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Alterations of fecal antibiotic resistome in COVID-19 patients after empirical antibiotic exposure.

ABSTRACT: As the COVID-19 pandemic spread globally, the consumption of antibiotics increased. However, no studies exist evaluating the effect of antibiotics use on the antibiotic resistance of intestinal flora in COVID-19 patients during the pandemic. To explore this issue, we collected 15 metagenomic data of fecal samples from healthy controls (HCs) with no use history of antibiotics, 23 metagenomic data of fecal samples from COVID-19 patients who received empirical antibiotics [COVID-19 (abx+)], 18 metagenomic data of fecal samples from antibiotics-naïve COVID-19 patients [COVID-19 (abx-)], and six metagenomic data of fecal samples from patients with community-acquired pneumonia [PC (abx+)] from the Sequence Read Archive database. A total of 513 antibiotic-resistant gene (ARG) subtypes of 18 ARG types were found. Antibiotic treatment resulted in a signiﬁcant increase in the abundance of ARGs in intestinal flora of COVID-19 patients and markedly altered the composition of ARG proﬁles. Grouped comparisons of pairs of Bray-Curtis dissimilarity values demonstrated that the dissimilarity of the HC versus the COVID-19 (abx+) group was signiﬁcantly higher than the dissimilarity of the HC versus the COVID-19 (abx-) group. The mexF, mexD, OXA_209, major facilitator superfamily transporter, and EmrB_QacA family major facilitator transporter genes were the discriminative ARG subtypes for the COVID-19 (abx+) group. IS621, qacEdelta, transposase, and ISCR were significantly increased in COVID-19 (abx+) group; they greatly contributed toward explaining variation in the relative abundance of ARG types. Overall, our data provide important insights into the effect of antibiotics use on the antibiotic resistance of COVID-19 patients during the COVID-19 epidemic.

SUBMITTER: Kang Y

PROVIDER: S-EPMC8664710 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Gut ecosystem has profound effects on host physiology and health. Gastrointestinal (GI) symptoms were frequently observed in patients with COVID-19. Compared with other organs, gut antiviral response can result in more complicated immune responses because of the interactions between the gut microbiota and host immunity. However, there are still large knowledge gaps in the impact of COVID-19 on gut molecular profiles and commensal microbiome, hindering our comprehensive understanding of the pathogenesis of SARS-CoV-2 and the treatment of COVID-19. We performed longitudinal stool multi-omics profiling to systemically investigate the molecular phenomics alterations of gut ecosystem in COVID-19. Gut proteomes of COVID-19 were characterized by disturbed immune, proteolysis and redox homeostasis. The expression and glycosylation of proteins involved in neutrophil degranulation and migration were suppressed, while those of proteases were upregulated. The variable domains of Ig heavy chains were downregulated and the overall glycosylation of IgA heavy chain constant regions, IgGFc-binding protein, and J chain were suppressed with glycan-specific variations. There was a reduction of beneficial gut bacteria and an enrichment of bacteria derived deleterious metabolites potentially associated with multiple types of diseases (such as ethyl glucuronide). The reduction of Ig heave chain variable domains may contribute to the increase of some Bacteroidetes species. Many bacteria ceramide lipids with a C17-sphingoid based were downregulated in COVID-19. In many cases, the gut phenome did not restore two months after symptom onset. Our study indicates widely disturbed gut molecular profiles which may play a role in the development of symptoms in COVID-19. Our findings also emphasis the need for ongoing investigation of the long-term gut molecular and microbial alterations during COVID-19 recovery process. Considering the gut ecosystem as a potential target could offer a valuable approach in managing the disease.

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Alterations of fecal antibiotic resistome in COVID-19 patients after empirical antibiotic exposure.

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