Integrated Analysis of Gut Microbiota and Serum Metabolites in Bactrian Camels with Vaginal Myiasis Using 16S ribosomal DNA Sequencing and LC/MS-Based Metabolomics
Abstract
Background :Vaginal myiasis in Bactrian camels, caused by larval infestation of Wohlfahrtia magnifica in vaginal tissues, is characterized by clinical signs including anorexia and emaciation. However, the underlying mechanisms through which this condition influences the gut microbiota and serum metabolic profiles remain poorly understood. Results :In this study, we collected fecal and serum samples from both infected and healthy camels and employed an integrated approach combining 16S rDNA gene sequencing, LC/MS(Liquid Chromatography-Mass Spectrometry)-based metabolomics, and correlation analysis to investigate the relationship between gut microbial communities and serum metabolites. 16S rDNA sequencing revealed 74 bacterial genera exhibiting significant differences in abundance ( p < 0.05) at the genus level, as determined by the Wilcoxon rank-sum test. Functional prediction based on the Kyoto Encyclopedia of Genes and Genomes (KEGG) database identified 41 significantly altered metabolic pathways ( p < 0.05). Among the 16 pathways significantly enriched in the infected group, those associated with metabolism were predominant ( n = 7). Serum metabolomic profiling identified 171 significantly differential abundant metabolites ( p < 0.05), with KEGG enrichment analysis revealing 28 significantly impacted metabolic pathways ( p <0.05). Furthermore, Spearman correlation analysis identified 29 significant microbiota–metabolite pairs ( p < 0.05). Integrative analysis highlighted concurrent disruptions in glycerophospholipid metabolism and glycine, serine, and threonine metabolism. Conclusions :The present study reveals that vaginal myiasis disrupts the normal "Gut-microbiota-reproductive axis," triggering a systemic metabolic response in the host characterized by disturbances in glycerophospholipid metabolism and glycine, serine, and threonine metabolism. Based on these findings, we propose a novel microbiota-mediated mechanism: a distant parasitic infection induces dysbiosis of the core gut microbiota, which in turn impairs the production of key metabolites. This cascade disrupts host energy homeostasis and immune balance, ultimately manifesting as clinical symptoms including emaciation and anorexia. This work provides new insights into host-microbial interactions in parasitic diseases.
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