Search

Antimicrobial resistance (AMR) is a major threat to global public health, and antibiotic resistance genes (ARGs) are widely distributed across humans, animals, and environment. Farming environments are emerging as a key research area for ARGs and antibiotic resistant bacteria (ARB). While the skin is an important reservoir of ARGs and ARB, transmission mechanisms between farming environments and human skin remain unclear. Previous studies confirmed that swine farm environmental exposures alter skin microbiome, but the timeline of these changes is ill defined. To improve understanding of these changes and to determine the specific time, we designed a cohort study of swine farm workers and students through collected skin and environmental samples to explore the impact of daily occupational exposure in swine farm on human skin microbiome. Results indicated that exposure to livestock‐associated environments where microorganisms are richer than school environment can reshape the human skin microbiome and antibiotic resistome. Exposure of 5 h was sufficient to modify the microbiome and ARG structure in workers' skin by enriching microorganisms and ARGs. These changes were preserved once formed. Further analysis indicated that ARGs carried by host microorganisms may transfer between the environment with workers' skin and have the potential to expand to the general population using farm workers as an ARG vector. These results raised concerns about potential transmission of ARGs to the broader community. Therefore, it is necessary to take corresponding intervention measures in the production process to reduce the possibility of ARGs and ARB transmission. Highlights: Exposure to livestock‐associated environment, more microbially enriched than school environment, can remodel the human skin microbiome and antibiotic resistome.The 5 h of exposure is sufficient to alter the microbiota and antibiotic resistance genes (ARGs) structure of skin and these changes were retained once formed.ARGs carried by host microbes were transferred between the environment and workers' skin. [ABSTRACT FROM AUTHOR]

Correct and bias-free interpretation of the deep sequencing data is inevitably dependent on the complete mapping of all mappable reads to the reference sequence, especially for quantitative RNA-seq applications. Seed-based algorithms are generally slow but robust, while Burrows-Wheeler Transform (BWT) based algorithms are fast but less robust. To have both advantages, we developed an algorithm FANSe2 with iterative mapping strategy based on the statistics of real-world sequencing error distribution to substantially accelerate the mapping without compromising the accuracy. Its sensitivity and accuracy are higher than the BWT-based algorithms in the tests using both prokaryotic and eukaryotic sequencing datasets. The gene identification results of FANSe2 is experimentally validated, while the previous algorithms have false positives and false negatives. FANSe2 showed remarkably better consistency to the microarray than most other algorithms in terms of gene expression quantifications. We implemented a scalable and almost maintenance-free parallelization method that can utilize the computational power of multiple office computers, a novel feature not present in any other mainstream algorithm. With three normal office computers, we demonstrated that FANSe2 mapped an RNA-seq dataset generated from an entire Illunima HiSeq 2000 flowcell (8 lanes, 608 M reads) to masked human genome within 4.1 hours with higher sensitivity than Bowtie/Bowtie2. FANSe2 thus provides robust accuracy, full indel sensitivity, fast speed, versatile compatibility and economical computational utilization, making it a useful and practical tool for deep sequencing applications. FANSe2 is freely available at http://bioinformatics.jnu.edu.cn/software/fanse2/. [ABSTRACT FROM AUTHOR]

Mycophenolate mofetil (MMF) is commonly utilized for the treatment of neuromyelitis optica spectrum disorders (NMOSD). However, a subset of patients experience significant gastrointestinal (GI) adverse effects following MMF administration. The present study aims to elucidate the underlying mechanisms of MMF-induced GI toxicity in NMOSD. Utilizing a vancomycin-treated mouse model, we compiled a comprehensive data set to investigate the microbiome and metabolome in the GI tract to elucidate the mechanisms of MMF GI toxicity. Furthermore, we enrolled 17 female NMOSD patients receiving MMF, who were stratified into non-diarrhea NMOSD and diarrhea NMOSD (DNM) groups, in addition to 12 healthy controls. The gut microbiota of stool samples was analyzed using 16S rRNA gene sequencing. Vancomycin administration prevented weight loss and tissue injury caused by MMF, affecting colon metabolomes and microbiomes. Bacterial β-glucuronidase from Bacteroidetes and Firmicutes was linked to intestinal tissue damage. The DNM group showed higher alpha diversity and increased levels of Firmicutes and Proteobacteria. The β-glucuronidase produced by Firmicutes may be important in causing gastrointestinal side effects from MMF in NMOSD treatment, providing useful information for future research on MMF., Importance: Neuromyelitis optica spectrum disorder (NMOSD) patients frequently endure severe consequences like paralysis and blindness. Mycophenolate mofetil (MMF) effectively addresses these issues, but its usage is hindered by gastrointestinal (GI) complications. Through uncovering the intricate interplay among MMF, gut microbiota, and metabolic pathways, this study identifies specific gut bacteria responsible for metabolizing MMF into a potentially harmful form, thus contributing to GI side effects. These findings not only deepen our comprehension of MMF toxicity but also propose potential strategies, such as inhibiting these bacteria, to mitigate these adverse effects. This insight holds broader implications for minimizing complications in NMOSD patients undergoing MMF therapy.

We examined the prevalence and transmission of the fosA3 gene among Citrobacter freundii isolates from flowers and the retail environments. We identified 11 fosfomycin-resistant C. freundii strains (>256 μg/mL) from 270 samples that included petals ( n = 7), leaves ( n = 2), dust ( n = 1) and water ( n = 1). These 11 isolates were multidrug-resistant and most were simultaneously resistant to fosfomycin, cefotaxime, ciprofloxacin and amikacin. Consistently, all 11 isolates also possessed bla CTX-M- 14 , bla CMY- 65 / 122 , aac(6')-Ib-cr , qnrS1 , qnrB13/6/38 and rmtB . These fosA3 -positive isolates were assigned to two distinct PFGE patterns and one ( n = 9) predominated indicating clonal expansion of fosA3 -positive isolates across flower markets and shops. Correspondingly, fosA3 was co-transferred with bla CTX-M- 14 via two plasmid types by conjugation possessing sizes of 110 kb ( n = 9) and 260 kb ( n = 2). Two representatives were fully sequenced and p12-1 and pS39-1 possessed one and two unclassified replicons, respectively. These plasmids shared a distinctive and conserved backbone in common with fosA3 -carrying C. freundii and other Enterobacteriaceae from human and food animals. However, the fosA3 - bla CTX-M- 14 -containing multidrug resistance regions on these untypable plasmids were highly heterogeneous. To the best of our knowledge, this is the first report of fosA3 and bla CTX-M- 14 that were present in bacterial contaminants from flower shops and markets. These findings underscore a public health threat posed by untypable and transferable p12-1-like and pS39-1-like plasmids bearing fosA3 - bla CTX-M- 14 that could circulate among Enterobacteriaceae species and in particular C. freundi in environmental isolates., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Cheng, Fang, Ge, Wang, He, Lu, Zhong, Wang, Yu, Lian, Liao, Sun and Liu.)