Search Results (38)

Although poverty and tuberculosis are insidiously linked, knowledge of the relationship between social determinants of health (SDoHs) and post-tuberculosis lung disease (PTLD) is limited. This study aimed to analyze the association between physical function, pulmonary function, and SDoHs in individuals with PTLD (iwPTLD), considering the impact of social inequalities on physical performance. This cross-sectional study collected social data from 69 iwPTLDs using a standardized assessment form. The patients underwent pulmonary function testing via spirometry and body plethysmography, as well as respiratory muscle strength and quadriceps muscle strength (QMS) testing. They also completed the six-minute step test (6MST). The median value of steps climbed by participants on the 6MST was 88 (57–117), corresponding to 50.1% (34.9–73.2) of the predicted value. The mean QMS was 28.7 ± 11.9 kgf, with 11 participants (17.4%) showing QMS below the cutoff point. Spirometry revealed normal, obstructive, restrictive, and mixed patterns in 19 (27.5%), 20 (29%), 18 (26.1%), and 12 (17.4%) of the participants, respectively. Performance on the 6MST showed no statistically significant association with SDoHs. QMS showed a statistically significant association with treated sewage (W = 84, p = 0.026). Forced expiratory volume in one second showed significant correlations with education level (ρ = 0.248, p = 0.040), social protection (W = 207, p = 0.050, r = 0.238), and treated water (W = 24.5, p = 0.029, r = 0.264). Maximum inspiratory pressure showed significant correlations with education level (ρ = 0.246, p = 0.042) and treated water (W = 20, p = 0.021, r = 0.280). The regression model for 6MST and QMS performance showed that 12% and 45% of the variability was explained by the studied variables, respectively. In iwPTLD, impairments in physical function and damage to lung function are weakly associated with the deterioration of SDoHs. While this relationship is weak, it should not be ignored because it may operate through indirect pathways. Full article

Background: Tuberculosis (TB) remains a leading cause of global morbidity and mortality, yet its impact extends far beyond microbiological cure. Many TB survivors experience persistent structural lung damage or functional impairment consistent with post-TB lung disease, while growing evidence highlights long-term non-respiratory health outcomes. Synthesizing evidence across lung and non- respiratory health outcomes, along with their risk factors, is critical to inform long-term TB care. Methods: We conducted a scoping review including systematic reviews reporting on post-TB long-term health outcomes. A search was performed in PubMed/MEDLINE on 27 July 2025, using terms related to “tuberculosis,” “systematic review,” “meta-analysis,” “sequelae” and “long-term health outcomes,” without language restrictions. Results: Nine systematic reviews met inclusion criteria. Most focused on pulmonary outcomes and consistently demonstrated that TB is associated with chronic airflow obstruction, reduced lung function, and an increased long-term risk of lung cancer, although residual confounding from environmental, clinical, and socioeconomic factors cannot be excluded. While younger adults are more prone to developing COPD after TB in high TB burden settings, older individuals face a higher risk of broader post-TB lung sequelae. Evidence suggested that TB survivors are at increased risk of non-respiratory complications. HIV co-infection, low CD4 counts, older age, pre-existing hepatitis, prior TB treatment, and hypoalbuminemia were associated with post-TB liver injury, while baseline hearing impairment and HIV co-infection increased the likelihood of post-TB hearing loss. TB was also linked to elevated risk of several non-pulmonary cancers, including oesophageal, cervical, hematological, pancreatic, and gastric malignancies, with the highest risk within the first year after TB diagnosis and persisting, though attenuated, in subsequent years. Conclusion: TB should be viewed as a chronic condition with enduring lung and non-respiratory health outcomes. TB survivors face increased risks of COPD, lung cancer, and a range of non-respiratory health outcomes, including hepatic and auditory complications, particularly among high-risk groups, such as those living with HIV infection, along with baseline hearing and hepatic impairment. Public health programmes must extend care beyond microbiological cure to include integrated, post-TB long-term monitoring of lung, hepatic and hearing across all ages, including malignancy surveillance, after baseline assessments to identify high-risk TB survivors. Future research should also elucidate risk factors for post-TB malignancy, and clarify the relationship between neurological, renal, and musculoskeletal sequelae and TB to inform evidence-based TB survivorship care. Full article

