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Chapter 3 : Types of Human Pulmonary Tuberculosis

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Abstract:

Human tuberculosis most frequently occurs as a tiny inapparent lesion that stays dormant throughout the life of the host. If clinical disease is produced, it varies from the rapidly progressing, hematogenously spread disease that occurs in infants and immunosuppressed individuals to a chronic, slowly progressing cavitary disease that is commonly found in immunocompetent adults. In this chapter, the gross and histopathological characteristics of the childhood and adult types of pulmonary tuberculosis are described in more detail. Proliferative lesions, sometimes called “hard” tubercles, are more common when small quantities of bacilli and their tuberculin like products are present in a host with high resistance to tuberculosis. Exudative lesions are more common when the host is highly sensitive to tuberculin, especially when large quantities of bacilli and their tuberculin-like products are present at the local site. Miliary tuberculosis occurs when a massive dose of tubercle bacilli is discharged from a caseous or liquefied focus into the bloodstream and the resistance of the host is inadequate, as in early infancy, in old age, and in immunologically depressed persons of any age. Reinfection-type or adult-type tuberculosis consists of a small to large pulmonary lesion that is not accompanied by any marked enlargement of the hilar lymph nodes. In patients with HIV/AIDS, the histologic pattern of tuberculosis generally correlates with the degree of immunosuppression. Tuberculous humans are about 100 times more sensitive than rabbits to tuberculin. Therefore, caseous necrosis and eventual calcification more readily occur in humans.

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 1
FIGURE 1

Development, arrest, or progression of human pulmonary tuberculosis. Once a tiny (0.5 to 1.0 mm) pulmonary lesion is established, the person becomes tuberculin positive. The tiny lesion is usually arrested, but in about 5% of cases, it progresses to form a larger caseous lesion. Such a lesion may (i) stabilize with bacillary dormancy, (ii) progress with or without hematogenous spread of the disease, or (iii) liquefy and produce a cavity with or without bronchial spread of the disease. Any stabilized lesion may reactivate years later if liquefaction and cavity formation occur with extracellular bacillary growth. Antimicrobials can arrest the disease at any stage, unless the bacillus becomes drug resistant.

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 2
FIGURE 2

A 10-day lesion, produced in a rabbit by the intravenous injection of BCG. Alveolar macrophages, staining darkly for β-galactosidase (our marker for macrophage activation), have accumulated in the surrounding alveolar area (rather far from the bacilli in the small caseous center). Around the caseous center are viable, young, β-galactosidase-negative macrophages from the bloodstream, which control the fate of the tuberculous lesion. Within the caseous center are disintegrated β-galactosidase-negative macrophages and more than 10 faintly stained tubercle bacilli (not easily seen in this photograph). Stained with 5-bromo-4-chloro-3-indolyl-β--galactoside, carbolfuchsin, and hematoxylin. Magnification, ×330. Reprinted with permission from reference 33.

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 3
FIGURE 3

Left lung of a 57-year-old woman showing an arrested Ghon complex. A calcified arrested primary tuberculous lesion is present subpleurally in the lower lobe, and an inactive caseous lymph node is present at the hilus. The pulmonary lesion was probably acquired during childhood. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 4
FIGURE 4

A proliferative type of miliary tubercle in the liver of an 8-month-old male infant. Parts of four Langhans’ giant cells are seen. Stained with hematoxylin and eosin. Magnification, ×130. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 5
FIGURE 5

A well-encapsulated fibrocaseous pulmonary lesion formed from confluent tubercles in a 5-month-old infant dying of tuberculous meningitis. The central area of necrosis is surrounded by smaller satellite necrotic areas. One Langhans’ giant cell is visible. This was a small proliferative tubercle that exacerbated as the patient became terminally ill. Stained with hematoxylin and eosin. Magnification, ×123. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 6
FIGURE 6

An exudative type of tuberculous lesion in the lung of a 47-year-old man. Depicted is an area of tuberculous pneumonia. A necrotic exudate fills the alveolar spaces, and the alveolar walls are thickened by infiltrating cells. Stained with hematoxylin and eosin. Magnification, ×266.

