Search bioRxiv⌕ Search

bioRxiv · 10.1101/814459

AB_SA: Tracing the source of bacterial strains based on accessory genes. Application to Salmonella Typhimurium environmental strains

Abstract

The partitioning of pathogenic strains isolated in environmental or human cases to their original source is challenging. The pathogens usually colonize multiple animal hosts, including livestock, which contaminate food-producing and environment (e.g. soil and water), posing additional public health burden and major challenges in the identification of the source. Genomic data opens new opportunities for the development of statistical models aiming to infer the likely source of pathogen contamination. Here, we propose a computationally fast and efficient multinomial logistic regression (MLR) source attribution classifier to predict the animal source of bacterial isolates based on \"source-enriched\" loci extracted from the accessory-genome profiles of a pangenomic dataset. Depending on the accuracy of the models self-attribution step, the modeler selects the number of candidate accessory genes that better fit the model for calculating the likelihood of (source) category membership. The accessory genes-based source attribution (AB_SA) method was applied on a dataset of strains of Salmonella Typhimurium and its monophasic variants (S. 1,4,[5],12:i:-). The model was trained on 69 strains with known animal source categories (i.e., poultry, ruminant, and pig). The AB_SA method helped to identify eight genes as predictors among the 2,802 accessory genes. The self-attribution accuracy was 80%. The AB_SA model was then able to classify 25 over 29 S. Typhimurium and S. 1,4,[5],12:i:-isolates collected from the environment (considered as unknown source) into a specific category (i.e., animal source), with more than 85% of probability. The AB_SA method herein described provides a user-friendly and valuable tool to perform source attribution studies in few steps. AB_SA is written in R and freely available at https://github.com/lguillier/AB_SA.\n\nAuthor NotesAll supporting data, code, and protocols have been provided within the article and through supplementary data files.\n\nSupplementary material is available with the online version of this article.\n\nAbbreviationsAB_SA, accessory-based source attribution; MLR, multinomial logistic regression; SNPs, single nucleotide polymorphisms; GFF, general feature format; AIC, Akaike information criteria.\n\nData SummaryO_LIThe AB_SA model is written in R, open-source and freely available Github under the GNU GPLv3 licence (https://github.com/lguillier/AB_SA).\nC_LIO_LIAll sequencing reads used to generate the assemblies analyzed in this study have been deposited in the European Nucleotide Archive (ENA) (http://www.ebi.ac.uk/ena) under project number PRJEB16326. Genome metadata and ENA run accession ID for all the assemblies are reported in the supplementary material.\nC_LI\n\nImpact StatementThis article describes AB_SA (\"Accessory-Based Source Attribution method\"), a novel approach for source attribution based on \"source enriched\" accessory genomics data and unsupervised multinomial logistic regression. We demonstrate that the AB_SA method enables the animal source prediction of large-scale datasets of bacterial populations through rapid and easy identification of source predictors from the non-core genomic regions. Herein, AB_SA correctly self-attribute the animal source of a set of S. Typhimurium and S. 1,4,[5],12:i:- isolates and further classifies the 84% of strains contaminating natural environments in the pig category (with high probability ranging between [~]85 and [~]99%).

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

GUILLIER, L., Gourmelon, M., Lozach, S., Cadel-Six, S., Vignaud, M.-L., Munck, N. S., Hald, T., Palma, F.. 2019-10-31. AB_SA: Tracing the source of bacterial strains based on accessory genes. Application to Salmonella Typhimurium environmental strains. https://doi.org/10.1101/814459

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Reverse Transcription Loop-Mediated Isothermal Amplification Combined with Lateral Flow Assay (RT-LAMP-LFA) for Rapid Detection of the 2026 Bundibugyo Virus (BDBV) Outbreak Strain

