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Chapter 24 : Summary and Conclusions

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Summary and Conclusions, Page 1 of 2

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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.

Citation: Dannenberg, Jr. A. 2006. Summary and Conclusions, p 367-372. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch24
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Figures

Image of FIGURE 1
FIGURE 1

Changes in the number of human-type tubercle bacilli in the lungs of Lurie’s natively resistant and natively susceptible rabbits at different intervals after aerosol infection. By 7 days after infection, the resistant rabbits had inhibited the growth of the bacilli 20 to 30 times more effectively than did the susceptible rabbits, but, from then on, the two curves were parallel. At 4 to 5 weeks, the lungs of susceptible rabbits contained about 13 times the number of primary pulmonary tubercles that the lungs of resistant rabbits contained. The means and their standard errors are shown. (The y axis of this figure is on a log scale.) Reproduced with permission from reference 3.

The number of tubercle bacilli in the lungs of the resistant rabbits failed to decrease during the period illustrated, because liquefaction with extracellular multiplication of the bacillus readily occurred in these rabbits. Liquefaction did not occur in the susceptible rabbits, possibly because only low levels of hydrolytic enzymes developed in their macrophages.

The logarithmic and stationary phases of this bacillary growth curve also occur in mice and guinea pigs, following the inhalation of virulent tubercle bacilli (see chapter 15).

Citation: Dannenberg, Jr. A. 2006. Summary and Conclusions, p 367-372. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch24
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References

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1. Dannenberg, A. M., Jr. 1999. Pathophysiology: basic aspects. I. Pathogenesis of tuberculosis. II. Immunology of tuberculosis, p. 1747. In D. Schlossberg (ed.), Tuberculosis and Nontuberculous Mycobacterial Infections, 4th ed. The W. B. Saunders Co., Philadelphia, Pa.
2. Dannenberg, A. M., Jr. 1993. Immunopatho-genesis of pulmonary tuberculosis. Hosp. Pract. 28:3340 (Off. ed. 51–58).
3. Lurie, M. B.,, P. Zappasodi, and, C. Tickner. 1955. On the nature of genetic resistance to tuberculosis in the light of the host-parasite relationships in natively resistant and susceptible rabbits. Am. Rev. Tuberc. Pulmon. Dis. 72:297329.
4. Allison, M. J.,, P. Zappasodi, and, M. B. Lurie. 1962. Host-parasite relationships in natively resistant and susceptible rabbits on quantitative inhalation of tubercle bacilli: their significance for the nature of genetic resistance. Am. Rev. Respir. Dis. 85:553569.
5. Weber, J. R.,, P. Moreillon, and, E. I. Tuomanen. 2003. Innate sensors for Gram-positive bacteria. Curr. Opin. Immunol. 15:408415.
6. McCullers, J. A., and, E. I. Tuomanen. 2001. Molecular pathogenesis of pneumococcal pneumonia. Front. Biosci. 6:d877d889.

Tables

Generic image for table
TABLE 1

Multiplication of tubercle bacilli, the type of disease, and the host immune response a

Citation: Dannenberg, Jr. A. 2006. Summary and Conclusions, p 367-372. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch24
Generic image for table
TABLE 2

General characteristics of acute and chronic bacterial infections a

Citation: Dannenberg, Jr. A. 2006. Summary and Conclusions, p 367-372. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch24

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