A novel mechanism of streptomycin resistance in Yersinia pestis: Mutation in the rpsL gene
PLOS Neglected Tropical Diseases·
- DOI
- 10.1371/journal.pntd.0009324
- PMID
- 33886558
- PMCID
- PMC8096067
- OpenAlex
- W3153398736
- Study type
- Journal article
- Publisher
- Public Library of Science (PLoS)
- Article type
- journal-article
- Integrity
- current
Why this research matters now
The abstract characterizes streptomycin resistance in Yersinia pestis as a public health concern and indicates that resistance assessment should consider rpsL mutations in addition to plasmid-associated mechanisms. The supplied evidence does not establish treatment outcomes or the extent of this mechanism in current populations.
Structured evidence summary
Research question
The study examined streptomycin susceptibility among Yersinia pestis strains in China and investigated the genetic basis of high-level resistance in a resistant isolate.
Study design
The authors assessed minimum inhibitory concentrations in 536 isolates, screened selected resistance-associated genes by PCR, and used genome sequencing and allelic replacement experiments to investigate the resistant strain.
Population and setting
The sample comprised 536 Yersinia pestis strains from China. The resistant isolate was obtained from a pneumonic plague outbreak in Tibet in 1996 and was associated with the Marmota himalayana Qinghai-Tibet Plateau plague focus.
Main findings
One clinical isolate showed high-level streptomycin resistance, with a reported MIC of 4,096 mg/L. The study linked this phenotype to a K43R amino-acid substitution in the rpsL gene, rather than the previously described conjugative-plasmid mechanism.
Public-health relevance
The abstract characterizes streptomycin resistance in Yersinia pestis as a public health concern and indicates that resistance assessment should consider rpsL mutations in addition to plasmid-associated mechanisms. The supplied evidence does not establish treatment outcomes or the extent of this mechanism in current populations.
Important limitations
The supplied material does not state explicit study limitations. This summary is limited to the supplied single-article abstract and metadata; the original paper is required for decision-grade assessment of sampling, methods, representativeness, and clinical implications.
GIDS interpretation
The article is discoverable as evidence concerning plague, antimicrobial resistance, China, and outbreak investigation. It provides context about a documented resistance mechanism but does not confirm or characterize any live surveillance signal.
Related GIDS surveillance
Literature context does not validate, explain, or change a surveillance signal. Exact and contextual relationships are shown separately.
Evidence relationships
This article has 8 auditable classifier relationships to diseases, places, topics, and study design.