(TB) induces a pronounced thromboinflammatory state during active disease, characterized by elevated fibrinogen, D-dimer, and thrombin-related activity, reduced levels of endogenous anticoagulants, impaired fibrinolysis, platelet activation, and endothelial dysfunction. Although many of these abnormalities improve after treatment initiation, accumulating evidence suggests that microbiological cure may not fully restore vascular, immune, and hemostatic homeostasis. This raises the possibility that TB leaves a persistent thromboinflammatory imprint after cure. This narrative synthesizes current evidence on tuberculosis-associated hypercoagulability during active disease and after treatment, and proposes a conceptual framework for post-tuberculosis thromboinflammatory memory grounded in cellular persistence, tissue remodeling, and extracellular vesicle-mediated signaling. Candidate storage compartments include hematopoietic stem and progenitor cells, monocyte/macrophage lineages, alveolar macrophages, remodeled pulmonary endothelium, and fibrotic post-TB lung tissue. EVs may function as mobile vectors that transfer procoagulant phospholipids, tissue factor, inflammatory proteins, and regulatory microRNAs between these compartments, thereby linking local post-TB remodeling to systemic vascular and coagulation pathways. A mechanistic evidence ladder is proposed, encompassing phenotypic persistence, EV cell-of-origin attribution, molecular persistence, paired longitudinal validation, functional transfer, and clinical outcome linkage. Current data support the biological plausibility of this framework but remain insufficient to establish post-TB thromboinflammatory memory as a defined clinical entity. Direct evidence in long-term TB survivors is still lacking, particularly with respect to persistent EV signatures, cell-specific reservoirs, and the functional transfer of procoagulant phenotypes. Longitudinal, cell-resolved, multi-omic, and functionally validated studies are required to determine whether TB leaves a durable thromboinflammatory memory, where it is stored, and whether it contributes to long-term thrombotic and cardiovascular risk. This article should be interpreted as a narrative review with a conceptual framework rather than as evidence that post-tuberculosis thromboinflammatory memory is already a formally established clinical entity. Full article

Background/Objective: Chronic obstructive pulmonary disease (COPD) and tuberculosis (TB) are among the most prevalent respiratory disorders worldwide and frequently coexist in the same patient. However, the contribution of active TB and post-tuberculosis lung disease to COPD exacerbations and long-term prognosis remains incompletely defined. This paper aim to evaluate the prevalence, clinical correlates, and prognostic significance of tuberculosis and its sequelae in patients with COPD. Materials and methods: We conducted a population-based retrospective cohort study using de-identified data from the regional healthcare information system. The cohort included all adults aged 18 years or older with a recorded diagnosis of COPD (ICD-10 code J44). Tuberculosis was identified by codes A15–A19 and B90. The primary outcomes were COPD exacerbations and all-cause mortality. Group comparisons, cluster analysis, Kaplan–Meier survival analysis, Cox proportional hazards modeling, and multivariable logistic regression were performed. Results: Tuberculosis and/or its sequelae were identified in 267 of 16,714 patients (1.60%): post-TB sequelae (B90) in 197 (73.8%), active TB (A15–A19) in 22 (8.2%), and both in 48 (18.0%). Compared with patients without TB, those with COPD-TB were younger (63.5 ± 14.2 vs. 65.7 ± 14.7 years; p = 0.018), more often male (75.3% vs. 52.0%; p < 0.001), and had higher mortality (16.5% vs. 10.6%; p = 0.003). COPD-TB was associated with bronchiectasis (OR = 6.07; 95% CI, 3.03–12.16), pulmonary fibrosis (OR = 5.67; 95% CI, 3.40–9.45), and pneumonia (OR = 2.01; 95% CI, 1.50–2.71), but with lower prevalences of obesity, diabetes mellitus, and hypertension. Patients with TB experienced more COPD exacerbations, including recurrent exacerbations. In multivariable models, tuberculosis was associated with COPD exacerbations after adjustment for age and sex (adjusted OR = 1.43; 95% CI, 1.05–1.96); this association was attenuated and lost significance after further adjustment for post-tuberculosis structural lung disease, indicating that it is largely mediated by post-TB sequelae. Tuberculosis remained associated with mortality after adjustment for available covariates, both in logistic regression (adjusted OR = 1.61; 95% CI, 1.14–2.28) and in Cox analysis (hazard ratio = 1.37; 95% CI, 1.01–1.85). Conclusions: Tuberculosis and post-tuberculosis lung disease are clinically accessible risk markers associated with COPD exacerbations and mortality. These findings support recognizing patients with COPD and a history of TB as a high-risk subgroup requiring intensified follow-up, proactive exacerbation prevention, and prioritized vaccination counseling. In the context of personalized medicine, a documented history of tuberculosis and post-tuberculosis lung changes represents a clinically accessible marker that can be used to stratify individual risk and to tailor monitoring and prevention in patients with COPD. Full article

