene expression profiling identified key Cuproptosis-related genes, including Slc31a1. Pharmacological inhibition of Cuproptosis effectively reversed the Cuproptosis process in both in vitro and in vivo models and significantly reduced fibrotic pathological changes. At the cellular level, knockdown of Slc31a1 mimics the protective effect of TTM; however, its efficacy in whole animal models is limited. CONCLUSION: This study identifies cuproptosis as a significant contributor to the pathogenesis of pulmonary fibrosis. Pharmacological inhibition of this pathway alleviates disease phenotypes, supporting the feasibility of targeting copper metabolism.
Mucormycosis, a disease encompassing life-threatening fungal infections by members of the Mucorales group, is characterized by significant heterogeneity, poor clinical outcomes, and globally rising incidences. Although showing clear outbreak potential, the disease remains poorly understood. Mucorales infections are characterized by rapid progression and extensive tissue destruction, often requiring disfiguring surgical interventions. Moreover, intrinsic resistance and high drug tolerance limit antifungal effectiveness, contributing to the disease's high mortality. To overcome the challenges associated with these infections, a deeper understanding of mucormycosis is urgently needed. Valuable translational insights traditionally derive from in vivo host models. However, current systems are limited by single-endpoint invasive analysis, offering only a narrow view of infection progression and treatment effects. To address these critical shortcomings and enhance experimental models, bioluminescent Mucor lusitanicus reporter strains were generated to establish models that allow for real-time, longitudinal monitoring of infection in individual animals. Codon optimization, targeted integration of the firefly luciferase gene, and control of expression using highly active promoters resulted in the successful establishment of two mucormycosis models: Galleria mellonella larvae as an intermediate infection model and a translational mouse model. In the murine model, the integration of micro-CT imaging further enhanced the characterization of host-pathogen interactions by enabling noninvasive assessment of tissue responses over time. Overall, our approach enables enhanced temporal resolution for quantitative assessment of fungal burden and host responses. Using M. lusitanicus as a model organism, this methodology establishes a foundation and technical expertise for application toward clinically relevant Mucorales infection and antifungal research.
Crimean-Congo Hemorrhagic Fever (CCHF) was first described in the 1930s and 40s, yet there is no study that has examined global research landscape of this important zoonosis. We undertook the first global and holistic bibliometric analysis on CCHF aimed at revealing gaps, trends and collaborative networks. We applied the SPAR-4-SLR protocol together with an expansive set of keywords to search and retrieve relevant studies from the Scopus database. Using our pre-defined inclusion criteria and removal of duplicates, a final dataset of 2540 studies were included for analysis. The dataset were analysed in Biblioshiny, VOSviewer, and R software. A total of 2,540 CCHF publications (1981-2025) were included in the final analysis. Overall, the number of studies showed a steady annual growth rate of 6.79%, with a sharp rise in outputs and citations after 2010. The correlation coefficient stood at R2 = 0.79. The research landscape was dominated by multi-authored collaborations, strong international partnerships, and a high share of original articles. Key contributors were from Iran, Turkey, the United States (USA), and Europe, with major funding driven by NIAID, NIH, and the European Commission. Funders and authors from African and other poorer regions were disproportionately lower despite the Congo (Africa) being the co-origin of the virus. Highly cited papers highlight advances in epidemiology, diagnostics, and tick-virus ecology. Frequently used keywords reflect strong focus on humans, CCHF virus, and surveillance. Core journals include Emerging Infectious Diseases, Antiviral Research, and PLoS Neglected Tropical Diseases. Keyword analysis showed a gradual transition from early basic studies to mechanistic, molecular, and One Health-oriented investigations. The CCHF research landscape is growing steadily, driven by strong international collaborations and major funding agencies. Persistent focus on surveillance and public health preparedness indicates a maturing, globally coordinated research landscape essential for controlling CCHF and protect public health.
