Fig. 6

Schematic overview of the effect of repurposed drugs on biofilm and its outcome on tuberculosis treatment: Under stress like conditions Mycobacteria secrete exogenous layer of matrix that forms a physical barrier for entry of drugs. The cells within the matrix continuously secrete to develop a biomass of biofilm that enables the cells to withstand high minimum inhibitory concentration (MIC) of drugs. As a result, higher dosage of drugs is required to kill the cells. Cells at the core of the biofilm matrix are least affected by drugs and evolve in due time so as to withstand even higher concentration of drugs. This confers drug tolerance and leads to drug toxicity, increased treatment cost and mortality. Cyclosporine-A, acarbose and GaNP inhibit the activity of PpiB that play crucial role in biofilm formation. Treatment with these drugs suppresses formation of biofilm and the bacterium is exposed directly to the drugs. As a result the drug is effective at low MIC values. Treatment with these drugs also reduces the MIC of existing anti-tubercular drugs resulting in decreased toxicity. The end result is that patient mortality and treatment cost may be reduced significantly. Regular and dotted arrows in the figure denote confirmed and putative roles respectively