Phylodynamic analysis of a prolonged meningococcal epidemic reveals multiple introductions and pre-epidemic expansion

IF 2.6 4区 医学 Q3 INFECTIOUS DISEASES Infection Genetics and Evolution Pub Date : 2025-02-07 DOI:10.1016/j.meegid.2025.105726
Zuyu Yang , Heather Davies , Jane Clapham , Liza Lopez , Holly B. Bratcher , Audrey Tiong , Xavier Didelot , Martin C.J. Maiden , Philip E. Carter , Xiaoyun Ren
{"title":"Phylodynamic analysis of a prolonged meningococcal epidemic reveals multiple introductions and pre-epidemic expansion","authors":"Zuyu Yang ,&nbsp;Heather Davies ,&nbsp;Jane Clapham ,&nbsp;Liza Lopez ,&nbsp;Holly B. Bratcher ,&nbsp;Audrey Tiong ,&nbsp;Xavier Didelot ,&nbsp;Martin C.J. Maiden ,&nbsp;Philip E. Carter ,&nbsp;Xiaoyun Ren","doi":"10.1016/j.meegid.2025.105726","DOIUrl":null,"url":null,"abstract":"<div><div><em>Neisseria meningitidis</em> is the causative agent of invasive meningococcal disease (IMD), a form of bacterial meningitis and septicaemia, leading to isolated cases, outbreaks, and epidemics worldwide. Between 1991 and 2008, Aotearoa/New Zealand (NZ) experienced a prolonged hyperendemic group B IMD outbreak caused by the NZMenB epidemic strain, belonging to clonal-complex 41/44 (cc41/44) and identified by the PorA variant P1.7–2,4 (B:4:P1.7–2,4:cc41/44). NZMenB continues to account for approximately one-quarter of group B meningococcal disease cases in NZ. To understand NZMenB origin and initiation we used phylodynamic tools to analyse approximately 97 % of all NZMenB isolates submitted to the NZ Meningococcal Reference Laboratory from 1990 to 2019. We found NZMenB can be divided into three major clades: clade41, clade154, and clade42, each with distinct origins and expansion patterns. Our evidence from molecular dating and clonal expansion analysis suggests that NZMenB was circulating and had expanded before the epidemic. Comparison with international data showed multiple importations and re-introductions of NZMenB into NZ, while not suggesting close relationships with international variants. The recent COVID-19 health emergency and differing governmental responses have brought societal and environmental contributions to epidemics and pandemics into focus. We propose the NZMenB epidemic may have been triggered by increasing societal inequality and household crowding resulting from government policies at the time.</div></div>","PeriodicalId":54986,"journal":{"name":"Infection Genetics and Evolution","volume":"129 ","pages":"Article 105726"},"PeriodicalIF":2.6000,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Infection Genetics and Evolution","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1567134825000152","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"INFECTIOUS DISEASES","Score":null,"Total":0}
引用次数: 0

