The Resistance of Mycobacterium Tuberculosis

by  Annika Bright

Tuberculosis is known to be one of the most endemic communicable diseases worldwide - caused by exposure to the Mycobacterium Tuberculosis organism. Although the prevalence of the bacterium has varied greatly throughout centuries, it continues to persist today in countries afflicted with numerous immunosuppressive diseases, in addition to those with a high poverty rate. Thus, why is it that Mycobacterium Tuberculosis is so resistant to mainstream healthcare treatments? 

The bacterium is inhaled through the nasal cavity and enters the lungs via the trachea where the organism aggregates within the alveoli. Once collected within the alveolar sacs, the bacteria divide rapidly by binary fission which occurs over a timespan of 18-24 hours. In normal circumstances, the bacteria are identified by their immune system which subsequently release M1 macrophages - a category of phagocytic cell - which attempt to completely engulf the Mycobacterium Tuberculosis bacteria in order to completely eliminate their effects. Furthermore, by the tenth week, a granuloma (an accumulation of macrophages surrounding a bacterium) is produced by the immune system which aims to prevent any ensuing symptoms that may occur. Despite the formation of a granuloma, in situations where the immune system is suppressed, the granuloma may be destroyed and release the replicated bacteria into the bloodstream whilst the microorganism uses the oxygen within the lungs to multiply. This ultimately results in a symptomatic period in which the person is able to transmit the bacterium to another.

The reason for the exceptional resistance of Mycobacterium Tuberculosis to antibiotics lies in the fact that once the bacterium is engulfed by the macrophage, it cannot by hydrolysed by the lysozymes as it inhibits the lysosome’s function. This allows the bacteria to copy itself, rather than being eliminated from the phagosome body. Moreover, the microorganism can only replicate at the site of abundant oxygen levels, thus, is likely to remain predominantly within the lungs and result in complications of pulmonary tuberculosis. As a result of this, the levels of the bacterium within the body remain extremely high throughout the infection, causing further mutations and strains to develop.