Chapter 24 : Summary and Conclusions

Abstract:

The pathogenesis of tuberculosis can be considered a series of battles between the host and the tubercle bacillus, each of which has its own weapons that can be used against the other. In addition, both the host and the bacillus have sites of vulnerability that can be exploited by the adversary. The weapons of the host are: cell-mediated immunity (CMI), which activates macrophages so that they can kill or inhibit tubercle bacilli that they ingest; and delayed-type hypersensitivity (DTH), which stops the intracellular growth of bacilli in nonactivated macrophages by killing these macrophages. DTH transforms an environment that is favorable for the bacillus into an environment that is inhibitory, i.e., solid caseous tissue. In general, each stage of tuberculosis is won by the host with increasing difficulty. Furthermore, in the same lung, some lesions may progress while other lesions may regress. Tuberculosis is a locally controlled disease that depends on the growth of bacilli in nonactivated macrophages or in liquefied caseum, or on the inhibition of bacilli in activated macrophages or in solid caseum. To control bacillary multiplication, both CMI and tissue-damaging DTH are required. This statement was proved by correlating bacillary growth curves with the observed gross pathology and histopathology. The type of tuberculosis described in the susceptible rabbits resembles that found in infants and immunocompromised adults. Acute and chronic bacterial infections show a spectrum of host responses. At one end of the spectrum is typical pneumococcal pneumonia, a rapidly progressing acute disease somewhat like anthrax and plague.