北京基因型对肺结核潜伏感染、肺结核疾病风险和肺结核病例聚集的影响。

IF 2.6 4区 医学 Q3 INFECTIOUS DISEASES Infection Genetics and Evolution Pub Date : 2024-07-25 DOI:10.1016/j.meegid.2024.105648
Michael Asare-Baah , Marie Nancy Séraphin , LaTweika A.T. Salmon-Trejo , Lori Johnston , Lina Dominique , David Ashkin , Krishna Vaddiparti , Awewura Kwara , Anthony T. Maurelli , Michael Lauzardo
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引用次数: 0

摘要

背景:结核分枝杆菌(Mtb)的北京基因型引发了有关其毒性和传播性的争论。本研究通过评估其对潜伏肺结核感染(LTBI)风险、接触者活动性肺结核(TB)疾病以及已知肺结核病例聚集的影响,为这一讨论做出了贡献:我们利用 2009 年至 2023 年间向佛罗里达州卫生局报告的 4457 名经培养确诊的肺结核患者及其接触者(20448 人)的记录进行了一项回顾性队列研究。研究采用单变量和多变量分析来评估北京菌株对LTBI、接触者活动性结核病风险和病例聚集的影响:我们的研究表明,北京基因型与非北京基因型在接触者中的传播性无明显差异。LTBI发病率为19.9%,非北京基因型略高于北京基因型(20.2% vs. 15.5%,p 结论:北京基因型不会增加接触者的LTBI发病率,但会增加非北京基因型的发病率:虽然北京基因型不会增加接触者感染迟发性肺结核或活动性肺结核的风险,但它显示出更高的病例聚集趋势。因此,干预措施应优先考虑该基因型流行的人群。
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Effects of the Beijing genotype on latent tuberculosis infection, TB disease risk, and clustering of TB cases

Background

The Beijing genotype of Mycobacterium tuberculosis (Mtb) has sparked debate regarding its virulence and transmissibility. This study contributes to this discussion by assessing its effect on the risk of latent tuberculosis infection (LTBI), active tuberculosis (TB) disease among contacts, and clustering of known TB cases.

Methods

We conducted a retrospective cohort study using the records of 4457 culture-confirmed TB patients and their contacts (20,448) reported to the Florida Department of Health between 2009 and 2023. Univariate and multivariate analyses were used to evaluate the effect of the Beijing strain on LTBI, active TB risk among contacts, and case clustering.

Results

Our study revealed no significant difference in transmissibility between the Beijing and non-Beijing genotypes among contacts. LTBI prevalence was 19.9%, slightly higher in non-Beijing than Beijing genotypes (20.2% vs. 15.5%, p < 0.001). The prevalence of active TB was 1.8%, with no significant difference between the Beijing and non-Beijing genotypes (1.4% vs. 1.8%, p = 0.296). Increased LTBI risk was associated with older age, male sex, Hispanic ethnicity, multidrug-resistant TB exposure, household exposure, and a longer exposure duration. Active TB risk was higher for males, HIV-positive individuals, and contacts with more prolonged exposure to index cases. The Beijing genotype was associated with increased TB case clustering (aOR = 1.98, 95%CI: 1.53, 2.55, p < 0.001) as compared to the non-Beijing genotypes. US birthplace (aOR = 2.75, 95%CI: 2.37, 3.19, p < 0.001), pulmonary disease (aOR = 1.27, 95%CI: 1.04, 1.56, p < 0.020), cavitary TB (aOR = 1.25, 95% CI: 1.08, 1.44, p < 0.003), previous year alcohol use (aOR = 1.68, 95%CI: 1.38, 2.04, p < 0.001), and recreational drug use (aOR = 1.32, 95%CI: 1.04, 1.67, p < 0.024) were also associated with an increased risk of TB case clustering.

Conclusion

While the Beijing genotype did not increase the risk of LTBI or active TB among contacts, it showed a higher tendency for case clustering. Hence, interventions should prioritize populations where this genotype is prevalent.

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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 .
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