SARS-CoV2 can induce an acute respiratory distress syndrome (ARDS), provoked by a dysregulated hyper-inflammatory pulmonary immune response. Here, we used the keratinocyte-18 humanized angiotensin converting enzyme-2 (K18-hACE2) mouse model of SARS-CoV2, where expression of the CoV2 spike protein receptor, hACE-2, is restricted to epithelia, to characterize inflammatory pulmonary immune responses post-intranasal infections with the delta isolate SARS-CoV2(∆) B.1.617.2. Immune-profiling by focused transcript analysis, inflammatory protein array, and multi-color flow cytometry, confirmed that clinically relevant markers of COVID-19 (IL-6, GM-CSF, neutrophils, inflammatory monocytes) were significantly elevated in lungs of mice at day 5 post-infection and that remdesivir antiviral active metabolite (GS441524) treatment significantly modified SARS-CoV2∆ viral loads and pulmonary inflammation. Chemokine ligands of CCR2 (CCL2/7/8) were among the top 5% upregulated pulmonary transcripts in a focused human infection response array to SARS-CoV2∆. CCL2 was confirmed as elevated in protein assays in SARS-CoV2∆ infected lungs. To address the functional relevance of the CCR2 pathway of inflammatory cell recruitment to the lungs mediating disease, mice were administered with anti-CCR2 antibody daily at the point of infection for up to 6 d. Anti-CCR2 treated mice showed significant improved welfare scores, were protected from weight loss, modified myeloid pneumonitis, and displayed significantly blunted cytokine and chemokine response in the lungs, despite not affecting pulmonary viral loads. Our data supports therapeutic benefit of modifying CCR2-dependent cell recruitment in the treatment of viral-induced ARDS.
Prohibitive costs associated with high-field MRI systems have resulted in reduced access in resource-limited areas with consequential healthcare inequities. This has renewed interest in purposefully designed low-field (LF) systems that, despite inherently lower signal-to-noise ratios, have advantages in terms of cost, portability, and accessibility. This pilot study successfully translated a previously developed LF (0.05 T) MRI canine cadaver brain protocol for in vivo application and compared the acquired images with paired 1.5 T images from 21 different canine patients. The visibility of 15 anatomic features was ordinarily scored (scale 1-3) on transverse T1-weighted post-contrast (21/21 patients) and T2-weighted (17/21 patients) sequences. Lateral ventricles were easily visualized (89.3%-100% scored 3/3) across all sequence‒system combinations, with T2-weighted sequences also providing good identification of the mesencephalic aqueduct (56.3%-100%), fourth ventricle (77.1%-100%), and thalamus (68.8%-100%). Absolute visual grading characteristics (VGC) analysis confirmed comparable performance of the LF system to the 1.5 T MRI for these features, a particularly relevant finding given the system's originally intended application for pediatric hydrocephalus neuroimaging in resource-limited areas. This study represents the first in vivo usage and evaluation of a 0.05 T MRI in a clinical veterinary context.
[Formula: see text] Dr. Tayade earned a Doctor of Veterinary Medicine, Masters, and PhD in Immunology from the Indian Veterinary Research Institute. He then completed a postdoctoral fellowship at the University of Guelph. He joined Queen's University in 2009 as an Assistant Professor and is currently working as a Vice Dean, and the Director of MD PhD Program in the Faculty of Health Sciences. The central theme of Dr. Tayade's research focusses on how immune dysfunction contributes to endometriosis pathophysiology, and identifying immune-based markers for diagnostic and therapeutic interventions. Dr. Tayade has published over 100 peer-reviewed articles in journals such as JCI Insight, Journal of Immunology, American Journal of Pathology, American Journal of Obstetrics and Gynecology, and Trends in Molecular Medicine. He has received competitive funding from the Canadian Institutes of Health Research (CIHR), the Natural Sciences and Engineering Research Council of Canada (NSERC), and the Endometriosis Foundation of America; and industrial funding from Bayer, Aurinia Pharmaceutical, and AbbVie. For his outstanding contributions to research, Dr. Tayade has received numerous special recognitions. In 2012, he won both the Early Researcher Award from the Ministry of Research and Innovation, as well as the Christian J Herr Award for Outstanding Contributions in Reproductive Immunology from the American Society for Reproductive Immunology. In 2014, he earned the Mihran and Mary Basmajian Award for Research Excellence from the Queen's Faculty of Health Sciences.
