@ERSpublications With proper management all TB patients have a chance to be cured; it should never be thought that a TB case is incurable http://ow.ly/ksm5gTuberculosis (TB) is most probably the disease that has caused more damage to the human species throughout its history in terms of number of patients and, above all, death toll. There have been thousands of years spent fighting against Mycobacterium tuberculosis in which the human species could only rely on the efficiency of the immune system [1]. We must recall its importance as, in the pre-antibiotic era, the immune system alone could ensure important achievements such as: 1) only 50% of the people exposed to M. tuberculosis contract the infection [2]); 2) only 10% of those infected progress to active disease; and 3) up to 30% of patients with advanced TB disease heal spontaneously ( fig. 1) [3,4]. In spite of this, the fate of TB patients in the pre-chemotherapy period was very bleak, with a mortality of .50% within 5 years after the onset of disease [3,4]. For centuries, several empirical treatments were attempted to trying to change this fateful prognosis. Additionally, sanatoriums were built throughout the world for many decades ( fig. 2). However, all these interventions were not really effective, and none of them contributed significantly to improve the doom of TB patients [4]. Then, fortunately, their fate changed dramatically with the advent of the antibiotic era. The two decades from the discovery of streptomycin in 1943 to that of rifampicin in 1963 changed a devastating disease into a relatively easy to cure one. Not only were up to 11 different drugs with activity against M. tuberculosis discovered (streptomycin, p-aminosalicylate (PAS), thiacetazone, isoniazid (H), pyrazinamide, cycloserine, kanamycin, ethionamide, ethambutol, capreomycin and rifampicin (R)), but, based on multiple randomised clinical trials, the basic fundamentals of TB treatment were also established [4,5]. Probably the most essential of these was the need to combine at least two to three drugs to which the patient was sensitive, as M. tuberculosis can develop resistance to single drugs.The ability of M. tuberculosis to develop resistances to antibiotics was described in the very first randomised clinical trial conducted with streptomycin and published in 1948 [6]. The first great lesson learnt from early randomised clinical trials was that using TB drugs in monotherapy, or in poor combinations, would lead to the selection of resistance to these drugs [5]. Thus, as a result of the misuse of the available drugs, monoresistant TB started to develop, followed by poly-resistant TB (resistance to two or more drugs), multi-drug resistant (MDR)-TB (resistance to at least H+R), and extensively-drug resistant (XDR)-TB (defined as MDR-TB plus resistance to at least one fluoroquinolone (FQ) and one second-line injectable drug). The need for definitions beyond XDR-TB is a currently an issue of debate.The definitions in the field of anti-TB drug resistance should be based on two main fact...