4.5 Article

Emergence of nosocomial associated opportunistic pathogens in the gut microbiome after antibiotic treatment

Journal

Publisher

BMC
DOI: 10.1186/s13756-021-00903-0

Keywords

Antibiotic resistance; Metagenomics; Nosocomial; Microbiota; Antibiotic therapy

Funding

  1. Research Participation Program at the Center for Drug Evaluation and Research
  2. Office of Medical Policy at US Food and Drug Administration (FDA)
  3. FDA

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The study aimed to confirm gut microbiota shifts in an animal model of antibiotic treatment and found that antibiotic therapy reduced detectable species of bacteria and increased opportunistic pathogens in the gut microbiota. Furthermore, antibiotic treatment selected for antibiotic-resistant gene enriched subpopulations for many of these pathogens.
Introduction According to the Centers for Disease Control's 2015 Hospital Acquired Infection Hospital Prevalence Survey, 1 in 31 hospital patients was infected with at least one nosocomial pathogen while being treated for unrelated issues. Many studies associate antibiotic administration with nosocomial infection occurrence. However, to our knowledge, there is little to no direct evidence of antibiotic administration selecting for nosocomial opportunistic pathogens. Aim This study aims to confirm gut microbiota shifts in an animal model of antibiotic treatment to determine whether antibiotic use favors pathogenic bacteria. Methodology We utilized next-generation sequencing and in-house metagenomic assembly and taxonomic assignment pipelines on the fecal microbiota of a urinary tract infection mouse model with and without antibiotic treatment. Results Antibiotic therapy decreased the number of detectable species of bacteria by at least 20-fold. Furthermore, the gut microbiota of antibiotic treated mice had a significant increase of opportunistic pathogens that have been implicated in nosocomial infections, like Acinetobacter calcoaceticus/baumannii complex, Chlamydia abortus, Bacteroides fragilis, and Bacteroides thetaiotaomicron. Moreover, antibiotic treatment selected for antibiotic resistant gene enriched subpopulations for many of these opportunistic pathogens. Conclusions Oral antibiotic therapy may select for common opportunistic pathogens responsible for nosocomial infections. In this study opportunistic pathogens present after antibiotic therapy harbored more antibiotic resistant genes than populations of opportunistic pathogens before treatment. Our results demonstrate the effects of antibiotic therapy on induced dysbiosis and expansion of opportunistic pathogen populations and antibiotic resistant subpopulations of those pathogens. Follow-up studies with larger samples sizes and potentially controlled clinical investigations should be performed to confirm our findings.

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