Post-tuberculosis lung disease (PTLD) poses a significant clinical challenge in regions with a high burden of tuberculosis (TB). This review provides a comprehensive overview of PTLD, encompassing its pathogenesis, clinical manifestations, diagnostic modalities, management strategies, long-term outcomes, and public health implications. PTLD arises from residual lung damage following TB treatment and is characterized by a spectrum of pathological changes, including fibrosis, bronchiectasis, and cavitation. Clinical presentation varies widely, from chronic cough and hemoptysis to recurrent respiratory infections, which are oftentimes a diagnostic dilemma. Radiological imaging, pulmonary function tests, and careful consideration of patient history play pivotal roles in diagnosis. Management strategies involve pharmacological interventions to alleviate symptoms and prevent disease progression, which are influenced by the extent of lung damage, comorbidities, and access to healthcare. Rehabilitation programs and surgical options are available for select cases. Prognosis is influenced by the extent of lung damage, comorbidities, and access to healthcare. Prevention efforts through a TB control program and early detection are crucial in reducing the burden of PTLD. This review stresses the importance of understanding and addressing PTLD to mitigate its impact on individuals and public health systems worldwide.

Tuberculosis of the long bones/femur, especially in an immunocompetent person, is a challenging diagnosis. It is a rare entity, even in endemic settings. The non-specific clinical features, backed by a low suspicion about such presentations even in endemic settings, may result in delayed diagnosis and often unfavorable treatment outcomes. The situation becomes even more challenging in the absence of pulmonary foci and a contact history of tuberculosis. Here is a case of a young adult male who presented with complaints of pain over his left leg for three months. A diagnosis was achieved with magnetic resonance imaging and the isolation of the bacteria from a bone biopsy using a cartridge-based nucleic acid amplification test. Antituberculous treatment was promptly initiated.

Tuberculosis (TB) remains a significant global health concern, particularly with the emergence of multidrug-resistant tuberculosis (MDR-TB) and extensively drug-resistant tuberculosis (XDR-TB). Traditional methods for diagnosing drug resistance in TB are time-consuming and often lack accuracy, leading to delays in appropriate treatment initiation and exacerbating the spread of drug-resistant strains. In recent years, artificial intelligence (AI) techniques have shown promise in revolutionizing TB diagnosis, offering rapid and accurate identification of drug-resistant strains. This comprehensive review explores the latest advancements in AI applications for the diagnosis of MDR-TB and XDR-TB. We discuss the various AI algorithms and methodologies employed, including machine learning, deep learning, and ensemble techniques, and their comparative performances in TB diagnosis. Furthermore, we examine the integration of AI with novel diagnostic modalities such as whole-genome sequencing, molecular assays, and radiological imaging, enhancing the accuracy and efficiency of TB diagnosis. Challenges and limitations surrounding the implementation of AI in TB diagnosis, such as data availability, algorithm interpretability, and regulatory considerations, are also addressed. Finally, we highlight future directions and opportunities for the integration of AI into routine clinical practice for combating drug-resistant TB, ultimately contributing to improved patient outcomes and enhanced global TB control efforts.

Tuberculosis can present at various extrapulmonary sites. However, even in endemic countries, concomitant involvement of different sites in the same patient is rarely reported. Further, tuberculous pericarditis represents a fraction of all tuberculosis infections and is an uncommon form of extrapulmonary tuberculosis. In underdeveloped nations, it is the most frequent cause of massive pericardial effusion. Additionally, it is the most common cause of constrictive pericarditis in adults, which has a high death rate and a poor prognosis. Furthermore, concomitant pleural effusion due to Mycobacterium tuberculosis is infrequently reported. Herein, a case of concomitant pericardial and left-sided pleural effusion in an Indian female is reported. She came with complaints of breathlessness, chest pain, night sweats, and loss of appetite. A diagnostic pleural thoracentesis and pericardiocentesis helped establish the diagnosis, and she was commenced on antituberculous treatment for 168 days.

Tuberculosis can present in various atypical forms. The clinical manifestations could involve sites like bones. Tuberculosis of the scapula, humerus, and posterolateral thoracic wall is extremely rare, and diagnosis is challenging due to similarities with conditions like tumors. A young boy presented with swelling of the right shoulder joint for three months. The diagnosis was challenging due to similarities with Ewing\'s sarcoma on the initial radiometric workup. A clinical assessment and diagnostic workup with biopsy, a cartridge-based nucleic acid amplification test, and an advanced radiometric investigation resulted in a final diagnosis. He was started on antituberculous drugs for 12 months.

