Background: Childhood tuberculosis (TB) is a major but underappreciated threat to human health. Because diagnosis of tuberculosis in children is difficult, there are a lack of accurate global statistics. This study aimed to comprehensively assess the long-term global, regional, and age-specific burden of childhood TB from 1990 to 2021, to examine its temporal trends and socioeconomic inequalities, and to project future patterns through 2045. Methods: We used incidence and mortality data from the GBD 2021 database for TB in children ages 0-14 years from 1990 to 2021. Children were stratified into three age groups-<5, 5-9 and 10-14 years-and classified by region and Socio-Demographic Index (SDI). Multiple statistical approaches were employed, including average annual percentage change and Bayesian age-period-cohort models, to analyze spatiotemporal trends in disease burden and generate projections for the next 20 years. We used decomposition analysis to separate demographic from epidemiological drivers and concentration indices to quantify socioeconomic inequalities. Results: In 2021 there were, globally, an estimated 759,300 incident cases of childhood TB and 70,659 deaths. Since 1990, childhood TB incidence and mortality rates have declined at average annual rates of 2.61% and 4.48%, respectively. The SDI showed a significant negative correlation with both incidence and mortality of childhood TB (p < 0.05). In 2021, 78.01% of childhood TB deaths were in children under 5 years of age, and over 80% of global childhood TB deaths occurred in Sub-Saharan Africa. Epidemiological interventions were partly offset by rapid population growth in low-SDI regions. The trends show that the incidence and mortality will continue to decline through 2045, but not enough to meet the goal of eliminating childhood TB by 2035. Conclusions: Global efforts should adopt an age-specific framework that prioritizes universal preventive treatment to eliminate mortality in children under 5 years, and implements active case finding to reduce transmission chains among children 5-14 years. Sustaining the decrease in the TB burdens of low-SDI regions requires international financing strategies attuned to expanding populations to ensure epidemiological success is not erased by demographic growth.

The "modern" lineages of Mycobacterium tuberculosis (Lineages 2, 3, and 4) drive the global tuberculosis pandemic, yet the evolutionary dynamics of Lineage 3 (L3) remain poorly defined. Although historically stereotyped as geographically restricted and evolutionarily marginal, our analysis of 7,679 genomes reveals that L3 is far more widespread than previously appreciated. It circulates across five continents, diversifying along a trajectory independent of the canonical adaptive steps that facilitated the rise of Lineages 2 and 4. We resolve the dominant L3.1.1 clade—accounting for > 95% of all isolates—into six actively circulating sub-lineages (L3.1.1.i1–i6). These groups exhibit contrasting demographic histories, with three notably undergoing recent exponential expansion. Remarkably, we detect strong parallel positive selection on an identical set of twelve genes across all six sub-lineages, indicating a clear pattern of convergent adaptation intrinsic to the lineage rather than shaped by regional environments. While nine of these genes are associated with drug resistance, three ( Rv2082 , phoR , Rv3401 ) likely reflect adaptation to host or environmental pressures. Despite L3 exhibiting a high overall burden of drug resistance (~ 30%), this resistance rarely enhances transmission in most subpopulations. The L3.1.1.i6, however, represents a striking exception: nearly half of its isolates are resistant, and compensatory evolution has restored high transmissibility even among pre-XDR strains. This mirrors the convergence toward the high-transmission, high-resistance phenotype characteristic of Lineage 2. Collectively, these findings demonstrate that L3 is not a weakened derivative of other modern lineages but a globally dispersed pathogen advancing along a distinct adaptive path. The ongoing expansion of L3, particularly the emergence of the resistance-driven L3.1.1.i6, underscores the urgent need to reassess its epidemiological significance in the contemporary tuberculosis landscape.

