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Treatment Guidelines for Active Drug-Susceptible and Drug-Resistant Pulmonary Tuberculosis, and Latent Tuberculosis Infection
Published in Lloyd N. Friedman, Martin Dedicoat, Peter D. O. Davies, Clinical Tuberculosis, 2020
Lynn E. Sosa, Lloyd N. Friedman
Extensively drug-resistant tuberculosis (XDR-TB) is defined as resistance to isoniazid and rifampin, a fluoroquinolone, and one of the following three injectable agents: amikacin, kanamycin, or capreomycin.9
Microbiological Diagnosis of Tuberculosis
Published in Nancy Khardori, Bench to Bedside, 2018
Hitender Gautam, Urvashi B. Singh
During the past two decades, the increase in drug-resistant tuberculosis has added to the complexity of this disease especially multidrug resistant tuberculosis (MDR-TB) and extensively drug resistant tuberculosis (XDR-TB) which are much more challenging to treat than drug-susceptible disease (Gandhi et al. 2006). The estimated number of MDR-TB cases worldwide is approximately 5,00,000 described from at least 127 countries, and XDR-TB has been described from 105 countries (WHO 2015).
Streptomycin
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Multidrug-resistant tuberculosis (MDR-TB) is defined as resistance to at least rifampicin plus isoniazid. Extensively drug-resistant tuberculosis (XDR-TB), a subset of MDR-TB, is currently defined as MDR-TB plus resistance to any quinolone and any second line injectable agent (i.e. kanamycin, amikacin, capreomycin). Pre-XDR-TB is defined as MDR-TB with resistance to either a quinolone or a second-line injectable, but not both. None of these definitions include streptomycin despite its historical importance in the treatment of tuberculosis. In a recent review of 1047 cases of MDR-pre-XDR and XDR-TB from Korea, outcomes became progressively poorer by resistance category. However, in patients with pre-XDR-TB, resistance to streptomycin was associated with a poorer prognosis (Kim et al., 2010). In contrast, in a smaller study of patients with MDR-pre-XDR and XDR-TB at the National Jewish Medical and Research Center in Colorado USA, patients with quinolone-resistant pre-XDR-TB combined with streptomycin resistance still had an improved outcome compared with the XDR-TB group (Chan et al., 2009).
Systematic review and meta-analytic findings on the association between killer-cell immunoglobulin-like receptor genes and susceptibility to pulmonary tuberculosis
Published in Pathogens and Global Health, 2021
Melodi Omraninava, Sahar Mehranfar, Arezou Khosrojerdi, Sirous Jamalzehi, Jafar Karami, Morteza Motallebnezhad, Mohammad Reza Javan, Saeed Aslani, Hamed Mohammadi, Ahmad Kousha
For the past 25 years, tuberculosis (TB), which is caused by Mycobacterium tuberculosis (M. tuberculosis) infection, has been one of the global public health emergencies. According to the World Health Organization (WHO) reports, about 10 million new cases of TB occur in 2019 [1]. About 87% (8.7 million) of these individuals are from the WHO 30 high-burden countries [2,3]. Today, prevention of TB occurs in several ways, such as screening of persons at high risk, early detection and treatment of infected individuals, and vaccination with bacillus Calmette Guérin (BCG) vaccine of newborns [4,5]. One of the big challenges for the treatment of TB is the emergence of multidrug-resistant tuberculosis (i.e. MDR-TB) and extensively drug-resistant tuberculosis (i.e. XDR-TB). Moreover, strains resistant to the majority of drugs available have been seen globally [6,7]. Co-infection with the human immunodeficiency virus (HIV) increases the risk for pulmonary TB (PTB) and extra-pulmonary TB [8,9].
Anti-tubercular activity and molecular docking studies of indolizine derivatives targeting mycobacterial InhA enzyme
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Katharigatta N. Venugopala, Sandeep Chandrashekharappa, Pran Kishore Deb, Christophe Tratrat, Melendhran Pillay, Deepak Chopra, Nizar A. Al-Shar’i, Wafa Hourani, Lina A. Dahabiyeh, Pobitra Borah, Rahul D. Nagdeve, Susanta K. Nayak, Basavaraj Padmashali, Mohamed A. Morsy, Bandar E. Aldhubiab, Mahesh Attimarad, Anroop B. Nair, Nagaraja Sreeharsha, Michelyne Haroun, Sheena Shashikanth, Viresh Mohanlall, Raghuprasad Mailavaram
Tuberculosis (TB) is a communicable infectious disease and a major cause of illness, particularly in low-income countries. It is caused by the opportunistic bacillus Mycobacterium tuberculosis (MTB) which primarily attacks the lungs (pulmonary) but may later affect other parts (extra-pulmonary) of the body1. According to the World Health Organisation (WHO), TB is considered as one of the top 10 causes of death worldwide, and the leading cause of death from a single infectious agent1. In 2019, TB resulted in nearly 1.4 million deaths, including 208,000 deaths among human immunodeficiency virus (HIV) positive patients2. HIV-infected patients are 19 times more likely to develop TB than HIV-negative subjects3,4. Several factors have contributed to the continuous health threat of TB globally. This includes the development of drug resistance such as multidrug-resistant tuberculosis (MDR-TB), extensively drug-resistant tuberculosis (XDR-TB)5, and totally drug-resistant tuberculosis (TDR-TB)6; the co-morbidities with acquired immunodeficiency syndrome (AIDS)7,8 and the risks involved in developing diabetes mellitus among TB patients9,10.
Carrier-free combination dry powder inhaler formulation of ethionamide and moxifloxacin for treating drug-resistant tuberculosis
Published in Drug Development and Industrial Pharmacy, 2019
Mohammad A. M. Momin, Shubhra Sinha, Ian G. Tucker, Shyamal C. Das
Drug-resistant tuberculosis (DR-TB) is an emerging threat to the global tuberculosis control. Globally in 2016, about 600,000 people developed multidrug-resistant tuberculosis (MDR-TB) and 8,000 people developed extensively drug-resistant tuberculosis (XDR-TB) [1]. While MDR-TB is the resistance of TB bacteria to the two first-line anti-TB drugs, isoniazid and rifampicin, XDR-TB is defined as the resistance to isoniazid, rifampicin, any fluoroquinolone and at least one of the three second-line injectable drugs (capreomycin, kanamycin, and amikacin), and the total drug-resistant TB is the resistance to all the currently available anti-TB drugs [2]. Suboptimal levels of drugs at the infection site (i.e. lung) is one of the contributing factors of drug-resistance [3–5]. Inappropriate dosing and incorrect delivery route contribute to the suboptimal levels of drug at the target site [6]. The currently recommended treatment regimen for MDR-TB and XDR-TB is a combination of multiple anti-TB drugs administered via oral and parenteral routes for a duration of 20–28 months [7]. The oral and parenteral routes cannot provide adequate amounts of drugs to the poorly vascularized lung lesions, and the success rates of the current lengthy treatment regimen are only 54% (for MDR-TB) and 30% (for XDR-TB) [1]. Pulmonary delivery of drugs directly to the lungs may result in a higher drug concentration in the lungs than those achievable by oral and parenteral routes with the potential to shorten the treatment time and increase the treatment success [8,9].