Tuberculosis is usually seen in the lungs. However, the involvement of various extrapulmonary sites is due to the spread of the bacteria via blood, lymphatic, or direct inoculation. The present case is a rare presentation of tuberculosis in an Indian female who came with complaints of swelling in her right elbow joint, headache, and cough with expectoration. A diagnostic evaluation resulted in the isolation of Mycobacterium tuberculosis from the sputum samples and elbow joints, which was further supported by an exudative picture on the cerebrospinal fluid examination. The findings were supported by advanced radiometric techniques. She was commenced on an antituberculous treatment per her weight. Disseminated tuberculosis is a challenging diagnosis as there is often a delay in clinical presentation, a lack of awareness about the possibility of multiple sites with tuberculous infection in clinicians, and a time lag in the availability of the culture results.

UNASSIGNED: The emergence of drug-resistant Mycobacterium tuberculosis (Mtb) strains has underscored the urgent need for novel therapeutic approaches. Carbon-based nanomaterials, such as graphene oxide (GO), have shown potential in anti-TB activities but suffer from significant toxicity issues.
UNASSIGNED: This study explores the anti-TB potential of differently functionalized graphene quantum dots (GQDs) - non-functionalized, L-GQDs, aminated (NH2-GQDs), and carboxylated (COOH-GQDs) - alone and in combination with standard TB drugs (isoniazid, amikacin, and linezolid). Their effects were assessed in both axenic cultures and in vitro infection models.
UNASSIGNED: GQDs alone did not demonstrate direct mycobactericidal effects nor trapping activity. However, the combination of NH2-GQDs with amikacin significantly reduced CFUs in in vitro models. NH2-GQDs and COOH-GQDs also enhanced the antimicrobial activity of amikacin in infected macrophages, although L-GQDs and COOH-GQDs alone showed no significant activity.
UNASSIGNED: The results suggest that specific types of GQDs, particularly NH2-GQDs, can enhance the efficacy of existing anti-TB drugs. These nanoparticles might serve as effective adjuvants in anti-TB therapy by boosting drug performance and reducing bacterial counts in host cells, highlighting their potential as part of advanced drug delivery systems in tuberculosis treatment. Further investigations are needed to better understand their mechanisms and optimize their use in clinical settings.

Tuberculosis inflicting small bones is infrequently reported, even in endemic countries. A case of isolated involvement of the left second metacarpal in an adult Indian male with no pulmonary involvement is rare and has never been documented before in the medical literature. It\'s a diagnostic challenge due to non-specific clinical features, absence of constitutional signs of tuberculosis, ambiguity on radiograph films at early stages, and often results in delayed diagnosis. Moreover, it\'s a paucibacillary disease, and hence, diagnosis can be an arduous task. Herein, a case of a 20-year-old Indian male is presented who came with complaints of pain and swelling with a discharging sinus from the dorsum of his left hand. A detailed evaluation with the isolation of Mycobacterium tuberculosis on a cartridge-based nucleic acid amplification test helped in the diagnosis and initiation of appropriate antituberculous chemotherapy per his weight.

Tuberculosis is common in endemic countries. However, extrapulmonary tuberculosis is relatively rare, and primary extrapulmonary rifampicin mono-resistant tuberculosis of the cervical, mediastinal, and axillary lymph nodes simultaneously without pulmonary focus in an immunocompetent male has never been reported. Herein is a case of a 27-year-old Indian male with no previous history of tuberculosis who was diagnosed after an extensive clinical assessment with a radiometric and cartridge-based nucleic acid amplification assay of the swollen lymph nodes. He was put on antituberculous treatment per the all-oral longer regimen of the national program.

It is essential to understand the interactions and relationships between Mycobacterium tuberculosis (Mtb) and macrophages during the infection in order to design host-directed, immunomodulation-dependent therapeutics to control Mtb. We had reported previously that ornithine acetyltransferase (MtArgJ), a crucial enzyme of the arginine biosynthesis pathway of Mtb, is allosterically inhibited by pranlukast (PRK), which significantly reduces bacterial growth. The present investigation is centered on the immunomodulation in the host by PRK particularly the activation of the host\'s immune response to counteract bacterial survival and pathogenicity. Here, we show that PRK decreased the bacterial burden in the lungs by upregulating the population of pro-inflammatory interstitial macrophages (IMs) and reducing the population of Mtb susceptible alveolar macrophages (AMs), dendritic cells (DCs), and monocytes (MO). Additionally, we deduce that PRK causes the host macrophages to change their metabolic pathway from fatty acid metabolism to glycolytic metabolism around the log phage of bacterial multiplication. Further, we report that PRK reduced tissue injury by downregulating the Ly6C-positive population of monocytes. Interestingly, PRK treatment improved tissue repair and inflammation resolution by increasing the populations of arginase 1 (Arg-1) and Ym1+Ym2 (chitinase 3-like 3) positive macrophages. In summary, our study found that PRK is useful not only for reducing the tubercular burden but also for promoting the healing of the diseased tissue.