Abstract Mycobacterium abscessus (Mab) infections are increasingly associated with dominant circulating clones (DCCs), yet the evolutionary processes underlying their emergence remain poorly understood. Here, we analyzed 11,314 globally collected Mab genomes to investigate genome-wide evolutionary changes during the emergence of seven DCCs. We established a conservative core-genome analytical framework that integrates population-wide gene conservation with read-level validation to minimize the influence of assembly-derived variation on downstream evolutionary inference. Applying this framework to the global Mab population, we defined a stable core genome of 3,001 genes, representing a conservative lower bound across currently sequenced Mab populations. Core-genome analysis revealed a substantial decline in recombination relative to mutation following DCC expansion, indicating a broad shift towards mutation-dominated clonal evolution. Selective pressures also changed across this transition: 29 genes shifted from purifying to positive selection, consistent with continued adaptation during DCC expansion, whereas 19 showed the opposite pattern, suggesting increased functional constraint after clonal establishment. Although the accessory genes acquired differed among DCCs, gains consistently exceeded losses during DCC formation and showed functional convergence in environmental sensing, metabolism, metal homeostasis and stress responses. Together, these findings reveal consistent evolutionary shifts across independently emerged DCCs, with convergence occurring primarily in evolutionary processes and adaptive functions rather than through a single shared genetic determinant. Significance Mycobacterium abscessus is an emerging human pathogen increasingly associated with globally distributed dominant circulating clones, yet the evolutionary processes underlying their emergence remain poorly understood. By analyzing more than 11,000 genomes, we show that these independently emerged clones undergo convergent shifts in evolutionary dynamics, characterized by reduced recombination, increasingly clonal evolution, and targeted changes in selective pressures. Their emergence is also accompanied by lineage-specific accessory-genome remodeling that converges on functions involved in environmental sensing, metabolism, metal homeostasis, and stress responses. These findings reveal that successful bacterial clones can emerge through convergent evolutionary processes without requiring a universal set of genetic changes, providing a broader framework for understanding how pathogenic clones arise from genetically diverse bacterial populations.

Background Long-term epidemiological trends of respiratory infectious diseases (RIDs) and their associations with meteorological factors and air pollutants remain understudied in recent 10 years in China. This study investigates temporal patterns of seven major RIDs during 2004–2018 and quantifies their relationships with meteorological variables and ambient pollutants, with the aim of informing evidence-based health policy and environmental interventions. Methods Data on seven RIDs were collected from the National Notifiable Infectious Disease Surveillance System, meteorological and air pollutants data were obtained from the meteorological monitoring stations and national air quality monitoring stations, respectively. Descriptive analyses were used to present trends, and joinpoint regression models were used to examine changes in incidence and mortality for each respiratory infectious disease and to estimate average annual percentage changes. A Distributed Lag Non-Linear Model (DLNM) with relative risk was applied to analyze the impact of meteorological conditions and air pollutants on RIDs. We also applied a time-series decomposition approach based on locally weighted regression to present the seasonality of seven RIDs. Results A total of 23,444,640 cases and 45,291 deaths caused by seven respiratory infectious diseases were recorded in China, and the national mean age-standardized incidence and mortality were 115.87/100,000 and 0.23/100,000, respectively; the change of incidence and mortality differed by age groups. sulfur dioxide (SO2) and particulate matter <10 μm (PM10) in air pollutants and relative humidity and sunshine hours in climatic factors had significant effects on most respiratory diseases in this study. Additionally, meteorological factors had a stronger impact on RIDs with an acute and short-term lag effect compared with air pollutants. Conclusions The prevention and control strategies for RIDs need to be formulated based on their own characteristics and shift from a single biomedical intervention model to an integrated approach encompassing medicine, environmental science, climate science, and socioeconomics.

Abstract Mycobacterium abscessus (MAB) is a recently emerged bacterial pathogen causing an increasing number of human infections. Despite increasing recognition that different circulating clones contribute disproportionately to MAB population expansion, the global population dynamics and the evolutionary pressures underlying the emergence and spread of MAB clones remain incompletely understood. We analyzed 11,314 publicly available genomes of MAB isolates sampled from 30 countries and identified 38 recently emerged clones that have spread across multiple countries, including the seven previously described Dominant Circulating Clones (DCCs). There was a significant association between the time since the emergence of each circulating clone and its population size, with older clones generally having larger populations. Among the 26 circulating clones of M. abscessus subsp. abscessus , 12 carried the macrolide-susceptible erm(41) 28C genotype, highlighting clone-level variation in macrolide susceptibility. Genome-wide analyses identified 55 genes that were previously under purifying selection but showed evidence of positive selection during recent clade expansion. Collectively, our findings reveal that the recent global expansion of MAB comprises a broad continuum of newly emerged clones, accompanied by widespread shifts in gene-level selective pressures indicative of ongoing adaptation to new ecological environments.

