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Chapter 7 : Structural Components of Tuberculous Lesions

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Abstract:

In humans, rabbits, and guinea pigs, typical tubercles often have a caseous necrotic center. Surrounding this caseous center is tuberculous granulation tissue, which is rich in macrophages and lymphocytes and contains dendritic cells, plasma cells, polymorphonuclear leukocytes, eosinophils, fibroblasts, and many capillaries. This chapter describes the structural components of tuberculous lesions. In humans, tuberculous granulation tissue often contains ill-defined granulomas and areas of caseous necrosis, along with variable numbers of tubercle bacilli. In rabbits, guinea pigs, and humans, caseous necrosis first occurs at the end of the logarithmic (symbiotic) stage of tuberculosis when tuberculin sensitivity develops. When macrophages surrounding the caseous center are poorly activated, the bacillus again grows intracellularly, and again the damaging delayed-type hypersensitivity (DTH) reaction kills such cells. Liquefaction occurs when solid caseous material softens. In contrast to pyogenic abscesses, which liquefy soon after they form, the caseous foci of tuberculosis may not liquefy for months, if ever. In both humans and rabbits, the healing of small endogenous metastatic tubercles (and small tubercles of exogenous reinfection) involves basically the same mechanisms as healing of primary foci, i.e., the local accumulation and activation of macrophages at the site of infection. Different organs of the host have different susceptibilities to tubercle bacilli. Live bovine-type bacilli can apparently survive at a lower oxygen tension than can human type bacilli, which explains some of the differences found in the disease produced by the live strains.

Citation: Dannenberg, Jr. A. 2006. Structural Components of Tuberculous Lesions, p 155-160. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch7
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Figures

Image of FIGURE 1
FIGURE 1

The wall of a cavity from a genetically resistant rabbit, 8 weeks after the inhalation of human-type tubercle bacilli. The liquefied caseous tissue (right) and liquefying caseous tissue (left) are both swarming with (rod-shaped) acid-fast bacilli. Cavities can be produced by both virulent human-type tubercle bacilli (illustrated here) and virulent bovine-type tubercle bacilli (illustrated in chapter 4); the bacilli can grow profusely in cavities produced by either type. Magnification, ×620. Reproduced with permission from reference 25.

Citation: Dannenberg, Jr. A. 2006. Structural Components of Tuberculous Lesions, p 155-160. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch7
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References

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1. Dannenberg, A. M., Jr., and, J. F. Tomashefski, Jr. 1998. Pathogenesis of pulmonary tuberculosis, p. 24472471. In A. P. Fishman (ed.), Fishman’s Pulmonary Diseases and Disorders, 3rd ed., vol. 2. McGraw-Hill Co., Inc., New York, N.Y.
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Tables

Generic image for table
TABLE 1

Causes of tissue damage and caseous necrosis a

Citation: Dannenberg, Jr. A. 2006. Structural Components of Tuberculous Lesions, p 155-160. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch7
Generic image for table
TABLE 2

Causes and results of liquefaction a

Citation: Dannenberg, Jr. A. 2006. Structural Components of Tuberculous Lesions, p 155-160. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch7

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