Abstract

Neisseria meningitidis is the causative agent of invasive meningococcal disease (IMD), a form of bacterial meningitis and septicaemia, leading to isolated cases, outbreaks, and epidemics worldwide. Between 1991 and 2008, Aotearoa/New Zealand (NZ) experienced a prolonged hyperendemic group B IMD outbreak caused by the NZMenB epidemic strain, belonging to clonal-complex 41/44 (cc41/44) and identified by the PorA variant P1.7–2,4 (B:4:P1.7–2,4:cc41/44). NZMenB continues to account for approximately one-quarter of group B meningococcal disease cases in NZ. To understand NZMenB origin and initiation we used phylodynamic tools to analyse approximately 97 % of all NZMenB isolates submitted to the NZ Meningococcal Reference Laboratory from 1990 to 2019. We found NZMenB can be divided into three major clades: clade41, clade154, and clade42, each with distinct origins and expansion patterns. Our evidence from molecular dating and clonal expansion analysis suggests that NZMenB was circulating and had expanded before the epidemic. Comparison with international data showed multiple importations and re-introductions of NZMenB into NZ, while not suggesting close relationships with international variants. The recent COVID-19 health emergency and differing governmental responses have brought societal and environmental contributions to epidemics and pandemics into focus. We propose the NZMenB epidemic may have been triggered by increasing societal inequality and household crowding resulting from government policies at the time.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
长时间脑膜炎球菌流行的系统动力学分析揭示了多次引入和流行前扩张。
脑膜炎奈瑟菌是侵袭性脑膜炎球菌病(IMD)的病原体,IMD是细菌性脑膜炎和败血症的一种形式,可导致世界范围内的孤立病例、暴发和流行。1991年至2008年,新西兰奥特罗阿(Aotearoa/New Zealand, NZ)经历了由属于克隆复合体41/44 (cc41/44)的NZMenB流行毒株引起的长时间高流行B组IMD暴发,由PorA变体p1.7 -2,4 (B:4: p1.7 -2,4:cc41/44)鉴定。NZMenB继续占新西兰B群脑膜炎球菌病病例的约四分之一。为了了解NZMenB的起源和起始,我们使用系统动力学工具分析了1990年至2019年提交给新西兰脑膜炎球菌参考实验室的所有NZMenB分离株的约97% %。我们发现,NZMenB可以分为三个主要分支:clade41、clade154和clade42,每个分支都有不同的起源和扩展模式。我们从分子定年和克隆扩增分析得到的证据表明,NZMenB在疫情发生前就已经在传播和扩增。与国际数据比较显示,NZMenB多次输入和重新引入新西兰,而不表明与国际变体有密切关系。最近的COVID-19突发卫生事件和不同的政府应对措施使社会和环境对流行病和大流行的影响成为人们关注的焦点。我们认为,NZMenB的流行可能是由当时政府政策导致的社会不平等加剧和家庭拥挤引发的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Infection Genetics and Evolution
Infection Genetics and Evolution 医学-传染病学
CiteScore
8.40
自引率
0.00%
发文量
215
审稿时长
82 days
期刊介绍: (aka Journal of Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases -- MEEGID) Infectious diseases constitute one of the main challenges to medical science in the coming century. The impressive development of molecular megatechnologies and of bioinformatics have greatly increased our knowledge of the evolution, transmission and pathogenicity of infectious diseases. Research has shown that host susceptibility to many infectious diseases has a genetic basis. Furthermore, much is now known on the molecular epidemiology, evolution and virulence of pathogenic agents, as well as their resistance to drugs, vaccines, and antibiotics. Equally, research on the genetics of disease vectors has greatly improved our understanding of their systematics, has increased our capacity to identify target populations for control or intervention, and has provided detailed information on the mechanisms of insecticide resistance. However, the genetics and evolutionary biology of hosts, pathogens and vectors have tended to develop as three separate fields of research. This artificial compartmentalisation is of concern due to our growing appreciation of the strong co-evolutionary interactions among hosts, pathogens and vectors. Infection, Genetics and Evolution and its companion congress [MEEGID](http://www.meegidconference.com/) (for Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases) are the main forum acting for the cross-fertilization between evolutionary science and biomedical research on infectious diseases. Infection, Genetics and Evolution is the only journal that welcomes articles dealing with the genetics and evolutionary biology of hosts, pathogens and vectors, and coevolution processes among them in relation to infection and disease manifestation. All infectious models enter the scope of the journal, including pathogens of humans, animals and plants, either parasites, fungi, bacteria, viruses or prions. The journal welcomes articles dealing with genetics, population genetics, genomics, postgenomics, gene expression, evolutionary biology, population dynamics, mathematical modeling and bioinformatics. We also provide many author benefits, such as free PDFs, a liberal copyright policy, special discounts on Elsevier publications and much more. Please click here for more information on our author services .
期刊最新文献
Emergence of distinct Burkholderia pseudomallei lineages in Brazil: Phenotypic, genotypic, and phylogenetic agreement. Macrolide resistance mutations of Mycoplasma pneumoniae in children and adults in Yunnan and its correlation with P1 genotype. Land-use changes shape mosquito assemblages, host-feeding and arbovirus infection in Baringo County, Kenya. Trypanosomatid detection in Culicoides biting midges (Diptera: Ceratopogonidae) from leishmaniasis-endemic Songkhla Province, southern Thailand: Microscopy and nanopore metabarcoding reveal parasite diversity. Genomic profiling of digestion related enzymes in Anopheles aquasalis a major coastal neotropical malaria vector.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1