Objectives: Lesion-level dynamics may reveal pulmonary tuberculosis (PTB) heterogeneity and help identify factors associated with treatment outcomes. Methods: A total of 288 serial Computed Tomography (CT) scans from 125 PTB patients were obtained from the National Institute of Allergy and Infectious Diseases (NIAID) TB Portals database (2008-2023). Lesions were segmented and annotated to obtain volume and imaging features, and a conservative longitudinal volume quantification method was used to characterize dynamic volume patterns. The proportion of lesions with different patterns was analyzed at the patient level to assess trajectory diversity. Firth's penalized logistic regression was used to identify factors associated with treatment outcomes. Results: Among 435 lesions in 125 patients, five patterns emerged: Stable, Decrease, Increase, Mix-I-D (increase then decrease), and Mix-D-I (decrease then increase). Multiple patterns coexisted in 66.7% of treatment success patients and all treatment failure patients. Mix-D-I lesions were identified more frequently in treatment failure patients (25.0% vs. 1.4%, p = 0.027), and in multivariable analysis, the presence of Mix-D-I lesions was statistically associated with treatment failure (p = 0.024). Conclusions: PTB lesions showed high trajectory heterogeneity. The presence of Mix-D-I lesions may point to an unfavorable treatment course, suggesting lesion dynamics could serve as a potential indicator for poor outcomes. By quantifying lesion-level trajectories on serial CT scans, we extend PET/CT-based evidence and support the value of routine monitoring in clinical management of tuberculosis.

Mycobacterium abscessus complex (MABC) is an emerging pathogen with intrinsic multidrug resistance. Genomic sequencing technology has been widely applied to predict bacterial resistance in other bacteria, but the catalog of known resistance-determining genes to explain phenotypic resistance in the MABC is incomplete for many antibiotics. Eighty-one MABC strains were isolated from sputum samples of patients with pulmonary disease in the Beijing Chest Hospital. All isolates were tested for minimum inhibitory concentrations (MICs) to eight antibiotics and underwent whole-genome sequencing (WGS). Of the total 81 MABC isolates, six strains exhibited clarithromycin (CLM) resistance by day 3 in culture, but only one (16.7%, 1/6) contained a mutation in the rrl gene. All M. abscessus strains contained the erm (41)28T (100.0%, 49/49) polymorphism and exhibited CLM-induced resistance after 14 days in culture. Of the 61 imipenem-resistant strains, 12 (19.7%, 12/61) had mutations in the bla gene. Although there were four (4.9%) amikacin-resistant, nine (11.1%) linezolid-resistant, eight (9.9%) clofazimine-resistant, 23 (28.4%) bedaquiline-resistant, and 27 (33.3%) cefoxitin-resistant strains, no known mutations associated with resistance to these antibiotics were found. These results suggest that the explanatory power of known resistance genes for clinical MABC resistance is limited and that other unidentified genes or novel resistance mechanisms may be involved.

Objectives:For people living with HIV (PLWH) and tuberculous meningitis (TBM), current studies on risk stratification and poor prognosis lack a clear optimal threshold. To address this gap, this study aims to identify an optimal immunological threshold for risk stratification and explore predictors of poor prognosis in this population. Methods:We conducted a multicentre cross-sectional study enrolling PLWH with TBM from hospitals across eight provinces of China between January 2018 and December 2020. We extracted the demographic and clinical data, discharge outcomes, Medical Research Council staging and CD4+ T-lymphocyte count on admission. CD4 thresholds were determined using restricted cubic splines with knots at quintiles. Multivariable logistic regression of risk factors derived adjusted ORs with 95% CIs. Results:A total of 201 participants were included in the study. Of these, 173 (86.1%) improved with treatment. Restricted cubic spline analysis identified CD4+ T-lymphocyte count <50 cells/µL as the optimal threshold for predicting poor TBM outcomes; the median CD4+ count was significantly lower in patients who deteriorated (40 cells/µL) than in those who improved (69 cells/µL). Multivariable logistic regression confirmed CD4+ T-lymphocyte count <50 cells/µL and elevated blood urea nitrogen (BUN) as independent risk factors for adverse outcomes. Conclusions:In PLWH with TBM, a CD4+ T-cell count below 50 cells/µL defines a critical stratification threshold for clinical risk classification, with elevated BUN serving as an additional prognostic marker. These findings support the prioritisation of severely immunocompromised patients for targeted management and further mechanistic studies.

