An Overview of Mycobacterium Tuberculosis
According to the Centers for Disease Control and Prevention (CDC) nearly one –third of the world’s population is infected with the bacteria that cause tuberculosis, which is why tuberculosis remains one of the most deadly diseases. The CDC reports that tuberculosis caused nearly two million deaths every year, making it one of the world’s most fatal diseases. Tuberculosis is caused by an infection called Mycobacterium tuberculosis, a large rod-shaped bacterium. Mycobacterium tuberculosis can infect many parts of the body including the skin, joints, bones, lymph nodes, kidney, spine and nervous system. Since these bacteria need oxygen in order to grow, they most often infect the upper part of the lungs. Kenneth Todar PhD, in his book Text book of Bacteriology explained there is a small percent of mycobacterium progress to disease and even a smaller percent will progress all the way to stage five. Stage one begins when droplet nuclei are inhaled. One droplet nuclei contains no more than 3 bacilli. Droplet nuclei are so small that they can remain air-borne for extended periods of time. The most effective (infective) droplet nuclei tend to have a diameter of 5 micrometers. Droplet nuclei are generated by during talking coughing and sneezing. Coughing generates about 3000 droplet nuclei. Talking for 5 minutes generates 3000 droplet nuclei but singing generates 3000 droplet nuclei in one minute. Sneezing produces the most droplet nuclei by far, which can disperse to individuals up to 10 feet away (Todar , 2008). Droplet nuclei spread from one individual to another.
After droplet nuclei are inhaled, the bacteria are nonspecifically taken up by alveolar macrophages. However, the macrophages are not activated and are unable to destroy the intracellular organisms.

Tuberculosis begins when droplet nuclei reach the alveoli. Thus, when a person inhales air which contains droplets most of the larger droplets become embedded in the upper respiratory tract (the nose and throat), where infection is unlikely to develop. However, the smaller droplet nuclei may reach the small air sacs of the lung (the alveoli), where infection begins. Stage two begins seven to twenty-one days after initial infection. MTB multiplies virtually unrestricted within inactivated macrophages until the macrophages burst. Other macrophages begin to extravasate from peripheral blood. These macrophages also phagocytose MTB, but they are also inactivated and hence cannot destroy the bacteria. In stage three, lymphocytes begin to infiltrate. The lymphocytes, specifically T-cells, recognize processed and presented MTB antigen in context of MHC molecules. This results in T-cell activation and the liberation of cytokines including gamma interferon (IFN). The liberation of IFN causes in the activation of macrophages. These activated macrophages are now capable of destroying MTB.
It is at this stage that the individual becomes tuberculin-positive. This positive tuberculin reaction is the result of the host developing a vigorous cell mediated immune (CMI) response. A CMI response must be mounted to control an MTB infection. An antibody mediated immune (AMI) will not aid in the control of a MTB infection because MTB is intracellular and if