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Chapter 1 : Overview

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Overview, Page 1 of 2

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Abstract:

This chapter presents an overview of tuberculosis. Tuberculosis is still one of the major diseases of the world, especially in developing countries. It kills over 2 million people each year, more than any other infectious disease. From the primary parenchymal lesion, the bacilli frequently spread via lymphatics and cause caseous lesions of the hilar lymph nodes. The bacilli may also spread via the bloodstream and cause lesions elsewhere in the host. The primary lesion, as well as the metastatic lesions, often progresses until the host succumbs. Adult-type pulmonary tuberculosis is a disease of innately resistant hosts, a category that includes most immunocompetent persons. The active parenchymal lesion frequently forms a cavity, in which the bacilli may multiply extracellularly. If so, the bacilli may spread via the bronchial tree to other parts of the lung. Cavity formation perpetuates tuberculosis in humankind because coughing spreads bacilli from the lungs into the environment, where they may infect other people. Contracting clinical tuberculosis depends on (i) the size and physiological state of the bacillary particle, (ii) its virulence, and (iii) the native and acquired resistance of the host. The chapter discusses factors to protect a personnel against tuberculosis. UV lights (shielded to protect people’s eyes) or high efficiency particle (HEPA)-filtered air purifiers should be used more frequently in hospital areas where tubercle bacilli are likely to be present.

Citation: Dannenberg, Jr. A. 2006. Overview, p 7-21. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch1
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Image of FIGURE 1
FIGURE 1

Rapidly progressing miliary tuberculosis in an 11-month-old infant. The rabbit counterpart of this type of tuberculosis is shown in Fig. 3. Most of the multiple caseous tubercles are of hematogenous origin. The primary lesion is marked by an arrow. Note the large size of the homolateral caseous hilar lymph nodes (which seeded the blood entering the lungs; see text). From the collection of the late professors A. R. Rich and W. G. MacCallum, Department of Pathology, Johns Hopkins School of Medicine, Baltimore, Md.

Citation: Dannenberg, Jr. A. 2006. Overview, p 7-21. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch1
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Image of FIGURE 2
FIGURE 2

Miliary tuberculosis of the lungs in a 19-year-old young adult. The tubercles appear smaller than those in Fig. 1 merely because the lungs of this individual are so much larger than those of the infant. Caseous hilar lymph nodes were the source of most of these miliary tubercles. In this patient, caseous plaques (not shown) in branches of the pulmonary veins seeded tubercle bacilli into the general circulation and caused miliary tubercles in many other organs. From the collection of the late professors A. R. Rich and W. G. MacCallum, Department of Pathology, Johns Hopkins School of Medicine, Baltimore, Md.

Citation: Dannenberg, Jr. A. 2006. Overview, p 7-21. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch1
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Image of FIGURE 3
FIGURE 3

Organs of Lurie’s inbred susceptible rabbit F4-33, which died of a generalized progressive tuberculosis of 3.3 months’ duration. This rabbit had a large, single, completely caseous nonliquefied primary lesion in the middle of the left lung, massive enlargement and caseation of the homolateral hilar lymph nodes, and hematogenous spread of the disease to the lungs, kidney, pleura, and knee joint. The rabbit was naturally infected in a room containing airborne tubercle bacilli from rabbits with tuberculous kidneys (see chapter 12). Reproduced with permission from reference 3.

Note that the disease in this susceptible inbred rabbit was similar to the disease in humans shown in Fig. 1 and 2. The tubercles shown in these three figures could be almost the same size, because the photographs of the human specimens are so much smaller than the actual specimens.

Citation: Dannenberg, Jr. A. 2006. Overview, p 7-21. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch1
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Image of FIGURE 4
FIGURE 4

Bilateral tuberculous cavities in the upper lobes of a 39-year-old diabetic woman. Below each cavity are areas of caseous lung tissue. Although infected, the hilar lymph nodes are not markedly enlarged. In the lung on the right, an applicator stick marks the communication between the cavity and the bronchus. The rabbit counterpart of this type of tuberculosis is shown in Fig. 6. From the collection of the late professors A. R. Rich and W. G. MacCallum, Department of Pathology, Johns Hopkins School of Medicine, Baltimore, Md.