Granulomas play a crucial role in the pathology of tuberculosis, but the immune environment governing their formation remains largely unknown. To explore the dynamic changes in the immune microenvironment during the formation of tuberculous granulomas, we infected adult zebrafish with Mycobacterium marinum and then examined uninfected and infected kidneys, as well as large and small granulomas in the kidneys. Using single-cell RNA sequencing technology, we identified two major macrophage subpopulations in the hematopoietic tissue (kidney) of zebrafish under uninfected physiological conditions: monocyte derived and tissue-resident macrophages. Interestingly, the infection induced the emergence of epithelioid cells and a previously undescribed grna.2+ macrophage subpopulation. Depletion of grna.2+ macrophages with the nitroreductase-metronidazole ablation system resulted in shortened zebrafish survival after infection, increased bacterial load, and more granulomas, especially necrotic granulomas. Depletion of grna.2+ macrophages also produced a denser granuloma structure with fewer T cells. RNA-seq and flow cytometry analysis revealed that depletion of grna.2+ macrophages led to upregulated inflammatory signaling pathways, including tnfα and il1β, and increased macrophage lytic cell death. Similarly, in samples from tuberculosis patients, we also identified GRN-positive macrophages, which exhibit similar anti-inflammatory functions. This subset of grna.2+ macrophages present in developing granulomas can suppress excessive inflammatory responses to alleviate macrophage lytic death, reduce tissue damage, promote T cell infiltration and ultimately help control mycobacterial growth in vivo.

Mycobacterium abscessus (MAB) is intrinsically resistant to many antibiotics, but the evolution of acquired drug resistance is poorly understood. We analyzed published genomes of 5617 clinical MAB isolates from 20 countries and searched for signals of ongoing evolution in 35 drug resistance-associated genes. Of these, we found 14 genes that were subject to positive selection, and we identified novel mutational sites under selection. Among these, the erm(41) V80I mutation arose exclusively in strains with erm(41) 28T and affected 50.5% (1750/3465) of subsp abscessus isolates. The study provided evidence that MAB is evolving mutations in drug resistance-associated genes, and further research is needed to understand the functional consequences of these mutations.

Tuberculosis (TB), the leading cause of death from bacterial infections worldwide, results from infection with Mycobacterium tuberculosis (Mtb). The antitubercular agents delamanid (DLM) and pretomanid (PMD) are nitroimidazole prodrugs that require activation by an enzyme intrinsic to Mtb; however, the mechanism(s) of action and the associated metabolic pathways are largely unclear. Profiling of the chemical-genetic interactions of PMD and DLM in Mtb using combined CRISPR screening reveals that the mutation of rv2073c increases susceptibility of Mtb to these nitroimidazole drugs both in vitro and in infected mice, whereas mutation of rv0078 increases drug resistance. Further assays show that Rv2073c might confer intrinsic resistance to DLM/PMD by interfering with inhibition of the drug target, decaprenylphophoryl-2-keto-b-D-erythro-pentose reductase (DprE2), by active nicotinamide adenine dinucleotide (NAD) adducts. Characterization of the metabolic pathways of DLM/PMD in Mtb using a combination of chemical genetics and comparative liquid chromatography-mass spectrometry (LC-MS) analysis of DLM/PMD metabolites reveals that Rv0077c, which is negatively regulated by Rv0078, mediates drug resistance by metabolizing activated DLM/PMD. These results might guide development of new nitroimidazole prodrugs and new regimens for TB treatment.

BACKGROUND:Extrapulmonary tuberculosis (EPTB) without symptomatic pulmonary involvement has been thought to be non-transmissible, but EPTB with asymptomatic pulmonary tuberculosis (PTB) could transmit tuberculosis (TB). Genomic investigation of Mycobacterium tuberculosis (Mtb) isolates from EPTB may provide insight into its epidemiological role in TB transmission. METHODS:Between January 2017 and May 2020, 107 Mtb isolates were obtained from surgical drainage of bone TB patients at the Beijing Chest Hospital, and 218 Mtb strains were isolated from PTB cases. These 325 Mtb isolates were whole-genome sequenced to reconstruct a phylogenetic tree, identify transmission clusters, and infer transmission links using a Bayesian approach. Possible subclinical PTB in the bone TB patients was investigated with chest imaging by two independent experts. RESULTS:Among 107 bone TB patients, 10 were in genomic clusters (≤12 SNPs). Phylogenetic analysis suggested that three bone TB patients transmitted the infection to secondary cases, supported by epidemiological investigations. Pulmonary imaging of 44 bone TB patients revealed that 79.5 % (35/44) had radiological abnormalities suggestive of subclinical PTB. CONCLUSIONS:This study provides genomic evidence that bone TB patients without clinically diagnosed PTB can be sources of TB transmission, underscoring the importance of screening for subclinical, transmissible PTB among EPTB cases.