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 7
FIGURE 7

An exudative lesion similar to that shown in Fig. 6 but stained for tubercle bacilli, some of which may be discerned in this photograph (arrows). Stained with Ziehl-Neelsen, counterstained with methylene blue. Magnification, ×450. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 8
FIGURE 8

Part of a typical pulmonary tubercle that shows both proliferative and exudative features and a Langhans’ giant cell. It was from a 12-month-old infant with miliary tuberculosis. Stained with hematoxylin and eosin. Magnification, ×300.

Langhans’ giant cells form when macrophages surrounding bits of caseum fuse to each other. The nuclei of Langhans’ giant cells are in the periphery and may continue to divide. In tuberculous lesions, Langhans’ giant cells are a sign of chronicity. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 9
FIGURE 9

Miliary tuberculosis of the lung in a 19-year-old man. Caseous hilar lymph nodes are present. From caseous plaques (not shown) in the branches of the pulmonary veins, tubercle bacilli seeded the general circulation and were carried to other organs in the body. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 10
FIGURE 10

Early liquefaction in a small tubercle from a 12-month-old infant who died of miliary tuberculosis. The lesion is partly surrounded by fibrous tissue. Stained with hematoxylin and eosin. Magnification, ×108. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 11
FIGURE 11

A rabbit pulmonary tuberculous lesion showing tubercle bacilli that had grown profusely in the liquefied caseum. This lesion was probably beginning to cavitate, because some of the spaces in the liquefied caseum are larger than usual. Such profuse growth occurs only in some of the lesions with liquefied centers, presumably where the composition of the liquefied caseum is most favorable and/or the adaptation of the bacillus to extracellular growth is most complete. Similar bacillary growth has been found in many human cavitary lesions. Stained with carbol-fuchsin, counterstained with methylene blue. Magnification, ×600. Reprinted with permission from reference 34.

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 12
FIGURE 12

The wall of a pulmonary cavity in a rabbit showing tubercle bacilli that had grown profusely in the liquefied caseum. The bacilli are more numerous near the lumen of the cavity (on the left), presumably because the oxygen tension there is highest. Such profuse growth occurs only in the walls of some, not all, cavities. Stained with carbol-fuchsin, counterstained with methylene blue. Magnification, ×250. Reprinted with permission from reference 34.

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 13
FIGURE 13

Bilateral tuberculous cavities in the upper lobes in a 39-year-old diabetic woman. Caseous areas surround the cavities. 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. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 14
FIGURE 14

An apical cavity of moderate size in the left lung of an adult. Caseous pulmonary consolidation of pneumonic origin surrounds the cavity. Several caseous foci are also present in the other lung. The hilar lymph nodes contain a few caseous areas but are 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 15
FIGURE 15

A tissue section of a rabbit pulmonary cavity wall. On the left are disintegrating mature epithelioid cells (see Fig. 15 in chapter 4). On the right is a small blood vessel extending into the cavity’s lumen. Such exposed vessels are the source of blood in the sputum. In humans, when a larger blood vessel is similarly exposed in a cavity and ruptures, massive hemoptysis and sometimes fatal hemorrhage may occur. Glycol methacrylate-embedded tissue section stained with Giemsa. Magnification, ×400. Reprinted with permission from reference 35.

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 16
FIGURE 16

A cavity in the base of the upper lobe of the left lung of a 17-month-old infant. The apical portion was adherent to the chest wall and solidified with confluent proliferative tubercles and encapsulated caseous pneumonic foci. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 17
FIGURE 17

A portion of a large cavity in the lung of a rabbit, 18 weeks after the inhalation of about 5,000 virulent bovine-type tubercle bacilli. The liquefied caseum (below) is surrounded by a thick fibrous capsule. In this capsule are many fibroblasts, as well as some macrophages, lymphocytes, and plasma cells. At the right is an oval metaplastic alveolus next to a small blood vessel. Glycol methacrylate-embedded tissue section stained with Giemsa. Magnification, ×250. Reprinted with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 18
FIGURE 18

