ArticleMedicine2016
Two case reports: Whole genome sequencing of two clinical macrolide-resistant Mycoplasma pneumoniae isolates with different responses to azithromycin.
Article in Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Unravelling distinct patterns of metagenomic surveillance and respiratory microbiota between two P1 genotypes ofEmerging microbes & infections · 2025Article
- Mechanical thrombectomy for a 12-year-old boy with acute ischemic stroke: A case report.Medicine · 2020Article
- Refractory Mycoplasma pneumoniae pneumonia with concomitant acute cerebral infarction in a child: A case report and literature review.Medicine · 2018Review
- Mycoplasma pneumoniae from the Respiratory Tract and Beyond.Clinical microbiology reviews · 2017Review
- Mechanism of resistance acquisition and treatment of macrolide-resistantKorean journal of pediatrics · 2017Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCases of macrolide-resistant Mycoplasma pneumoniae have increased rapidly since 2000, especially in Asia. Patients infected with macrolide-resistant M pneumoniae usually present with severe M pneumoniae pneumonia. The aim of this study was to identify indicators for whether children at an early stage of M pneumoniae infection develop mild or severe pneumonia. CASE SUMMARY: Herein, we retrospectively reviewed 2 pediatric cases caused by macrolide-resistant M pneumoniae, but with markedly different severity of pneumonia. First, we compared the clinical courses of the patients, then isolated the pathogens and tested their response to macrolides, then finally, carried out whole genome sequencing of these isolates. Despite the difference in clinical presentation of the infection, both isolates exhibited a high level of resistance to macrolide antibiotics. Analysis of clinical data showed that the erythrocyte sedimentation rate in blood samples of the patients in the early stages of disease varied greatly. Genome sequence analysis revealed single nucleotide polymorphisms mainly focused on adhesin P1, which is involved in the pathogenicity of M pneumoniae.
conclusionThe differences of erythrocyte sedimentation rate in the early stage of M pneumoniae pneumonia and mutations in P1 protein may help us to distinguish between severe or mild disease after infection with macrolide-resistant M pneumoniae. These findings could lead to the development of screening assays that will allow us to distinguish severe or mild M pneumoniae pneumonia early.
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