Background The changes of respiratory infectious diseases’ epidemiological characteristics, and the relationship between respiratory infectious diseases and meteorological conditions and pollutants rarely explored in recent 10 years in China. Methods The seven respiratory infectious diseases’ data were collected from the NNIDSS, meteorological data and air pollutants data were from the meteorological monitoring stations and national air quality monitoring stations, respectively. Descriptive analyses were used to present trends, and joinpoint regression models were used to examine changes in incidence and mortality for each respiratory infectious disease and to estimate average annual percentage changes (AAPCs). A Distributed Lag Non-Linear Model (DLNM) with relative risk was applied to analyze the impact of meteorological conditions and air pollutants on respiratory infectious diseases. We also applied a time-series decomposition approach based on LOESS (locally weighted regression) to present the seasonality of seven respiratory infectious diseases. Results A total of 23,444,640 cases and 45,291 deaths caused by seven respiratory infectious diseases were recorded in China, and the national mean age-standardized incidence and mortality were 115.87/100,000 and 0.23/100,000, respectively; the change of incidence and mortality differed by age groups. SO2and PM10in air pollutants and relative humidity and air pressure in climatic factors had significant effects on most respiratory diseases in this study. Additionally, meteorological factors had a stronger impact on respiratory infectious diseases with an acute and short-term lag effect compared with air pollutants. Conclusions In view of the large regional difference in environmental factors, air pollutants, and geographical location, the prevention and control strategies for respiratory infectious diseases need to be formulated based on their own characteristics.

Tuberculosis (TB) is a common infectious disease linked to host genetics and the innate immune response. It is vital to investigate new molecular mechanisms and efficient biomarkers for Tuberculosis because the pathophysiology of the disease is still unclear, and there aren't any precise diagnostic tools. This study downloaded three blood datasets from the GEO database, two of which (GSE19435 and 83456) were used to build a weighted gene co-expression network for searching hub genes associated with macrophage M1 by the CIBERSORT and WGCNA algorithms. Furthermore, 994 differentially expressed genes (DEGs) were extracted from healthy and TB samples, four of which were associated with macrophage M1, naming RTP4, CXCL10, CD38, and IFI44. They were confirmed as upregulation in TB samples by external dataset validation (GSE34608) and quantitative real-time PCR analysis (qRT-PCR). CMap was used to predict potential therapeutic compounds for tuberculosis using 300 differentially expressed genes (150 downregulated and 150 upregulated genes), and six small molecules (RWJ-21757, phenamil, benzanthrone, TG-101348, metyrapone, and WT-161) with a higher confidence value were extracted. We used in-depth bioinformatics analysis to investigate significant macrophage M1-related genes and promising anti-Tuberculosis therapeutic compounds. However, more clinical trials were necessary to determine their effect on Tuberculosis.

Abstract Background This study was aimed to examine the effectiveness of App-assisted self-care in a Beijing community based on intelligent family physician-optimised collaborative model (IFOCM) program. Methods We conducted a survey of 12,050 hypertensive patients between Jan 2014 and Dec 2021. Generalized linear model was used to analyze the covariates that associated with blood pressure (BP) control. Decision tree and random forest algorithm was used to extract the important factors of BP outcome. Results The study included 5937 patients, mean age 66.2 ± 10.8, with hypertension in the baseline; 3108(52.4) were female. The community management resulted in mean systolic BP and diastolic BP reductions of 4.6 mmHg and 3.8 mmHg at follow-up. There were 3661 (61.6%) hypertension patients with BP control, increasing from 55.0% in 2014 to 75.0% in 2021. After adjusted for covariates, antihypertensive medication adherence, diabetes, and APP-assisted self-care were common predictors associated with BP control in GLM model and machine learning algorithm. Conclusion Community management based on IFOCM program significantly improved BP control in hypertensive patients. APP-assisted self-care would be beneficial for the management of chronic disease.