Rapidly progressing disseminated tuberculosis in an 11-month-old infant. Both hematogenous and bronchogenic spread from caseous hilar lymph nodes occurred in the lungs. Most of the caseous foci are hematogenous in origin. At the hilus in the lung on the right is an area of caseous pneumonia caused by the rupture of a tuberculous lymph node into a nearby bronchus. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 19
FIGURE 19

A large, rapidly formed tuberculous cavity in the upper lobe. Caseous pneumonia is present throughout the rest of the lung. Fibrosis is minimal. The hilar node is markedly enlarged and mostly caseous. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 20
FIGURE 20

Advanced fibrocaseous tuberculosis in an 11-year-old girl, who died before the advent of the antimicrobial era. The bilateral cavities in the upper lobes have caused adjacent areas of caseous bronchopneumonia. On the right is fibrous tissue from pleural adhesions. The hilar lymph nodes contain several caseous foci. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 21
FIGURE 21

Caseous bronchopneumonia originating from a large subapical cavity. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 22
FIGURE 22

Tuberculous laryngitis in a rabbit that had inhaled 300 virulent bovine-type tubercle bacilli 33 weeks previously. The lung of this rabbit had 14 lesions, 4 of which had formed cavities. The cavity in the right lower lobe of the lung had apparently discharged so many bacilli into the bronchial tree that the larynx became infected. This laryngeal lesion partly obstructed the airway. In humans, tuberculous laryngitis has been rare ever since antimicrobials for this disease became available. Magnification, ×5.4. Reprinted with permission from reference 35.

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 23
FIGURE 23

Extensive confluent caseous pneumonia in a 13-month-old infant, caused by the rupture of a large liquefied caseous hilar lymph node into an adjacent bronchus. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 24
FIGURE 24

A progressive Ghon complex in the mid portion of a lung from a 6-year-old boy who died of tuberculous meningitis. At the lower edge of the specimen is the primary subpleural caseous lesion. Near the center is a markedly enlarged caseous hilar lymph node. Many tubercles of hematogenous origin are also present. 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. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 25
FIGURE 25

Confluent, multidrug-resistant, tuberculous pneumonia in a patient with AIDS. The lung parenchyma was replaced by pale nodular zones of caseation necrosis. Reprinted with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 26
FIGURE 26

A tissue section from the lung depicted in Fig. 25. Caseosuppurative necrosis can be seen on the left, and poorly organized tuberculous granulation tissue is on the right. Stained with hematoxylin and eosin. Magnification, ×150. Reprinted with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 27
FIGURE 27

Progressive miliary tuberculosis and tuberculous pneumonia in the left upper lobe of an immunocompromised 42-year-old woman receiving corticosteroids for dermatomyositis. An infarct is present in the lower lobe. Reprinted with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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Image of FIGURE 28
FIGURE 28

