Genome Sequencing Verifies Relapsed Infection of Helicobacter cinaedi

Author:

Sawada Osamu1,Gotoh Yasuhiro2,Taniguchi Takako3,Furukawa Shota1,Yoshimura Dai4,Sasaki Satomi3,Shida Haruki1,Kusunoki Yoshihiro1,Yamamura Tsuyoshi1,Furuya Ken1,Itoh Takehiko4,Horita Tetsuya1,Hayashi Tetsuya2,Misawa Naoaki3

Affiliation:

1. Center of Nephrology and Connective Tissue Disease, Japan Community Health Care Organization Hokkaido Hospital, Japan

2. Department of Bacteriology, Faculty of Medical Sciences, Kyushu University, Japan

3. Center for Animal Disease Control, University of Miyazaki, Japan

4. Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Japan

Abstract

Abstract Background Recurrent infections of Helicobacter cinaedi are often reported, and long-term antimicrobial treatment is empirically recommended to prevent such infections. However, there have been no studies examining whether recurrent infections are relapses of former infections or reinfections with different clones. Methods A 69-year-old woman presented with recurrent H cinaedi bacteremia-associated cellulitis after a 51-day interval. We isolated 10 colonies from the blood cultures obtained during each of the 2 episodes and subjected them to whole-genome sequencing (WGS). High-confidence single-nucleotide polymorphisms (SNPs) were identified by an assembly based method. Heterogeneous SNP sites were identified by read mapping. The susceptibility of a representative isolate to 14 antimicrobials was also examined. Results Whole-genome sequence analysis revealed only 6 SNP sites among the 20 isolates at the whole-genome level. Based on the 6 SNPs, 5 within-host variants (referred to as genotypes) were identified. All 5 genotypes were detected in the first infection; however, only 2 genotypes were detected in the second infection. Although the H cinaedi clone showed a higher minimum inhibitory concentration to fluoroquinolones and macrolides and responsible mutations were identified, none of the 6 SNPs appeared related to additional resistance. Conclusions The second infection analyzed here was a relapse of the first infection. A certain level of within-host genomic heterogeneity of the H cinaedi clone was already present in the first infection. Our results suggest the importance of longer treatment courses to eradicate H cinaedi for preventing the relapse of its infection.

Funder

Japan Society for the Promotion of Science KAKENHI

Publisher

Oxford University Press (OUP)

Subject

Infectious Diseases,Oncology

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