AN IRREVERENT LOOK AT MYCOBACTERIUMTB

TB is one of the oldest diseases known to affect humanity.The Greeks called the disease "pthisis", but to everyone's infinite relief, the name didn't stick.
Strike up a conversation with any member of the Mycobacteriaceae family (for instance M.kansasii) and chances are that, before the minute is up, he will start to drop names. And the first name to be dropped will inevitably be that of the prince of Mycobacteriae, it's proudest son and facile princeps, Mycobacterium tuberculosis. Such is the primal position of M.TB in the family that the rest of the members are clubbed together and , rather disparagingly, referred to as NonTB mycobacteria.The record shows M.TB as being a slender, rod shaped aerobic bacterium ; "that Cassius has a lean and hungry look".

PATHOGENESIS
Day 0.Somewhere in India.
A patient with tuberculosis coughs, sneezes or talks, producing aerosolized, droplet nuclei pregnant with M.TB. An unsuspecting healthy fellow Indian inhales. A fraction of the bacilli inhaled filter down into his alveoli, where they are ingested by "nonspecifically activated" macrophages. These macrophages are omnivorous soldiers who ingest anything [and are therefore 'nonspecific'] which percolate down to the alveoli. Inside the macrophages the bacilli are showered with the usual cocktail of complement, free radicals, proteolytic enzymes and the like. In most instances the bacilli succumbs to this lethal mixture. It is thus the lot of most M.TB to die unsung in some macrophage's belly, choking on a free radical.
However, in a minority of cases, the bacilli weathers the storm and not only survives, but actually starts to multiply inside the the macrophages. The key to this survival is not brawn or brain , but fat !. Fat, in the form of the lipid rich cell wall and the glycolipid capsule. Now, with the bacteria multiplying, the boot is firmly in the other foot. The hunter has become the hunted. The bacilli are released, no doubt to thunderous ovation, with the death of the macrophages.
As far as the body's defenses are concerned, it's certainly time for PLAN B.
Four weeks later. Same place.
Plan B is set into motion. The plan is to launch a two pronged counter attack. The first of these responses is called the tissue damaging response. It involves sacrificing those brave, but losing macrophages with rapidly multiplying bacilli inside them. Hard choice that ; killing your own, but they have to be martyred for the greater common good. This response also involves damaging some tissue (which gives it its name) and causing tissue necrosis. This necrotic environment (with low O₂ tension and low ph) makes life pretty unpleasant for M.TB,which generally likes wide open spaces and a bit of fresh air. The bacilli are consequently inhibited.
The second type of response is called Macrophage activating response. These activated macrophages are no ordinary macrophages ; they are TB specialists. Their mission is "damage limitation and containment" and towards this end they take on some fancy names like 'epitheloid cells' and 'giant cells'. Along with some friendly lymphocytes, they then proceed to aggregate around the lesion's center and effectively neutralize the tubercle bacilli, without causing furthur tissue destruction. In the central part of the lesion there is caseation necrosis. If all goes well, the lesions may proceed to healing . However, it is less than accurate to describe them as "healed" lesions. What we actually have is a stalemate, because, though the bacteria are contained, viable M.TB remain within the macrophages and the necrotic material for years or even throughout the patient's lifetime. They lie waiting for an opportune time to strike.
Cavities:
In a minority of cases the macrophage activating response is weak and the only way to contain the bacteria is through an  intense tissue damaging response. The lesion tends to expand furthur as more and more tissue is destroyed. Bronchial walls and blood vessels are invaded and destroyed ;cavities are formed. Within the cavity walls, TB bacilli live merrily, multiply and spread into the airways and to the outside through expectorated sputum.......sputum, which we hope will find its way to the nearest microscopy center !