摘要
      肠道病原体会引起广泛的食源性疾病，并且越来越多地被发现具有抗微生物耐药性。然而，这些病原体对人类肠道微生物组和耐药性的生态影响尚未完全阐明。这项研究对60名肠道细菌感染患者（病例）的粪便进行了鸟枪宏基因组测序，并与从同一患者康复后（随访）收集的粪便进行比较。总体而言，与随访样本相比，病例样本携带更多的抗微生物耐药性基因（ARGs），并具有更大的耐药性多样性（p＜0.001），而随访样本的微生物组则更为多样（p＜001）。尽管病例主要由埃希氏菌、沙门氏菌和志贺菌属以及ARGs来定义多化合物和多药耐药性，随访发现，拟杆菌门和厚壁菌门以及四环素、大环内酯类、林可酰胺类和链菌素（MLS）的基因和氨基糖苷类耐药性更为丰富。宿主追踪分析显示，在病例和随访中，大肠杆菌都是ARGs的主要携带者，在感染期间出现了更高的丰度。在感染过程中发现了11种不同的超广谱β-内酰胺酶（ESBL），其中一些在恢复后似乎丢失或转移到不同的微生物宿主。食源性病原体引起的疾病发病率不断上升，加上它们在社区内携带和转移抗微生物耐药性决定因素方面的作用不断演变，有理由进一步研究肠道感染对人类肠道生态的影响。
Abstract
Enteric pathogens cause widespread foodborne illness and are increasingly found to harbor antimicrobial resistance. The ecological impact of these pathogens on the human gut microbiome and resistome, however, has yet to be fully elucidated. This study applied shotgun metagenome sequencing to stools from 60 patients (cases) with enteric bacterial infections for comparison to stools collected from the same patients’ post-recovery (follow-ups). Overall, the case samples harbored more antimicrobial resistance genes (ARGs) and had greater resistome diversity than the follow-up samples (p<0.001), while follow-ups had much more diverse microbiomes (p<0.001). Although cases were primarily defined by genera Escherichia, Salmonella, and Shigella along with ARGs for multi-compound and multidrug resistance, follow-ups had a greater abundance of Bacteroidetes and Firmicutes phyla and genes for tetracycline, macrolides, lincosamides, and streptogramins (MLS), and aminoglycoside resistance. A host-tracking analysis revealed that Escherichia was the primary carrier of ARGs in both cases and follow-ups, with a greater abundance occurring during infection. Eleven distinct extended spectrum beta-lactamases (ESBLs) were identified during infection, some of which appear to be lost or transferred to different microbial hosts upon recovery. The increasing incidence of disease caused by foodborne pathogens, coupled with their evolving role in harboring and transferring antimicrobial resistance determinants within communities, justifies further examination of the repercussions of enteric infection on human gut ecology.

https://www.biorxiv.org/content/10.1101/2023.01.13.523990v1.abstract