Background: Tuberculosis-related pulmonary changes may overlap radiologically and clinically with lung cancer, complicating diagnostic interpretation, staging, and therapeutic planning. This study evaluated the relationship between tuberculosis status, thoracic imaging patterns, and clinical characteristics in patients diagnosed with lung cancer. Methods: A retrospective cohort study was conducted between February 2020 and December 2025 at the Clinical Pneumophtisiology Hospital, Constanța, Romania. A total of 620 patients with lung cancer were analyzed. Patients were classified into three groups: no tuberculosis, post-tuberculosis sequelae, and active tuberculosis. Demographic, clinical, laboratory, histopathological, functional, and radiological variables were assessed. Associations between tuberculosis status and imaging findings were evaluated using chi-square testing, effect-size analysis, and multinomial logistic regression. Results: Post-tuberculosis sequelae were identified in 337 patients (54.4%), active tuberculosis in 51 patients (8.2%), and no tuberculosis-related disease in 232 patients (37.4%). Adenocarcinoma was the most frequent histological type, occurring in 359 patients (57.9%). Significant associations with tuberculosis status were observed for fibrotic/interstitial or bronchial changes, infectious-inflammatory changes, cavitary/destructive lesions, atelectatic/retractile changes, pulmonary opacities, pleural involvement, and mediastinal/hilar adenopathy. The strongest effects were found for fibrotic/interstitial changes, infectious-inflammatory changes, and cavitary/destructive lesions. In regression analysis, active tuberculosis was most strongly associated with infectious-inflammatory changes, cavitary lesions, pulmonary opacities, and fibrotic abnormalities, while post-tuberculosis sequelae were mainly associated with chronic fibrotic and structural pulmonary changes. Conclusions: Tuberculosis-related abnormalities frequently coexist with lung cancer and may mimic or obscure malignant findings. Recognition of these overlapping patterns is essential for accurate radiological interpretation and individualized clinical management. Full article

Background: Treatment monitoring in pulmonary tuberculosis increasingly requires assessment of residual inflammatory burden and structural lung damage beyond microbiologic response alone. High-resolution computed tomography (HRCT) can provide this information, but interpretation of serial examinations is time-consuming and partly subjective. This study did not aim to evaluate AI for the diagnosis of pulmonary tuberculosis. Instead, it explored whether artificial intelligence (AI)-assisted quantitative HRCT analysis could support longitudinal assessment of treatment-related imaging changes in patients with microbiologically confirmed pulmonary tuberculosis. Methods: We conducted a retrospective, single-center, exploratory longitudinal study of patients receiving treatment for pulmonary tuberculosis. HRCT examinations acquired at diagnosis and during follow-up were anonymized, reviewed by an expert thoracic radiologist, and processed using AVIEW Lung Texture (Coreline Soft v2.0). The software quantified total lung volume and six predefined parenchymal categories: normal lung, ground-glass opacity, consolidation, reticulation, honeycombing, and emphysema. Results: Ninety-six patients contributed 256 HRCT examinations. The most frequent software-detected abnormalities were ground-glass opacity, consolidation, and emphysema-labeled low-attenuation areas. Ground-glass opacity and consolidation showed the clearest decline across serial examinations, consistent with regression of active inflammatory disease during treatment. Reticulation showed a heterogeneous course, likely reflecting both inflammatory resolution and residual structural remodeling. Honeycombing was infrequent and quantitatively limited. Lung volume changed variably and did not consistently parallel visual improvement. A key methodological limitation was the absence of a dedicated cavity class. As a result, emphysema-labeled low-attenuation areas should not be interpreted as conventional emphysema alone, because tuberculous cavities and post-destructive abnormalities were frequently included in this category. Conclusions: AI-assisted HRCT quantification may support longitudinal assessment of pulmonary tuberculosis by providing structured and reproducible measures of interval change. However, tuberculosis-specific interpretation remains dependent on expert radiologic oversight, particularly in cavitary disease. Full article