Citation: Dannenberg, Jr. A. 2006. Overview, p 7-21. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch1
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Image of FIGURE 5
FIGURE 5

An apical cavity of moderate size in an adult patient. Below the cavity is an area of caseous consolidation of pneumonic origin. Several caseous foci are also present in the other lung, probably also pneumonic in origin. The hilar lymph nodes (not shown) contained a few caseous foci but were only slightly enlarged. From the collection of the late professors A. R. Rich and W. G. MacCallum, Department of Pathology, Johns Hopkins School of Medicine, Baltimore, Md.

Citation: Dannenberg, Jr. A. 2006. Overview, p 7-21. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch1
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Image of FIGURE 6
FIGURE 6

Organs of Lurie’s inbred resistant rabbit A2-6, which died of tuberculosis 9 months after its tuberculin skin test converted. A single primary encapsulated pulmonary cavity was present in the right lung, from which tubercle bacilli spread (via the bronchial tree) to the larynx and the intestines. No grossly visible tuberculous lesions were found in the hilar lymph nodes or in the kidneys. Nonprogressive secondary tubercles were present in both lungs (probably bronchogenic in origin). Like the susceptible rabbit depicted in Fig. 3, this resistant rabbit was naturally infected in a room containing airborne tubercle bacilli from rabbits with tuberculous kidneys (see chapter 12). Reproduced with permission from reference 3.

Note that the disease in this inbred resistant rabbit was similar to the cavitary disease in humans shown in Fig. 4 and 5.

Citation: Dannenberg, Jr. A. 2006. Overview, p 7-21. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch1
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Image of FIGURE 7
FIGURE 7

Tubercle bacilli growing profusely in the liquefied caseum in a pulmonary cavity of a rabbit that inhaled about 340 virulent bovine-type tubercle bacilli 33 weeks previously. Such profuse growth occurs only in some lesions with liquefied centers, presumably where the composition of the liquefied caseum is most favorable or the adaptation of the bacillus to extracellular growth is most complete. Similar bacillary growth has been found in many human cavitary lesions (20). Bacilli were stained with carbol-fuchsin and counterstained with methylene blue. Magnification, ×600. Photograph reproduced with permission from reference 59.

Citation: Dannenberg, Jr. A. 2006. Overview, p 7-21. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch1
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Image of FIGURE 8
FIGURE 8

An example of an effective disposable mask. This mask is made of HEPA-filtering material with an exhaust valve in the center. It is backed by a ring of foam rubber that fits tightly against one’s face (but not quite as tightly as the less flexible mask shown in Fig. 9). Similar masks are available from Lab Safety Supply, 401 S. Wright Road, Janesville, Wis. 53546. Tel: 1-800-356-0783. http://www.labsafety.com.

Citation: Dannenberg, Jr. A. 2006. Overview, p 7-21. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch1
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Image of FIGURE 9
FIGURE 9

3M 7200S Half-Facepiece Respirator with 7255 Easi-Air High Efficiency Filter (approved by the National Institute of Occupational Safety and Health [NIOSH]). Similar masks are available from Lab Safety Supply, Janesville, Wis. (See legend to Fig. 8.)

Citation: Dannenberg, Jr. A. 2006. Overview, p 7-21. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch1
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Image of FIGURE 10
FIGURE 10

3M Air-Mate High Efficiency Particle (HEPA) Powered Air Purifying Respirator (PAPR)—HEPA 10 Head Cover and HEPA 12 Hood—with the HEPA PAPR assembly shown in Fig. 11 (NIOSH approved). Available from Lab Safety Supply, Janesville, Wis. (See legend to Fig. 8.) Photograph is reproduced with permission from the 3M Occupational Health and Environmental Safety Division.

Citation: Dannenberg, Jr. A. 2006. Overview, p 7-21. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch1
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Image of FIGURE 11
FIGURE 11

Components of the 3M Air-Mate HEPA 10 Head Cover and Air-Mate HEPA 12 Hood with the HEPA PAPR assembly shown in Fig. 10 (NIOSH approved). Available from Lab Safety Supply, Janesville, Wis. (See legend to Fig. 8.) Photograph is reproduced with permission from the 3M Occupational Health and Environmental Safety Division.

Citation: Dannenberg, Jr. A. 2006. Overview, p 7-21. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch1
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