Tuberculosis is a disease that is caused by the bacterium tubercle bacillus. This disease develops slowly and mainly affects the lungs. When a person with tuberculosis – who is not undergoing treatment – coughs or sneezes, mists teeming with tubercle bacilli are dispersed, and those in the vicinity are liable to breathe in sufficient quantities of the tuberculosis-causing bacteria.
Once these tubercle bacilli settle in the lungs’ air sacs, they can cause a flu-like reaction. A few days later, they may spread into the bones, the other internal organs, and even the brain. As they multiply during a period of from three to ten weeks, the tubercle bacilli can cause an inflammatory reaction at the infected portions of the affected body parts. The reaction is marked by an accumulation of nodular, chronically inflamed tissues and white blood cells, or what is called granuloma.
A number of prescription drugs are being used to treat tuberculosis. Some examples are rifampin, ethambutol, isoniazid, and streptomycin. But how effective really are these prescription drugs in treating tuberculosis? Let’s direct the spotlight on the last one – streptomycin.
Probably one of the most discouraging findings in the areas of medical investigation and experimentation is the repeated observations that a drug initially very effective in fighting an infection fails to sustain its effectiveness in the long run. Such is the case in streptomycin.
A soil actinomycete (mold) product, streptomycin is, to an extreme extent, damaging to tubercle bacilli and is relatively innocuous to man. This makes its use initially effective in preventing the advance of tuberculosis. But continued use of streptomycin has proven to gradually decrease its effectiveness, even reaching the point where it may become totally useless. In the end, it is observed that tubercle bacilli in the treated individual exhibit extreme resistance to streptomycin which was earlier capable of destroying them.
What can perhaps explain the foregoing circumstance is that, at the onset, only a few tubercle bacilli are so formed as to withstand the injurious effect of streptomycin. The use of streptomycin at this point, therefore, results to something strikingly beneficial to the affected individual. But these few bacteria later increase rapidly in number, yielding a great number of resistant progenies, taking the place of the few streptomycin-resistant ones that were initially involved. At this point, streptomycin, for all practical purposes, has become ineffective; but the disease remains to be tuberculosis.
It may be appropriate to conclude that using streptomycin for minor infections without a doctor’s prescription exposes the individual to certain dangers. The importunate problem may be seemingly settled, but the growth of strains of bacteria that are resistant to the drug may be promoted in the process. Subsequent treatment of more serious infections in this regard may be perilously impaired.