PURPOSE: This study presents the first seroepidemiological investigation of anti-Kudoa spp. (Myxosporea: Multivalvulida) antibodies in the general population of the Canary Islands (Macaronesia, Spain), a region with high seafood consumption and pronounced geographic and climatic variability. METHODS: A total of 1,096 serum samples from all seven islands were randomly selected and analyzed by ELISA for IgG and IgE antibodies against Kudoa spp. pseudocyst antigens extracted from locally consumed fish. RESULTS: The overall seroprevalence for both IgG and IgE was 16.4%, indicating widespread exposure to Kudoa parasites. Marked geographic variation was observed: IgG seroprevalence was highest in Lanzarote (47%), Fuerteventura, and Gran Canaria (29.4%), while IgE prevalence peaked in La Gomera (63.3%), El Hierro (30.9%), and La Palma (27.4%). Sex-related differences were also detected, with higher IgE levels in males (p < 0.001). In addition, seropositivity varied by climate zone, with the dry desert zone showing the highest IgG prevalence (35.7%) and mild temperate zones the highest IgE prevalence (16.5%). CONCLUSION: These findings suggest that environmental, dietary, and behavioral factors strongly modulate host immune responses to fish-borne parasites. The results underscore the clinical and public health relevance of Kudoa spp., highlighting the need for ongoing surveillance and targeted preventive measures in populations with elevated seafood consumption. Overall, this research provides novel insights into the epidemiology, immune sensitization, and risk determinants of Kudoa exposure, contributing to improved management of seafood-borne zoonoses and evidence-based risk assessment for public health authorities.
Next-generation probiotics derived from gut commensals show promise for metabolic disease intervention, yet effective anti-obesity strains remain limited. Here, we demonstrate that oral administration of Christensenella massiliensis markedly alleviates obesity and metabolic dysfunction in high-fat diet-induced obese mice. Treatment reduced food intake, improved glucose tolerance and insulin sensitivity, lowered blood glucose and lipid levels, and attenuated hepatic steatosis and adipose accumulation. C. massiliensis increased the levels of plasma GLP-1 and ileal GLP-1 receptor expression while decreasing ghrelin level, suggesting modulation of gut hormone regulation. C. massiliensis also suppressed systemic and colonic inflammation, accompanied by upregulation of metabolic homeostasis-related genes (ppara, pparg, ucp2). Targeted and quantitative metabolomics identified altered gut metabolic profiles, particularly reduced kynurenine levels. In vitro assays further showed that C. massiliensis converted kynurenine into kynurenic acid, and its lysate reversed kynurenine-induced lipid accumulation, inflammation, and PPARγ suppression in hepatocytes, providing mechanistic support for the observed in vivo metabolic benefits. These findings support C. massiliensis as a promising next-generation probiotic for obesity management.
Hyalomma asiaticum is a dominant tick vector in arid and semi-arid regions. It transmits multiple pathogens affecting livestock health and production. Long-term spatiotemporal patterns of this tick and associated pathogens remain poorly characterized across the Belt and Road region. We systematically integrated 1970-2025 Chinese and English language literature to construct spatiotemporal distribution and pathogen risk databases for H. asiaticum. Standard deviational ellipse (SDE) analysis, kernel density estimation (KDE), and centroid shift methods were applied to quantify tick expansion and pathogen distribution. Host composition and environmental and human activity-related factors were evaluated as potential ecological correlates. H. asiaticum showed a literature-derived apparent spatial expansion pattern over the past half century. However, this pattern may partly reflect increased sampling effort and publication intensity over time. Five key pathogen groups (CCHFV, SFGR, Anaplasma spp., Coxiella burnetii, piroplasmids) displayed heterogeneous spatial patterns. For comparative interpretation, these pathogens were operationally grouped according to their major One Health risk relevance, primarily related to livestock production and trade or to public health. Livestock-associated pathogens showed higher detection metrics in hub regions, whereas public health risk pathogens showed no significant hub-region difference and only a weak HFP-related trend. This study provides a comprehensive, long-term assessment of H. asiaticum and its associated pathogens, highlighting livestock interfaces as key risk areas. Findings support targeted tick surveillance and cross-border biosecurity strategies, offering practical guidance for veterinary public health management along the Belt and Road corridor.
