期刊
MICROORGANISMS
卷 10, 期 5, 页码 -出版社
MDPI
DOI: 10.3390/microorganisms10050866
关键词
Shiga toxin-producing Escherichia coli (STEC); pangenome; pathogenicity islands; virulence genes
类别
资金
- USDA-ARS CRIS project [2030-42000-052-00D]
This study examines the pathogenic potential of Shiga toxin-producing Escherichia coli (STEC) O145:H28 in clinical and environmental strains using comparative genomics. The core genes-based tree failed to differentiate between environmental and clinical strains, while the accessory genes-based tree grouped all clinical strains together. Loss-of-function mutations were common in virulence genes related to adherence and secretion systems. Differences in pathogenicity islands and other genetic elements were observed between O145:H28 and reference strains. The study reveals the genetic diversity and evolution of virulence in STEC.
Shiga toxin-producing Escherichia coli (STEC) O145:H28 can cause severe disease in humans and is a predominant serotype in STEC O145 environmental isolates. Here, comparative genomics was applied to a set of clinical and environmental strains to systematically evaluate the pathogenicity potential in environmental strains. While the core genes-based tree separated all O145:H28 strains from the non O145:H28 reference strains, it failed to segregate environmental strains from the clinical. In contrast, the accessory genes-based tree placed all clinical strains in the same clade regardless of their genotypes or serotypes, apart from the environmental strains. Loss-of-function mutations were common in the virulence genes examined, with a high frequency in genes related to adherence, autotransporters, and the type three secretion system. Distinct differences in pathogenicity islands LEE, OI-122, and OI-57, the acid fitness island, and the tellurite resistance island were detected between the O145:H28 and reference strains. A great amount of genetic variation was detected in O145:H28, which was mainly attributed to deletions, insertions, and gene acquisition at several chromosomal hot spots. Our study demonstrated a distinct virulence gene repertoire among the STEC O145:H28 strains originating from the same geographical region and revealed unforeseen contributions of loss-of-function mutations to virulence evolution and genetic diversification in STEC.
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