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Multidrug therapy (MDT) regiment has been used for leprosy all over the world for more than 20 years. Drug resistances of Mycobacterium have been reported from many areas. The resistance mostly occurred due to mutation on the gene coding protein targeted by anti-leprosy drugs. Two hundreds and seventy M. leprae isolates from some area in Indonesia were examined for studying the profile of mutation among isolates collected during 2003-2011. Drug resistance determining region of the folP1 gene and the rpoB gene was sequenced. The results showed 5 isolates of M. leprae harboured mutation only in the folP1 gene and another isolate harbored mutation in both the folP1 and rpoB gene. The point mutation in the folP1 gene that was found in 2 isolates occurred in codon 53 (ACC→GCC; Thr→Ala). Double point mutations on codon 53 that was found in two isolates were ACC→AGA (Thr→Arg) and ACC→AGG (Thr→Arg). The point mutation in the folP1 geneoccurred in codon 55 were found in two isolates were CCC→CTC (Pro→Leu) and CCC→CGC (Pro→Arg). Whereas mutation in the rpoB gene in one isolate occurred in codon 410 was GAT→TAT (Asp→Tyr). These mutations that altered the amino acids of the protein revealed that isolates of M. leprae were resistant to drug with variable profiles

The drug resistant problem of Mycobacterium leprae has been developing since the last decade and this has become a leprosy elimination problem in several countries, including Indonesia. Using biological on molecular methods, it is now possible to test for drug resistant cases in relatively simple and less time consuming ways. The purpose of the study is to analyze the prevalence of drug resistance M. leprae to dapsone and rifampicin in East Java based on the etection of mutations in the folP and rpoB genes. All samples were obtained from multibacillary leprosy patients in East Java, who have admitted to the Dr Sutomo Hospital Surabaya in 2003-2005. Isolates were analyzed by PCR, and the presence of nucleotide sequence of the folP and rpoB genes from M. leprae were confirmed by direct sequencing. Of 94 specimens which were collected, all were analyzed for their folP and rpoB genome. From 94 isolates, 70 showed a positive result by the folP1-folPR test and 77 out of 94 isolates showed positive by the rpoBF-rpoBR test. From 70 isolates for folP gene examination, there were 3 isolates which had mutation in the amino acid at codon 53; 2 cases Threonin (ACC) became Alanin (GCC) and 1 case Threonin (ACC) became Arginin (AGA). These mutations are responsible to dapsone resistance. For the rpoB gene, no mutation was found. The result suggested that 3 isolates (4.3%), 1 from a new case and 2 from relapse cases in this experiment, were resistant to dapsone and all isolates (100%) were susceptible to rifampicin.