Gastric acid-suppressive medications, particularly proton pump inhibitors (PPIs), are commonly used in patients with alcohol-associated liver disease (ALD) to prevent and manage upper gastrointestinal bleeding, gastroesophageal reflux disease, and non-steroidal anti-inflammatory/aspirin-induced gastroesophageal damage. By inhibiting the gastric H⁺/K⁺-ATPase, PPIs suppress acid secretion and impair bacterial killing, thereby promoting gut dysbiosis that disrupts barrier integrity and enhances bacterial translocation, ultimately exacerbating liver injury. PPIs are frequently co-administered with antibiotics for indications such as gastrointestinal bleeding, Spontaneous Bacterial Peritonitis (SBP), other infections, or hepatic encephalopathy prophylaxis, but the consequences of this combined therapy on gut microbial ecology and disease outcomes remain unclear. Our study addresses this gap by showing how PPI use, alone or with antibiotics, reshapes the gut microbiome and aggravates liver disease progression. In previous studies, we showed that PPIs promote dysbiosis and ALD progression in mice and humans by facilitating intestinal expansion and hepatic translocation of Gram-positive Enterococcus. Fecal cytolysin, an Enterococcus faecalis exotoxin that induces hepatocyte death, predicts mortality in patients with alcohol-associated hepatitis (AH). In this study, we have examined the mechanism by which PPIs alone and in combination with non-absorbable antibiotics targeting Gram-positive bacteria influence ALD, as well as the disease mechanisms associated with cytolytic Enterococcus faecalis and the development of therapeutic strategies. In mice, alcohol administration during gastric acid suppression promoted expansion of Gram-positive taxa, including cytolysin-producing Enterococcus. Similarly, PPI use in patients with AH was associated with increased fecal Enterococcus and higher 30-d mortality, underscoring the translational relevance of our findings. Unexpectedly, treatment of acid-suppressed mice with non-absorbable antibiotics designed to suppress Gram-positive bacteria worsened ethanol-induced steatohepatitis: while Enterococcus abundance decreased, Streptococcus and other potentially pathogenic taxa expanded, leading to increased bacterial translocation and aggravated liver injury. In patients with cirrhosis or metabolic dysfunction-associated steatotic liver disease (MASLD), PPIs did not promote Enterococcus expansion, indicating etiology-dependent microbiome responses. Finally, we identified dipalmitoylphosphatidylcholine and Caspase-1 inhibitor as in vitro and in vivo modulators of cytolysin activity, highlighting potential therapeutic avenues. Collectively, our study demonstrates how PPIs and non-absorbable antibiotics targeting Gram-positive bacteria interact with the gut microbiome to drive ALD, underscoring the need for careful therapeutic management.
Free-roaming cats (Felis catus) can serve as reservoirs of various zoonotic parasites in urban settings. Despite a large population of free-roaming cats around New York City, studies assessing the prevalence and shedding of various parasites in the New York urban landscape are scarce. This study utilized fecal and blood samples opportunistically collected during the Trap Neuter Return (TNR) program from 87 free-roaming cats in New York City between May and July 2023. Samples were analyzed using centrifugal fecal flotation, coproantigen immunoassays, serologic assays, and PCR-based assays for gastrointestinal and vector-borne parasites. Fecal flotation (n = 87) results revealed that 57.5% (50/87; 95% CI: 46.9-67.4) of cats were infected with at least one species of parasite. The most prevalent infection was Toxocara spp. (54%; 95% CI: 43.4-64.3), followed by Ancylostoma spp. (13.8%; 95% CI: 8.2-22.6) and coccidia (11.5%; 95% CI: 6.4-19.9). Coproantigen testing (n = 43) identified Giardia spp. in 11.6% (5/43; 95% CI: 5.1-24.5) and Cryptosporidium spp. in 2.3% (1/43; 95% CI: 0.4-12.1) of cats. Antibodies to Toxoplasma gondii were detected in 8.9% (4/45; 95% CI: 3.5-20.7) of serum samples; no Dirofilaria immitis antigen and Cytauxzoon felis DNA were found in the blood samples (n = 45). Male cats were significantly more likely to be infected with Toxocara spp. (OR = 4.36) and, along with juvenile cats (<1 year), shed significantly higher numbers of eggs (p < 0.05), identifying young males as high-intensity "super-shedders" driving environmental contamination. The high prevalence of zoonotic helminths, particularly Toxocara spp., underscores the public health risks associated with unmanaged feline populations in densely populated urban centers. These findings highlight the utility of integrating disease surveillance into TNR programs to monitor urban ecosystem health and mitigate zoonotic risks.
