Abstract
1. Immunity to reinfection is a function of the increased capacity of the mononuclear phagocytes to destroy tubercle bacilli and varies directly with the extent of the primary lesion; however it is rarely sufficient to annihilate completely the microorganism. This acquired immunity is superimposed on the natural resistance of a given organ. 2. In the presence of sufficient immunity, such as occurs with the persistence of an extensive primary lesion, small numbers of tubercle bacilli are destroyed by the mononuclear cells in situ without local or general infiltration of the tissues by polymorphonuclear or mononuclear leucocytes. Larger numbers of bacilli are destroyed within 24 hours by an accelerated formation of sharply localized nodules of mononuclear phagocytes. These progress no further and are absorbed or result in inconspicuous microscopic collections of epithelioid and giant cells. 3. In the presence of less immunity, such as occurs when the primary lesion has almost completely healed, the immediate inflammatory reaction is more intense and diffuse and persists longer. It results in a less rapid disappearance of the bacilli and in a more extensive formation of tubercles. These appear much earlier than in the normal animal and soon resolve. 4. Tubercle bacilli of reinfection may be destroyed even though the primary lesion in the lung and kidney is progressive. This is due to an unhindered extracellular multiplication of the bacilli in the caseous foci that undergo softening and excavation. Resistance may be overwhelmed by the spread of tremendous numbers of living bacilli from these foci through the bronchi or renal tubules, while the moderate numbers of reinfecting bacilli reaching the organs by way of the blood stream are destroyed.