Stenotrophomonas muris- First discovered as an urgent human pathogen with strong virulence associated with bloodstream infections

Author:

Liu Jiaying,Dong Xu,Yu Yuyun,Wu Tiantian,Xiang Yanghui,Yuan Xin,Cao Dan,Bi Kefan,Zhang Hanyin,Zhu Lixia,Zhang Ying

Abstract

AbstractFor the first time,Stenotrophomonas muris(S. muris) has been identified to be associated with human infections while studying the virulence ofStenotrophomonas maltophilia(S. maltophilia) clinical isolates. Previously,S. muriswas only isolated from the intestines of mice but its pathogenic potential for humans has never been reported. In this work, the phenotype ofS. murisvirulence, the potential genes that encode higher virulence ofS. muris, and host responses toS. murisinfection were investigated for the first time. It was found that S9 (S. murisno.9, isolated from patient’s bloodstream infection) was more virulent than both S8 (S. murisno.8, isolated from patient’s sputum) and S1 (S. maltophilia), where S8 and S9 were subsequently identified asS. murisby whole genome sequencing analysis. Candidate genes which may encode higher virulence of S9 were identified, includingvirB6, dcm, hlyD, and 14 other genes involved in porphyrin metabolism, pyrimidine metabolism, DNA methylation, two component system, and biofilm formation. Transcriptome analysis of host cells (THP-1 cells) infected by S8 and S9 (S9 with strong virulence over S8 with weak virulence) showed that 12 candidate genes involved in ion transport function and calcium signaling pathway were down-regulated and require special attention. Antibiotic susceptibility testing indicated that compared withS. maltophilia, theS. murisstrains, though more susceptible to minocycline, are highly resistant to last resort antibitoics colistin and polymyxin B and are also resistant to cephalosporin and fluoroquinolone. Because of the above differences in virulence properties and antibiotic susceptibility, it is critical thatS. murisbe distinguished fromS. maltophiliain clinical setting for improved care. This work provides the basis for future studies on pathogenic mechanisms ofS. murisand for developing improved treatment in the future.

Publisher

Cold Spring Harbor Laboratory

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