Background: Pulmonary tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis (M. tuberculosis). Drug-resistant TB remains a major public health challenge and calls for new approaches to drug development. Targeted delivery of antibacterial agents using nanoscale carriers represents one such approach. A decisive factor for efficient targeting is the judicious selection of the carrier platform. Methods: In the present study, diamond nanoparticles were evaluated as a prospective vehicle for conveying anti-TB drugs to lung cells. Conventional and analytical transmission electron microscopy were used to analyze the localization of the nanodiamonds (NDs) in the lungs of M. tuberculosis-infected mice 30 days after nanoparticle administration and 44 days post-infection. Results: The study shows that the NDs co-localize with M. tuberculosis in foamy macrophages of the lung, residing in the same cellular compartments—phagosomes/phagolysosomes and lipid droplets. These in vivo results demonstrate a high degree of macrophage-specific accumulation of NDs relative to M. tuberculosis. Conclusions: Consequently, NDs can be considered a promising carrier for targeted delivery of anti-TB therapeutics to the lungs during TB-induced inflammation. Full article

Background: Pulmonary tuberculosis (PTB) and lung cancer (LC) are major causes of global respiratory morbidity and mortality. Increasing evidence suggests that tuberculosis may induce persistent pulmonary alterations that extend beyond microbiological cure, potentially facilitating lung carcinogenesis. This review synthesizes current epidemiological and mechanistic evidence linking PTB to subsequent LC development. Methods: A structured narrative appraisal of the literature was conducted using PubMed, Web of Science, Scopus, ScienceDirect, MDPI Journals, and Google Scholar, focusing on studies published between 2020 and 2025. Eligible publications included cohort studies, meta-analyses, observational reports, and mechanistic investigations addressing the TB–LC association. Studies were thematically categorized into epidemiological evidence, pathogenic mechanisms, diagnostic challenges, and therapeutic implications. Results: Population-based studies consistently demonstrate a two- to threefold increased risk of LC among individuals with prior PTB, independent of smoking and other major confounders. Mechanistically, the post-tuberculous lung is characterized by chronic inflammation, oxidative stress, fibrotic remodeling, immune checkpoint activation (including PD-1/PD-L1 signaling), dysregulated microRNA expression, and metabolic reprogramming. Clinically, overlapping radiological and histopathological features may delay cancer diagnosis. A history of TB may also influence therapeutic decisions, particularly regarding immune checkpoint inhibitors due to potential infection reactivation. Conclusions: PTB may represent an independent risk factor for LC through sustained structural and immunological remodeling. Structured post-TB surveillance and risk-adapted screening strategies may be warranted in selected high-risk populations. Full article

Background: Pulmonary inflammation is a widely recognized characteristic of active tuberculosis (TB). Although standard TB treatment is effective, a substantial proportion of mycobacteriologically cured TB patients experience persistent pulmonary inflammation, which can lead to long-term lung impairment, post-tuberculosis lung disease (PTLD) and potentially TB recurrence. Methods: We conducted a case–control study to compare host serum biomarker profiles in individuals with minimal (TLG < 50 SUVbw*mL, n = 37) versus extensive (TLG ≥ 50 SUVbw*mL, n = 34) persistent lung inflammation following completion of standard drug-sensitive TB treatment. Lung inflammation was measured by 18F-FDG PET/CT scan using total lung glycolysis (TLG) as a surrogate marker. All participants had negative sputum cultures at four months of TB treatment, and blood samples were collected at treatment completion (month six). A Luminex^® multiplex assay performed on the Bio-Plex^® 200 platform was used to analyze 48 host serum biomarkers involved in cytokine/chemokine signaling. Results: Following multiple t-test analysis, fifteen biomarkers were significantly elevated (p < 0.05) in participants with extensive persistent lung inflammation compared to those with minimal inflammation. Among these, 14 demonstrated potential as discriminatory markers, with area under the curve (AUC) values ranging from 0.707 to 0.806, sensitivities ranging from 47.06% to 73.53%, and specificities ranging from 70.27% to 83.78%. Notably, 13 of these 16 candidate biomarkers significantly correlated with TLG values, further supporting their potential clinical utility. Conclusion: We report associations between serum inflammatory mediators and persistent pulmonary inflammation following mycobacterial clearance in TB patients, highlighting their potential as diagnostic biomarkers that could potentially meet the target product profile (TPP) criteria. Full article