(A) Tissue section of an exudative tuberculous lesion from the lung shown in Fig. 27, showing extensive caseous necrosis without granuloma formation or Langhans’ giant cells. Within the adjacent alveoli (on the right) is an exudate of fibrin and caseous debris. Stained with hematoxylin and eosin. Magnification, ×170. (B) Numerous intracellular and extracellular acid-fast bacilli found at the edge of a necrotic area in the lung from the same patient. Stained with Ziehl-Neelsen, counterstained with methylene blue. Magnification, ×1,700. Reprinted with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3
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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.), Pulmonary Diseases and Disorders, 3rd ed., vol. 2. McGraw-Hill Book Co., New York, N.Y.
2. 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.
3. Canetti, G. 1955. The Tubercle Bacillus in the Pulmonary Lesion of Man, p. 130. Springer Publishing Company, Inc., New York, N.Y.
4. Poole, J. C. F., and, H. W. Florey. 1970. Chronic inflammation and tuberculosis, p. 11831224. In H. W. Florey (ed.), General Pathology, 4th ed. The W. B. Saunders Co., Philadelphia, Pa.
5. Rich, A. R. 1951. The Pathogenesis of Tuberculosis, 2nd ed. Charles C Thomas Publisher, Springfield, Ill.
6. Iseman, M. D. 2000. A Clinician’s Guide to Tuberculosis. Lippincott Williams & Wilkins, Philadelphia, Pa.
7. Hopewell, P. C., and, R. M. Jasmer. 2005. Overview of clinical tuberculosis, p. 1531. In S. T. Cole,, K. D. Eisenach,, D. N. McMurray, and, W. R. Jacobs, Jr. (ed.), Tuberculosis and the Tubercle Bacillus. ASM Press, Washington, D.C.
8. Medlar, E. M. 1955. The behavior of pulmonary tuberculous lesions. A pathological study. Am. Rev. Tuberc. 71:1244.
9. Wolinsky, E. 1989. Tuberculosis, p. 465519. In G. L. Baum and, E. Wolinsky (ed.), Textbook of Pulmonary Diseases, 4th ed., vol. I. Little, Brown & Co., Boston, Mass.
10. Tomashefski, J. F., Jr. 1994, Tuberculosis and atypical mycobacterial infections, p. 451463. In M. J. Saldana (ed.), Pathology of Pulmonary Disease. Lippincott Williams & Wilkins, Philadelphia, Pa.
11. Lurie, M. B. 1964. Resistance to Tuberculosis: Experimental Studies in Native and Acquired Defense Mechanisms. Harvard University Press, Cambridge, Mass.
12. Schlesinger, L. S. 1993. Macrophage phagocytosis of virulent but not attenuated strains of Mycobacterium tuberculosis is mediated by mannose receptors in addition to complement receptors. J. Immunol. 150:29202130.
13. Schlesinger, L. S.,, C. G. Bellinger-Kawahara,, N. R. Payne, and, M. A. Horwitz. 1990. Phagocytosis of Mycobacterium tuberculosis is mediated by human monocyte complement receptors and complement component C3. J. Immunol. 144:27712780.
14. Dannenberg, A. M., Jr. 1991. Delayed-type hypersensitivity and cell-mediated immunity in the pathogenesis of tuberculosis. Immunol. Today 12:228233.
15. Dannenberg, A. M., Jr. 1993. Immunopatho-genesis of pulmonary tuberculosis. Hosp. Pract. 28:3340 (Office edition, 51–58).
16. Kenyon, T. A.,, S. E. Valway,, W. W. Ihle,, I. M. Onorato, and, K. G. Castro. 1996. Transmission of multidrug-resistant Mycobacterium tuberculosis during a long airplane flight. N. Engl. J. Med. 334:933938.
17. Wenzel, R. P. 1996. Airline travel and infection. N. Engl. J. Med. 334:981982.
18. Grosset, J. 2003. Mycobacterium tuberculosis in the extracellular compartment: an underestimated adversary. Antimicrob. Agents Chemother. 47:833836.
19. Balasubramanian, V.,, E. H. Wiegeshaus, and, D. W. Smith. 1994. Mycobacterial infection in guinea pigs. Immunobiology 191:395401.
20. Hruban, R. H., and, G. M. Hutchins. 1993. Mycobacterial infections, p. 331350. In D. H. Dial and, S. P. Hammar (ed.), Pulmonary Pathology. Springer-Verlag, New York, N.Y.