ABSTRACT The World Health Organization recommends culture-based techniques as the gold standard for rifampicin-resistant (RR) tuberculosis. However, as rapid molecular assays are rolled out, discordance in resistance has been observed. The current study compared 516 clinical isolates on Lowenstein–Jenson (LJ) and Mycobacteria Growth Indicator Tube (MGIT) drug susceptibility testings (DSTs) with rpoB sequencing. The discordance rate was higher in MGIT DST (24%) compared to LJ (9.4%). We report discordant results for RpoB mutations 430P (MGIT: 14/20; LJ: 19/20), 435Y (MGIT: 5/21; LJ: 17/21), 445N (MGIT: 11/18; LJ: 15/18), 445L (MGIT: 0/9; LJ: 8/9), 452P (MGIT: 5/20; LJ: 17/20), and 445C (MGIT: 1/6; LJ: 2/6) on LJ and MGIT DSTs, respectively. Mutations N438K and T444A, sensitive on LJ and MGIT DSTs, are novel. Two novel discordant mutations, Q436H+N437del and S428I, were also detected. One novel large deletion (Del) ggaccagaacaacccg/G (Del of DQNNP at positions 435–439) demonstrated concordance on LJ and MGIT DST. Numerous double and triple mutations including some novel combinations, M434V+H445N, L430R+D435Y, H445N+S450W, S428R+L430P, M434L+H445N, D435G+A451V, and M434I+D435G+A451V, have also shown higher discordant results on MGIT DST. The discordance results of RR are higher in MGIT DST compared to LJ. We suggest that the genotypic result should be preferred instead of phenotypic DST in case of discordant mutations. Physicians should be aware of such discordance to prescribe an effective treatment. Untargeted whole-genome sequencing to capture MGIT-sensitive and large deletions may be reconsidered for better treatment outcomes in high-burden countries. IMPORTANCE An accurate diagnosis of drug resistance in clinical isolates is an important step for better treatment outcomes. The current study observed a higher discordance rate of rifampicin resistance on Mycobacteria Growth Indicator Tube (MGIT) drug susceptibility testing (DST) than Lowenstein–Jenson (LJ) DST when compared with the rpoB sequencing. We detected a few novel mutations and their combination in rifampicin resistance isolates that were missed by MGIT DST and may be useful for the better management of tuberculosis (TB) treatment outcomes. Few novel deletions in clinical isolates necessitate the importance of rpoB sequencing in large data sets in geographic-specific locations, especially high-burden countries. We explored the discordance rate on MGIT and LJ, which is important for the clinical management of rifampicin resistance to avoid the mistreatment of drug-resistant TB. Furthermore, MGIT-sensitive isolates may be subjected to molecular methods of diagnosis for further confirmation and treatment options.

The recent population dynamics of the global tuberculosis epidemic are heavily shaped by Mycobacterium tuberculosis complex (MTBC) strains with enhanced transmissibility. The infamous Beijing family strain stands out because it has rapidly spread throughout the world.

Background Understanding multidrug-resistant tuberculosis (MDR-TB) transmission patterns is crucial for controlling the disease. We aimed to identify high-risk populations and geographic settings of MDR-TB transmission. Methods We conducted a population-based retrospective study of MDR-TB patients in Beijing from 2018 to 2020, and assessed MDR-TB recent transmission using whole-genome sequencing of isolates. Geospatial analysis was conducted with kernel density estimation. We combined TransPhylo software with epidemiological investigation data to construct transmission networks. Logistic regression analysis was utilized to identify risk factors for recent transmission. Results We included 241 MDR-TB patients, of which 146 (60.58%) were available for genomic analysis. Drug resistance prediction showed that resistance to fluoroquinolones (FQs) was as high as 39.74% among new cases. 36 (24.66%) of the 146 MDR strains were grouped into 12 genome clusters, suggesting recent transmission of MDR strains. 44.82% (13/29) of the clustered patients lived in the same residential community, adjacent residential community or the same street as other cases. The inferred transmission chain found a total of 6 transmission events in 3 clusters; of these, 4 transmission events occurred in residential areas and nearby public places. Logistic regression analysis revealed that being aged 25–34 years-old was a risk factor for recent transmission. Conclusions The recent transmission of MDR-TB in Beijing is severe, and residential areas are common sites of transmission; high levels of FQs drug resistance suggest that FQs should be used with caution unless resistance can be ruled out by laboratory testing.