Premises Identification (PID) programs in Canada assign unique identification numbers to locations where animals, such as livestock and poultry, are kept. These programs are provincial and territorial, with a purpose of supporting various animal disease outbreaks, natural disaster emergencies, and animal traceability. While most PID programs have been operating since early 2000s, there has been no study reporting on PID programs in Canada. This qualitative study explored PID programs across Canada through the perspectives of government-employed stakeholders to (1) describe PID programs in participating Canadian provinces and territories, and (2) identify the strengths and weaknesses across PID programs. Stakeholders from nine provinces and one territory (N = 22) participated in online one-on-one interviews or focus groups. Data were analyzed inductively using codebook thematic analysis. Findings suggest that PID programs must build trust with farmers through transparent communication of intended data usage, ideally through familiar social networks. Furthermore, compliance with PID appears to be stronger when there are robust cross-compliance measures in place that have proportional incentives and enforcement measures. Programs with increased capacity and resources were better equipped to maintain data quality, which was achieved by some programs by narrowing the eligibility criteria for PID around the species of interest. This study provides valuable insights for improving the effectiveness of PID programs in Canada. Future research should explore the perspectives of other stakeholders, such as farmers eligible for the program.
BACKGROUND: Influenza A viruses are a significant cause of global morbidity, mortality, and economic losses. Swine are considered an important host for pandemic emergence; however, knowledge on the ecology and evolution of swine influenza viruses in relation to pig production and exchange systems is limited. The PigFluCam+ project was first initiated in 2019 as a One Health-focused research collaboration between public and animal health stakeholders in Cambodia. OBJECTIVE: The primary objectives of the project were to (1) describe the epidemiology and diversity of swine influenza A viruses (swIAVs) in the Cambodian pig sector, (2) assess the risk of zoonotic influenza transmission across different occupations, (3) characterize the pig trade network, (4) develop mathematical models of swIAV transmission to target control activities, and (5) promote in-country One Health research and surveillance. This paper presents the methods and approaches used by the project, serving as a resource for future research initiatives with similar aims. METHODS: These approaches consist of systematic sample collections and survey studies. Influenza surveillance in pigs was conducted over 2 years through repeated (monthly) cross-sectional sampling at 18 slaughterhouses across 4 provinces. Phylogenetic analysis was used to describe the diversity of swIAVs detected and was used to develop antigens for Luminex xMAP assays for screening human and pig sera. Cross-sectional surveys among actors in the pig value chain characterized pig production practices and trading networks. In parallel, a cohort study was carried out involving households with and without occupational exposure to live pigs to compare the seroprevalence of influenza A viruses among different swine-associated occupational groups. RESULTS: The surveys began in 2020 and despite disruptions caused by the COVID-19 pandemic and the introduction of African Swine Fever into the region, the project has generated a wealth of data. Over 4000 pigs were sampled at slaughterhouses, and network surveys collected pig production and trading data from 379 study participants. Higher influenza A seroprevalence (960/2399, 40%) and prevalence (37/2413, 1.5%) were found among pigs from commercial farms, compared to smallholder farms (seroprevalence 8.9%, 95/1066; prevalence 0.6%, 6/1071). Duration at slaughterhouse and seroprevalence correlated positively, suggesting potential transmission after leaving the farm. A total of 997 individuals were recruited into the cohort study, with 775 consenting to provide at least 1 serum sample. Funding for the project ended in September 2025; 3 results papers and 1 PhD thesis have been published, with analysis and publication expected to be completed by the end of 2026. CONCLUSIONS: This project has developed surveillance protocols and modern technologies for establishing active zoonotic disease surveillance. These efforts support the region's capability to effectively identify zoonotic pathogens and enhance the prediction and response to zoonotic outbreaks and pandemic risk associated with pig production systems in the Lower Mekong region.
