**1. Introduction**

An understanding of the epidemiology of multidrug resistant tuberculosis (MDR-TB) and the extensively drug-resistant tuberculosis (XDR-TB) is critical for effective control of the global burden of tuberculosis (TB) which is caused by the organisms belonging to the *Mycobacterium tuberculosis* complex. Epidemiology of MDR-TB and XDR-TB will be reviewed here.

The history of tuberculosis treatment has observed sequential development of resistance to anti-tuberculosis drugs over the decades. Para amino salicylic acid (PAS) and isoniazid (INH) were introduced to reduce the development of streptomycin (SM) resistance, which heralded the era of combination treatment for tuberculosis [1]. Within 20 years, resistance to both INH and SM was already a challenge in the use of INH, SM and PAS as the standard anti-tubercu‐ losis regimen. With the discovery of rifampicin (RMP) in 1966 [2] and the expansion of its use between 1970 and 1990, patients who were already carriers of isoniazid (INH) resistant *Mycobacterium tuberculosis* strains became resistant to RMP. This was the start of a progressively growing problem, multi drug resistant tuberculosis (MDR-TB), which has reached epidemic proportions in some countries. In the last two decades, with the misuse of other drugs with anti-tuberculosis action, in particular the fluoroquinolones (FQs), the most effective among the second-line drugs, resistance has dramatically increased to extensively drug-resistant TB (XDR-TB) which is defined as resistance to at least RMP and INH (the definition of multidrugresistant tuberculosis (MDR-TB)), in addition to any fluoroquinolone, and at least one of the three injectable anti-tuberculosis (TB) drugs capreomycin, kanamycin and amikacin [3].