Making accurate diagnosis is a critical first step in patient management and control for emerging and re-emerging disease outbreaks. Bundibugyo virus (BDBV) is a filovirus that causes Ebola disease, and the 2026 outbreak highlights the need for rapid diagnostic approaches that can be deployed in settings with limited laboratory infrastructure. Here, we developed a reverse transcription loop-mediated isothermal amplification-lateral flow assay (RT-LAMP-LFA) for rapid detection of the 2026 BDBV outbreak strain. LAMP primers were designed based on the genome sequence of the 2026 outbreak strain, and the conservation of the primer binding sites among all available 2026 outbreak genomes was confirmed in silico. LAMP primers were evaluated for analytical specificity and sensitivity using in vitro-transcribed RNA (ivtRNA) from BDBV and other filoviruses, as well as RNA derived from arboviruses and mammalian cells. Amplification products were detected using a Chromatography-Printed Array Strip (C-PAS) lateral flow platform. The newly designed primers specifically detected the presence of BDBV RNA without nonspecific amplification of the other viral or cellular RNA samples tested. Consistent amplification was observed down to 103 copies per reaction. In addition, BDBV viral RNA was successfully amplified, and the amplification products were detected using C-PAS, with the total workflow being completed within 25 min. These findings demonstrate the analytical specificity and sensitivity of the developed RT-LAMP-LFA assay and its compatibility with rapid visual lateral flow detection, supporting its potential application as a point-of-care approach for BDBV detection.

microbiology↗

Divergent methane production and microbial community responses to carbon enrichment in freshwater wetland sediments

Methane (CH4) accumulation in wetland sediments reflects interactions among organic matter, sediment chemistry, and microbial communities. We combined depth-resolved field characterization across four wetland habitats in northern Israel with complementary incubations to examine methane accumulation and responses to labile-carbon enrichment. Sediment cores were characterized using Rock-Eval analysis, porewater chemistry, oxygen profiling at three sites, and mcrA amplicon sequencing. High CH4 concentrations occurred under contrasting conditions: Ein Nimfit (EN) contained approximately 12% total organic carbon and reached 2.1 mM CH4, whereas Ein Afek site EA2 contained approximately 5% carbon and accumulated 0.7-1.7 mM CH4. Both showed sulfate depletion, but EN exhibited pronounced sulfide accumulation, whereas EA2 showed greater dissolved iron and nutrient enrichment. Their classified methanogenic assemblages also differed. EA1 remained methane poor despite increasing carbon content with depth, while EA3 combined low carbon content and CH4 accumulation with detectable methanogens and lower methanogenic diversity. In a 36-day bottle experiments using sediments from two of the four wetland habitats, sucrose-amended EA3 exhibited a transient maximum of 18.8 mmol collected CH4 kg-1 wet sediment during Days 22-29, whereas EN reached its highest collected amount during Days 29-36. Methane proportions increased before the large output increase in EA3 but remained comparatively stable and high in EN. Soluble chemical oxygen demand trajectories and microbial community changes also differed. These findings identify distinct biogeochemical settings supporting methane accumulation and demonstrate methanogenic potential in low-CH4 sediment, emphasizing the complementary information provided by field profiles, microbial characterization, and exploratory enrichment experiments.

microbiology↗

The absence of microbiome in germ-free mice exacerbates the pathogenicity of mouse-adapted SARS-CoV-2 MA10

Germ-free mice, which are devoid of microbiota, provide a powerful system to define the contribution of the microbiome to host responses during infection. Severe COVID-19 outcomes are associated with multiple comorbidities that are themselves characterized by microbiome dysbiosis; however, the causal role of the microbiota in SARS-CoV-2 pathogenesis remains poorly understood. Here, we use germ-free mouse models to evaluate the impact of the microbiome on disease severity following infection with mouse-adapted SARS-CoV-2 MA10. Comparison with conventionally housed mice revealed that the absence of the microbiome markedly exacerbates SARS-CoV-2-induced disease in both C57BL/6 and Swiss Webster backgrounds. Germ-free mice exhibited greater weight loss, impaired lung function, worsened pulmonary pathology, and pronounced alterations in circulating cytokine and chemokine profiles compared with conventional controls. These findings show that resident microbiota limit SARS-CoV-2 pathogenicity and establish germ-free COVID-19 models as a powerful platform to identify protective microbial taxa and microbiota-based interventions to reduce severe disease.

microbiology↗