Objective: The transition from acute kidney injury (AKI) to chronic kidney disease (CKD) is a major cause of poor prognosis in renal injury, and preventing the progression from AKI to CKD has important clinical significance. Finerenone exerts renoprotective effects, however, its role in the AKI-CKD transition remains unclear.Methods: An ischemia-reperfusion (IR)-induced AKI mouse model was established in male C57BL/6 mice by unilateral renal artery clamping combined with contralateral nephrectomy. Finerenone was administered at doses of 10 mg/kg or 15 mg/kg, and renal function, aldosterone levels, podocyte injury, inflammatory responses, and renal fibrosis were evaluated at days 8 and 28 to investigate pathological mechanisms underlying the AKI-CKD transition.Result: Finerenone significantly attenuated IR-induced renal injury and improved renal function during the acute phase and throughout the subsequent AKI-CKD transition. Compared with 10 mg/kg, finerenone at 15 mg/kg more effectively reduced podocyte injury, dampened the inflammatory response, and attenuated renal fibrosis. Mechanistically, finerenone suppressed the p38 phosphorylation and reduced nuclear factor kappa-B (NF-κB) activation during the AKI-CKD transition.Conclusion: Finerenone exerts dose-dependent renoprotective effects during AKI progression and the subsequent AKI-CKD transition, potentially by suppressing podocyte mineralocorticoid receptor overactivation and concomitant reductions in renal inflammation and fibrosis, accompanied by attenuation of p38 phosphorylation and NF-κB activation during the AKI-CKD transition.
Monkeypox (Mpox) is a zoonotic disease caused by MPXV and remains a threat to global public health. MPXV Clade Ib has higher mortality, whereas Clade IIb exhibits widespread international transmission. WHO has twice designated mpox epidemics as a Public Health Emergency of International Concern (PHEIC). This highlights that the virus is not only pathogenic but also has the potential to cause a global pandemic, posing a challenge to the international public health system. The rapid transmission of MPXV between and within hosts is related to two key virus particles: IMV and EEV. Antigenic proteins (A29L, M1R, B6R, and A35R) on these particles mediate viral invasion, dissemination, and immune evasion. Clinical management of mpox remains supportive, and there is a lack of specific antiviral drugs. Although smallpox-related drugs (such as tecovirimat, cidofovir, and brincidofovir) show potential, their clinical efficacy needs to be verified. The existing vaccines recommended by the WHO are facing challenges, such as side effects or limited duration of immune protection in application, prompting the research and development of novel vaccines and antibody therapeutics. Research on the mechanism of invasion and surface proteins of viruses will continue to provide a scientific foundation for the development of medications and vaccines. Prevention and control rely on a stronger monitoring system, timely risk warnings, and public health education. This article reviews the recent progress in MPXV detection, vaccine development, and antibody-based therapy, providing new insights for mpox prevention and control.
Carbapenem-resistant Providencia (CRP) is a formidable opportunistic pathogen with extensive drug resistance, posing an increasing threat to human, animal, and environmental health. However, its global genomic epidemiology and resistome-plasmidome co-evolution within a One Health context remain poorly understood. Here, we conducted a comprehensive population genomic and plasmid analysis of 1197 CRP isolates from 35 countries spanning 2012-2025. We reclassified the CRP population into nine Providencia species, identifying P. stuartii and P. rettgeri as established epidemic species alongside the rapid emergence of P. hangzhouensis and P. huashanensis. We pinpointed 2019 as a critical inflection point, marking the transition from endemic stability to rapid global epidemic expansion (80.8% isolates in 2019-2025). Ten intercontinentally disseminated high-risk sequence types (e.g., ST46, ST79), each with strict species-ST specificity, were responsible for global spread. The bla NDM-1 gene (62.4% prevalence) was the predominant carbapenem gene, exhibiting strong geographic and species specificity and mutual exclusion with other major carbapenem genes. Plasmids encoded approximately 80% of antimicrobial resistance (AMR) genes, with 78.0% of these plasmids belonging to 75 stable clusters. These clusters evolved a dual specialist-generalist strategy, with the broad-host-range cluster 72 mediating interspecies AMR transmission and cluster 7 acting as a super-vector carrying six carbapenem genes. Importantly, CRP circulated across interconnected human, animal, and environmental reservoirs, with distinct host-associated species distributions suggesting ecological niche adaptation and potential cross-host dissemination of resistance determinants. These findings demonstrate that the global expansion of CRP is driven by the combined evolution of high-risk clones and mobile genetic elements across interconnected ecological sectors, underscoring the need for integrated One Health surveillance and coordinated interventions spanning clinical, veterinary, agricultural, and environmental settings.
