The Association between PHYLOGENETIC LINEAGE AND THE SUBCLINICAL Phenotype OF PULMONARY TUBERCULOSIS: A retrospective 2-Cohort study.

pulmonary tuberculosis

Journal

The Journal of infection
ISSN: 1532-2742
Titre abrégé: J Infect
Pays: England
ID NLM: 7908424

Informations de publication

Date de publication:
15 Dec 2023
Historique:
received: 04 08 2023
revised: 01 12 2023
accepted: 11 12 2023
medline: 18 12 2023
pubmed: 18 12 2023
entrez: 17 12 2023
Statut: aheadofprint

Résumé

Subclinical pulmonary tuberculosis (PTB) is an asymptomatic disease state between established TB infection and symptomatic (clinical) TB disease. It is present in 20-25% of PTB patients in high-income countries. Mycobacterium tuberculosis complex (MTBC) genetic heterogeneity, and differential host immunological responses, have been implicated in its pathogenesis. To determine the association between MTBC lineage and PTB disease phenotype, we used two retrospective cohorts of PTB patients in Canada and two independent lineage attribution methods (DNA fingerprinting and genome sequencing). The first cohort, Cohort 1, consisted of consecutively diagnosed PTB patients between 2014 and 2020. The second, Cohort 2, consisted of newly-arrived foreign-born PTB patients who either were or were not referred for post-landing medical surveillance between 2004 and 2017. Univariable and multivariable logistic regression models were sequentially fitted to both cohorts, adjusting for age, sex, disease type, drug resistance and HIV. Evolution of radiographic features was correlated to lineage in Cohort 2. Cohort 1 and 2 included 874 (209 subclinical) and 111 (44 subclinical) patients, respectively. In both cohorts, subclinical patients were more likely than clinical patients to have relapse/retreatment disease, be smear-negative, have longer times-to-culture positivity and to harbour an ancestral MTBC lineage (Indo-Oceanic or Mycobacterium africanum). Relapse/retreatment disease and ancestral MTBC lineage were independent predictors of subclinical disease (ORs and 95% CIs in Cohort 1, 1.85 [1.07,3.28], p<0.029 and 2.30 [1.66,3.18], p<0.001, respectively, and Cohort 2, 5.74 [1.37-24.06], p<0.017 and 3.21 (1.29,7.97], p<0.012, respectively). A strong phylogeographic population structure was observed among isolates from Cohort 1 patients. Non-progressive lung disease was more common in patients infected with ancestral than modern lineages in Cohort 2, 56.0% vs 25.4%, p<0.005. MTBC lineage is a strong predictor of PTB disease phenotype. The genetic drivers of this association, and the relative contribution of other explanatory variables, are unknown.

Sections du résumé

BACKGROUND BACKGROUND
Subclinical pulmonary tuberculosis (PTB) is an asymptomatic disease state between established TB infection and symptomatic (clinical) TB disease. It is present in 20-25% of PTB patients in high-income countries. Mycobacterium tuberculosis complex (MTBC) genetic heterogeneity, and differential host immunological responses, have been implicated in its pathogenesis.
METHODS METHODS
To determine the association between MTBC lineage and PTB disease phenotype, we used two retrospective cohorts of PTB patients in Canada and two independent lineage attribution methods (DNA fingerprinting and genome sequencing). The first cohort, Cohort 1, consisted of consecutively diagnosed PTB patients between 2014 and 2020. The second, Cohort 2, consisted of newly-arrived foreign-born PTB patients who either were or were not referred for post-landing medical surveillance between 2004 and 2017. Univariable and multivariable logistic regression models were sequentially fitted to both cohorts, adjusting for age, sex, disease type, drug resistance and HIV. Evolution of radiographic features was correlated to lineage in Cohort 2.
FINDINGS RESULTS
Cohort 1 and 2 included 874 (209 subclinical) and 111 (44 subclinical) patients, respectively. In both cohorts, subclinical patients were more likely than clinical patients to have relapse/retreatment disease, be smear-negative, have longer times-to-culture positivity and to harbour an ancestral MTBC lineage (Indo-Oceanic or Mycobacterium africanum). Relapse/retreatment disease and ancestral MTBC lineage were independent predictors of subclinical disease (ORs and 95% CIs in Cohort 1, 1.85 [1.07,3.28], p<0.029 and 2.30 [1.66,3.18], p<0.001, respectively, and Cohort 2, 5.74 [1.37-24.06], p<0.017 and 3.21 (1.29,7.97], p<0.012, respectively). A strong phylogeographic population structure was observed among isolates from Cohort 1 patients. Non-progressive lung disease was more common in patients infected with ancestral than modern lineages in Cohort 2, 56.0% vs 25.4%, p<0.005.
INTERPRETATION CONCLUSIONS
MTBC lineage is a strong predictor of PTB disease phenotype. The genetic drivers of this association, and the relative contribution of other explanatory variables, are unknown.

Identifiants

pubmed: 38104727
pii: S0163-4453(23)00592-3
doi: 10.1016/j.jinf.2023.12.006
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2023 The British Infection Association. Published by Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest none

Auteurs

Richard Long (R)

Department of Medicine,University of Alberta, Alberta Public Laboratories, Alberta Precision Laboratories. Electronic address: richard.long@ualberta.ca.

Matthew Croxen (M)

Department of Laboratory Medicine and Pathology, University of Alberta, Alberta Public Laboratories, Alberta Precision Laboratories; Faculty of Medicine and Dentistry, University of Alberta, Alberta Public Laboratories, Alberta Precision Laboratories; Li Ka Shing Institute of Virology, University of Alberta; Women and Children's Health Research Institute, University of Alberta.

Robyn Lee (R)

Department of Medicine, Faculty of Medicine and Health Sciences, McGill University.

Alexander Doroshenko (A)

Department of Medicine,University of Alberta, Alberta Public Laboratories, Alberta Precision Laboratories.

Angela Lau (A)

Department of Medicine,University of Alberta, Alberta Public Laboratories, Alberta Precision Laboratories.

Leyla Asadi (L)

Department of Medicine,University of Alberta, Alberta Public Laboratories, Alberta Precision Laboratories.

Courtney Heffernan (C)

Department of Medicine,University of Alberta, Alberta Public Laboratories, Alberta Precision Laboratories.

Catherine Paulsen (C)

Department of Medicine,University of Alberta, Alberta Public Laboratories, Alberta Precision Laboratories.

Mary Lou Egedahl (ML)

Department of Medicine,University of Alberta, Alberta Public Laboratories, Alberta Precision Laboratories.

Colin Lloyd (C)

Li Ka Shing Institute of Virology, University of Alberta; Public Health Agency of Canada, National Microbiology Laboratory.

Vincent Li (V)

Faculty of Medicine and Dentistry, University of Alberta, Alberta Public Laboratories, Alberta Precision Laboratories.

Gregory Tyrrell (G)

Department of Laboratory Medicine and Pathology, University of Alberta, Alberta Public Laboratories, Alberta Precision Laboratories; Li Ka Shing Institute of Virology, University of Alberta.

Classifications MeSH