Effectiveness of MDT: FAQ
Can MDT prevent the resistance of M. leprae to anti-leprosy drugs?
Yes, it can. MDT was developed mainly because of the widespread emergence of dapsone resistance, and the regimens were designed on the principle that they would be effective against all the strains of M. leprae regardless of their susceptibility to dapsone. It is estimated that an advanced, untreated lepromatous leprosy patient harbours about 11 logs live organisms. Out of these, the proportion of naturally-occurring drug-resistant mutants is estimated to be 1 in 7 logs for rifampicin; 1 in 6 logs each for dapsone and clofazimine. The organisms resistant to one drug will be susceptible to the other drugs in MDT as their mechanisms of action are different. As of today, very few patients have relapsed after treatment with MDT and re-treatment with the WHO-MDT regimen has been effective in all cases of relapses.
Does MDT help to bring about skin smear negativity earlier than with dapsone monotherapy?
The main function of MDT is to kill all viable organisms, which can be achieved in a relatively short period. The clearance of dead bacilli depends largely on the individual's immune response which, especially in individuals suffering from MB leprosy, is defective. The results of several large-scale, long-term field trials show that the rate of clearance of dead bacilli is about 0.6 to 1.0 logs per year and is not enhanced by MDT.
Is there any evidence that the drugs included in MDT can antagonize each other's antibacterial activity?
All experimental and clinical evidence indicates that there is no antagonism among the drugs included in MDT. The experience with MDT so far has shown the combination to be the most effective.