Clostridioides difficile infection (CDI) is a major cause of antibiotic-associated diarrhea, with frequent recurrences closely linked to antibiotic-induced dysbiosis of the gut microbiota and bile acid metabolism. Parabacteroides distasonis, a potential probiotic capable of converting primary to secondary bile acids, has shown therapeutic promise in several metabolic and inflammatory diseases. This study evaluated the preventive and therapeutic effects of P. distasonis against CDI and explored the underlying mechanisms. We characterized the probiotic properties of four P. distasonis strains and investigated the inhibitory activity of strain 1190003 against C. difficile, as well as its protective and therapeutic efficacy in mouse models. Gut microbiota structure and bile acid metabolic profiles were analyzed by integrating 16S rRNA gene sequencing and metabolomics. The four P. distasonis strains exhibited strong acid and bile salt tolerance as well as auto-aggregation ability. Supernatants from P. distasonis co-cultured with cholic acid (4 mM and 8 mM) significantly inhibited C. difficile growth, toxin expression and spore formation, with deoxycholic acid identified as the key inhibitory metabolite. Both live P. distasonis and its culture supernatant alleviated disease severity in CDI mouse models and ameliorated gut microbiota dysbiosis. Notably, the relative abundance of Parabacteroides goldsteinii was increased following supernatant treatment. Furthermore, intervention with either live P. distasonis or its supernatant elevated the level of hyodeoxycholic acid. In summary, P. distasonis acts as a potential probiotic that alleviates CDI by ameliorating gut microbiota dysbiosis and remodeling bile acid metabolism. These findings provide experimental evidence for its use as a microbiota-based therapeutic strategy.
BVA's director of policy and governance, Amelia Findon, reports from the recent Federation of Veterinarians of Europe (FVE) general assembly in Rovaniemi, Finland, where, alongside RCVS, we form the UK delegation.
Opisthorchis viverrini infection remains a major public health concern in Southeast Asia, particularly in the Greater Mekong Subregion. Although animal reservoirs contribute to sustaining parasite transmission, comprehensive evidence on infections in these hosts remains limited. This study conducted a systematic review and meta-analysis to assess O. viverrini infection in animal reservoirs (cats and dogs). Pooled prevalence and infection intensity were estimated using random-effects models and meta-regression, and associated factors were synthesized. Subgroup analyses were performed to examine variability, and heterogeneity was evaluated using the Q statistic and the I² index. The pooled prevalence of O. viverrini infection in animal reservoirs was 4.76% (95% confidence interval (CI): 2.83-7.90%, prediction interval (PI): 0.15-61.76%). After trim-and-fill adjustment, the estimate increased to 16.31% (95% CI: 10.00-25.49%, PI: 0.28-93.09%), with wide prediction intervals indicating substantial heterogeneity. Cats showed significantly higher prevalence (11.97%) than dogs (1.89%; p < 0.01). Infection intensity followed a similar pattern, with mean eggs per gram (EPG) higher in cats (151.07) than in dogs (45.77; p < 0.01). No significant difference in overall prevalence was observed between Thailand (4.36%) and Lao PDR (13.44%; p = 0.19), although significant subgroup differences were detected for cats (p = 0.01) and dogs (p < 0.01). Overall reservoir-host prevalence was higher in endemic areas (5.64%) than in non-endemic regions (2.28%; p < 0.001); this difference was significant in cats but not in dogs. Meta-regression showed no significant temporal trend. Linear regression revealed positive associations between human and animal infections, with stronger correlation for cats (R² = 0.86, p < 0.01) than dogs (R² = 0.62, p = 0.02). These findings support an important role of animal reservoirs, particularly cats, in transmission and emphasize the need for improved surveillance and integrated control strategies.