Chronic obstructive pulmonary disease (COPD) and tuberculosis (TB) increasingly co-occur in low- and middle-income countries and aging populations. Prior pulmonary TB is a robust, smoking-independent determinant of COPD and is linked to persistent systemic inflammation, endothelial dysfunction, dyslipidemia, and hypercoagulability axes that also amplify cardiovascular disease (CVD) risk. We conducted a targeted narrative non-systematic review (2005–2025) of PubMed/MEDLINE, Embase, Scopus, and Web of Science, selecting studies for clinical relevance across epidemiology, clinical phenotypes, pathobiology, biomarkers, risk scores, sleep-disordered breathing, and management. No quantitative synthesis or formal risk-of-bias assessment was performed. Accordingly, findings should be interpreted as a qualitative synthesis rather than pooled estimates. Prior TB is associated with a distinctive COPD phenotype characterized by mixed obstructive–restrictive defects, reduced diffusing capacity (DLCO), radiographic sequelae, and higher exacerbation/hospitalization burden. Mechanistic insights: Convergent mechanisms chronic immune activation, endothelial injury, prothrombotic remodeling, molecular mimicry, and epigenetic reprogramming provide biologic plausibility for excess CVD, venous thromboembolism, and pulmonary hypertension. Multimarker panels spanning inflammation, endothelial injury, myocardial strain/fibrosis, and coagulation offer incremental prognostic value beyond clinical variables. While QRISK4 now includes COPD, it does not explicitly model prior TB or COPD-TB outcomes, but data specific to post-TB cohorts remain limited. Clinical implications: In resource-constrained settings, pragmatic screening, prioritized PAP access, guideline-concordant pharmacotherapy, and task-shifting are feasible adaptations. A history of TB is a clinically meaningful modifier of cardiopulmonary risk in COPD. An integrated, multimodal assessment history, targeted biomarkers, spirometry/lung volumes, DLCO, 6 min walk test, and focused imaging should guide individualized care while TB-aware prediction models and implementation studies are developed and validated in high-burden settings. Full article

Tuberculosis (TB) continues to be the world’s deadliest infectious disease, with an estimated 10.8 million new cases reported in 2023, of which India alone accounted for 28% of the global burden. This study aims to evaluate the impact of tuberculosis on pulmonary function and exercise tolerance, and to examine how these impairments affect health-related quality of life (HRQoL). In a cross-sectional design, 96 bacteriologically confirmed TB patients and 96 age- and sex-matched community controls underwent spirometry, six-minute-walk test (6 MWT), and HRQoL evaluation. DR-TB was detected in 27 patients (28.1%): Isoniazid monoresistance 59.3%, rifampicin monoresistance 11.1%, and XDR-TB 29.6%. Dyspnoea (70.8%) and cough (37.5%) were the most commonly reported symptoms among TB patients. Mean values of FEV₁, FVC, and FEV₁/FVC were significantly lower in TB patients compared to controls (62.8%, 65.97%, and 70.08% vs. 82.55%, 80.09%, and 78.08%, respectively; p < 0.001). Recurrent or DR-TB was associated with reduced spirometric indices and 6 MWT distances (241 m vs. 358 m in drug-sensitive TB). St. George’s respiratory questionnaire (SGRQ) scores indicated significantly poorer health-related quality of life (HRQoL) in patients compared to controls across all domains—symptoms (23.7 vs. 10.7), activity (33.3 vs. 14.2), and impact (20.6 vs. 9.4; p < 0.05). SGRQ scores were inversely correlated with lung function parameters (r = −0.42 to −0.56). These findings underscore the persistent health burden TB poses post-therapy, highlighting the need for routine post-TB functional screening and robust DR-TB control to achieve End-TB goals. Full article

Background: Pulmonary tuberculosis (TB) frequently leads to long-term lung complications that contribute to increased mortality. Understanding the pathogenesis of post-TB lung impairments is crucial for improving long-term outcomes in TB patients; yet this area remains poorly researched. Methods: Our study assessed circulatory inflammatory markers in patients who completed TB treatment more than one year before enrolment (population 1) and patients receiving in-hospital treatment for active drug-sensitive TB (population 2). Results: IL-6 was seven times higher in both populations compared to the normal range. IL-8 was below the limit of detection (LOD) in population 1, while it was approximately 2.5 times higher in population 2 compared to the normal range. TNF-α was 21 times higher in population 1 and 19 times higher in population 2 compared to the normal range. CRP was almost 49 times higher in both populations, and IL-1Ra was below the LOD in population 1, while it was ~1.5 times higher in population 2 compared to the normal range. Conclusions: These inflammatory biomarkers correlated well with lung function in the post-TB state, and their high levels suggest a persistent pro-inflammatory state post-TB, which may contribute to post-TB lung disease. More research is warranted to better understand this phenomenon, but these findings may highlight a need to consider anti-inflammatory therapy for patients with post-TB lung disease, especially since these high levels of cytokines can directly contribute to lung damage. Full article

