By incorporating a known tuberculostatic agent on one end of a surface-active molecule, an increased in vitro effect on the tubercle bacillus has been obtained.
This activity is presumably due to the concentration of the drug molecules at or beneath the mycobacterial cell boundary.
Whether the surface-active drug actually penetrates the lipid, or lipoprotein complex that is so characteristic of the mycobacteria is only problematic. According to comparable purely physical-chemical experiments, such a penetration is quite likely.
Increase in tuberculostatic effect of over 1000-fold has been attained by rendering surface-active the drugs included in this study. The quantitative evaluation of this increase in activity has been obtained by measuring drug action both when its surface-active properties are functional, and when these properties have been selectively abolished by a specific surface-active antagonist.
It is believed that the molecular orientation of a surface-active drug about a bacterial cell accounts for one component of its antibacterial action. Certain previously described surface-active antituberculous drugs and antibiotics have been examined in light of this interpretation.
It may be anticipated that the more potent tuberculostatic drugs such as streptomycin could be made more effective by incorporating the molecule into a surface-active compound, according to the principles herein described.