21. West, J. B. 2000. Respiratory Physiology. The Essentials, 6th ed., p. 5059. Lippincott Williams & Wilkins, Philadelphia, Pa.
22. Bennett, W. D.,, M. S. Messina, and, G. C. Smal-done. 1985. Deposition (normalized for lung volume) is generally greater in basal region of lung than in apical region. Effect of exercise on deposition and subsequent retention of inhaled particles. J. Appl. Physiol. 59:10461054.
23. Lurie, M. B.,, A. G. Heppleston,, S. Abramson, and, I. B. Swartz. 1950. An evaluation of the method of quantitative airborne infection and its use in the study of the pathogenesis of tuberculosis. Am. Rev. Tuberc. 61:765797.
24. Kaplan, G.,, F. A. Post,, A. L. Moreira,, H. Wainwright,, B. N. Kreiswirth,, M. Tanverdi,, B. Mathema,, S. V. Ramaswamy,, G. Walther,, L. M. Steyn,, C. E. Barry III, and, L.-G. Bekker. (2003) Mycobacterium tuberculosis growth at the cavity surface: a microenvironment with failed immunity. Infect. Immun. 71:70997108.
25. Lillebaek, T.,, A. Dirksen,, E. Vynnycky,, I. Baess,, V. O. Thomsen, and, A. B. Andersen. 2003. Stability of DNA patterns and evidence of Mycobacterium tuberculosis reactivation occurring decades after initial infection. J. Infect. Dis. 188:10321039.
26. Zhang, Y. 2004. Persistent and dormant tubercle bacilli and latent tuberculosis. Front. Biosci. 9:11361156.
27. Barnes, P. F.,, A. B. Bloch,, P. T. Davidson, and, D. E. Snider, Jr. 1991. Tuberculosis in patients with human immunodeficiency virus infection. N. Engl. J. Med. 324:16441650.
28. Hill, A. R.,, P. Somasundaram,, S. Brustein,, K. Vaidya,, S. Powell,, P. Li, and, B. Suster. 1991. Disseminated tuberculosis in the acquired immunodeficiency syndrome era. Am. Rev. Respir. Dis. 144:11641170.
29. Lucas, S., and, A. M. Nelson. 1994. Pathogenesis of tuberculosis in human immunodeficiency virus-infected people, p. 503513. In B. R. Bloom (ed.), Tuberculosis: Pathogenesis, Protection, and Control. ASM Press, Washington, D.C.
30. Lindgren, I. 1961. Anatomical and roentgeno-logic studies of tuberculosis infection in BCGvaccinated and non-vaccinated subjects, with biophysical investigations of calcified foci. Acta Radiol. 209(Suppl.):1101.
31. Lindgren, I. 1965. The pathology of tuberculous infection in BCG-vaccinated humans. Adv. Tuberc. Res. 14:202234.
32. Sutherland, I., and, I. Lindgren. 1979. The protective effect of BCG vaccination as indicated by autopsy studies. Tubercle 60:225231.
33. Shima, K.,, A. M. Dannenberg, Jr.,, M. Ando,, S. Chandrasekhar,, J. A. Seluzicki, and, J. I. Fabrikant. 1972. Macrophage accumulation, division, maturation, and digestive and microbicidal capacities in tuberculous lesions. I. Studies involving their incorporation of tritiated thymidine and their content of lysosomal enzymes and bacilli. Am. J. Pathol. 67:159180.
34. Converse, P. J.,, A. M. Dannenberg, Jr.,, T. Shigenaga,, D. N. McMurray,, S. W. Phalen,, J. L. Stanford,, G. A. W. Rook,, T. Koru-Sengul,, H. Abbey,, J. E. Estep, and, M. L. M. Pitt. 1998. Pulmonary bovine-type tuberculosis in rabbits: bacillary virulence, inhaled dose effects, tuberculin sensitivity, and Mycobacterium vaccae immunotherapy. Clin. Diagn. Lab. Immunol. 5:871881.
35. Converse, P. J.,, A. M. Dannenberg, Jr.,, J. E. Estep,, K. Sugisaki,, Y. Abe,, B. H. Schofield, and, M. L. M. Pitt. 1996. Cavitary tuberculosis produced in rabbits by aerosolized virulent tubercle bacilli. Infect. Immun. 64:47764787.

Tables

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TABLE 1

Basic types of pulmonary tuberculosis a

Citation: Dannenberg, Jr. A. 2006. Types of Human Pulmonary Tuberculosis, p 34-64. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch3

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