Because the apices of the lungs are most commonly involved in chronic cavitary histoplasmosis (CCPH), it has been assumed by many to have a pathogenesis which is similar to post-primary tuberculosis. Fungi such as Aspergillus may colonize pulmonary bullae. Although less common, colonization by Histoplasma capsulatum in a heavily endemic area is possible or even probable. In chronic obstructive pulmonary disease (COPD), apical bullae are characteristic. Since COPD is common and CCPH is rare, the pathogenesis of CCPH remains incompletely understood. What is presently known about the pathogenesis of CCPH has not changed appreciably since 1976. A cellblock from a patient with CCPH was analyzed with histochemical stains for T cells, B cells, plasma cells, and macrophages to better understand the pathogenesis of CCPH. The pathogenesis of cavitary disease in histoplasmosis has been assumed to resemble that of tuberculosis. However, liquefaction of a caseous focus in lung apices which resulted from blood-borne tubercle bacilli is distinctly unlike CCPH, as caseation is unusual. Rather, repeated colonization of the apical and other bullae by propagules (microconidium, macroconidium, hyphal fragment) of H. capsulatum in patients with COPD who have resided in heavily endemic areas appears to be the primary event in CCPH. Immunohistochemical enumeration of specific cell types in a patient with CCPH has not been previously carried out to our knowledge, but is only a first step in understanding the disease. In future studies, identification of the varieties of macrophages and cytokines in CCPH may reveal whether the process is pro-inflammatory, anti-inflammatory, or both. Full article

Background: Despite “successful” treatment, some lung tuberculosis (TB) patients develop long-term lung impairments that includes damage to the parenchyma and reduced function, which may predispose them to diseases like pulmonary hypertension. However, this is not well understood. Therefore, we investigated whether previous or current TB patients would display elevated biomarkers of endothelial dysfunction and vascular remodeling. Methods: We performed assays for ADMA, VCAM-1, VEGF, angiopoietin-1, TBARS, NT-pro-BNP, and cardiac troponin-I. We further stratified the patients based on 1, 2, 3, and >3 previous TB episodes, and 1–5 yrs, 5–10 yrs, 10–15 yrs and >15 yrs after the last TB treatment completion. We also assessed correlations between the biomarkers and the number of previous TB episodes or the time since the completion of the last TB treatment. Results: ADMA was 70 times higher, VEGF was 2000 times higher and angiopoietin-1 was 6500 times higher than the normal range. NT-pro-BNP and cardiac troponin-I were undetected, and TBARS levels were low. There was a positive linear relationship between the number of previous TB episodes and angiopoietin-1, and between VEGF and the number of previous TB episodes. ADMA, VCAM-1 and TBARS exhibited a weak and negative linear association with the number of previous TB episodes. A negligible negative linear association was observed between the time since the completion of the last TB treatment and angiopoietin-1, VEGF and ADMA. Conclusions: Therefore, having >1 previous TB episode, despite the successful completion of TB treatment, associates with an increased risk of endothelial dysfunction/angiogenesis or vascular remodeling. Full article

Goats are natural hosts of Mycobacterium (M.) bovis, and affected herds can be the cause of significant economic losses. Similarites in disease course and lesions of M. bovis infections in goats and M. tuberculosis in humans make goats good models for human tuberculosis. The aim of this investigation was to characterize M. bovis challenge models in goats. For this, goats were endobronchially inoculated with three doses of M. bovis or culture medium. Clinical signs, shedding, and immune responses were monitored until 146 days post inoculation (dpi). At necropsy, lesions were examined by computed tomography, histology, and bacteriological culture. Infected goats did not develop clinical signs. M. bovis was cultured from feces, but never from nasal swabs. IGRAs were positive from 28 dpi onwards, antibodies at 140 dpi, and SICCT at 146 dpi. The increase in CD25⁺, IFN-γ⁺, and IFN-γ-releasing T-cell subpopulations was time-related, but not dose-dependent. All infected goats developed paucibacillary granulomas in the lungs and regional lymph nodes. M. bovis was regularly cultured. Dose-dependent effects included the size of pulmonary lesions, caverns, intestinal lesions, and early generalization in the high-dose group. In summary, reproducible challenge models with dose-dependent differences in lesions were established, which may serve for testing vaccines for veterinary or medical use. Full article