Objective: To investigate the overall distributions of key virulence genes in , especially the hypervirulent -positive (Hv-(+)-KP).
Methods: A total of 521 complete genomes of from GenBank were collected and analyzed. Multilocus sequence typing, molecular serotyping, antibiotic-resistance, virulence genes and plasmid replicon typing were investigated.
Results: Positive rates of virulence genes highly varied, ranging from 2.9 () to 99.6% (). Totally 207 strains presented positive , , and and 190 showed positive , , , and , which were the two primary modes. A total of 94, 165 and 29 strains were denoted as hypervirulent (HvKP), (+)-KP and Hv-(+)-KP. ST11 accounted for 17 among the 29 Hv-(+)-KP strains; Genes , and were positive in 28, 26 and 18 Hv-(+)-KP strains respectively. Among the 29 Hv-(+)-KP strains exhibiting four super clusters from GenBank, IncHI1B plasmids carrying virulence genes and IncFII ones with were responsible for both 23 strains respectively.
Conclusions: Positive rates of virulence genes vary remarkably in . Genes , and were primary ones inducing Hv-(+)-KP. IncHI1B plasmids carrying virulence genes and IncFII ones with constitute the primary combination responsible for Hv-(+)-KP. The making of Hv-(+)-KP is mostly (+)-KP acquiring another plasmid harboring virulence genes.
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http://dx.doi.org/10.3389/fcimb.2021.661218 | DOI Listing |
BMC Infect Dis
January 2025
Department of Clinical Laboratory, Key Laboratory of Clinical Laboratory Medicine of Guangxi Department of Education, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Background: In clinical practice, the emergence of ST11-K64 carbapenem-resistant Klebsiella pneumoniae (ST11-K64 CRKP) has become increasingly alarming. Despite this trend, limited research has been conducted to elucidate the clinical and molecular characteristics of these strains.
Objectives: This study aimed to comprehensively investigate the clinical characteristics, antimicrobial resistance patterns, resistance and virulence-associated genes, and molecular epidemiology of ST11-K64 CRKP in Southwest China.
Phytopathology
January 2025
Virginia Polytechnic Institute and State University, School of Plant and Environmental Science, Blacksburg, Virginia, United States;
Diseases that affect the vascular system or the pith are of great economic impact since they can rapidly destroy the affected plants, leading to complete loss in production. Fast and precise identification is thus important to inform containment and management, but many identification methods are slow because they are culture-dependent and they do not reach strain resolution. Here we used culture-independent long-read metagenomic sequencing of DNA extracted directly from stems of two tomato samples that displayed wilt symptoms.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Xiangya Hospital, Central South University, Changsha, Hunan, China.
Background: Single nucleotide polymorphism (SNP)-based genetic studies have identified many risk genes for Alzheimer's disease (AD), but only explain part of the heritability. Structural variation (SVs) may account for some of this otherwise unexplained heritability. In this study, we sequenced 1,519 AD patients and 2,010 controls using 30X whole-genome sequencing (WGS).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
Background: The Longitudinal Early-onset Alzheimer's Disease Study (LEADS) is analyzing the genetic etiology of early onset (40-64 years) cognitive impairment, including amyloid-positive early-onset Alzheimer's disease (EOAD) and amyloid-negative early-onset Alzheimer's disease (EOnonAD). One goal of this investigation is to identify novel or under-characterized genetic variants.
Methods: Cognitively impaired (CI) LEADS participants, including amyloid-positive and amyloid-negative early-onset cases, were whole exome or genome sequenced (N = 361).
Alzheimers Dement
December 2024
The Jackson Laboratory, Bar Harbor, ME, USA.
Background: Altered lipid profiles and lipid processing genes are associated with Alzheimer's disease (AD). There is a reported genetic interaction between the AD risk gene APOE and cholesterol ester transfer protein (CETP). Mice lack functional CETP which is critical to the balance of circulating lipoproteins; this imparts cardioprotective effects and may make mice resistant to AD.
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