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Chapter 12 : Natural Airborne Infection
Author:
Arthur M. Dannenberg, Jr.1
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Affiliations:
1: Center for Tuberculosis Research Departments of Environmental Health Sciences, Molecular Microbiology and Immunology, and Epidemiology, Bloomberg School of Public Health Department of Pathology, School of Medicine Johns Hopkins University, Baltimore, Maryland 21205
Content Type: Monograph
Publication Year:
2006
Category: Clinical Microbiology; Bacterial Pathogenesis
Book DOI:
10.1128/9781555815684
Chapter DOI:
10.1128/9781555815684.ch12
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Abstract:
Using natural airborne infection of virulent bovine-type tubercle bacilli over many months, Lurie showed that resistance to the establishment of tuberculosis and resistance to its progress are separate phenomena: his inbred resistant rabbits converted their tuberculin skin tests an average of 2.7 months sooner than did his inbred susceptible rabbits. The separation of the establishment and progress of tuberculosis is only applicable to experiments in which occasional fully virulent tubercle bacilli are inhaled over many months. Airborne infection of laboratory animals over many months has, however, established other concepts directly applicable to tuberculosis in humans. (i) Only a single grossly visible primary pulmonary lesion will be produced, despite the continuous presence of virulent tubercle bacilli in the air. The immunity developed in response to the primary lesion is evidently sufficient to prevent other occasionally inhaled tubercle bacilli from causing grossly visible lesions. (ii) Some animals (and perhaps a few humans) may convert their dermal tuberculin reactions, and yet show no grossly visible primary lesions in their lungs at necropsy. This occurrence may be due to the early spread of inhaled bacilli out of the lungs to the hilar lymph nodes, where the growth of tubercle bacilli can be more easily controlled. These concepts are consistent with what Riley found when he exposed guinea pigs for months to air from a ward containing sputum-positive tuberculous patients.
Citation:
Dannenberg, Jr. A.
2006.
Natural Airborne Infection,
p 215-229.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch12
Figures
Natural Airborne Infection
Citation:
Dannenberg, Jr. A.
2006.
Natural Airborne Infection,
p 215-229.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch12
/content/10.1128/9781555815684.ch12.ch12fig01
FIGURE 1
A diagram of the rabbit cages that Lurie used for natural airborne infection. Thirty commercial rabbits, many of which were shedding virulent bovine-type tubercle bacilli (Ravenel) in their urine, were distributed into the three rabbit runs (rear of the diagram). As the rabbits moved throughout the runs, they caused tubercle bacilli in the urine-dampened bedding to become airborne.
Noninfected inbred resistant and susceptible rabbits were placed in 30 cages (front of the diagram). These rabbits inhaled occasional tubercle bacilli over a period of many months. The cages were moved daily, so that during the course of 30 days, each cage resided in each position for 1 day. Reproduced with permission from reference 2.
Noninfected inbred resistant and susceptible rabbits were placed in 30 cages (front of the diagram). These rabbits inhaled occasional tubercle bacilli over a period of many months. The cages were moved daily, so that during the course of 30 days, each cage resided in each position for 1 day. Reproduced with permission from reference 2.
10.1128/9781555815684/f0216-01_thmb.gif
10.1128/9781555815684/f0216-01.gif
FIGURE 1
A diagram of the rabbit cages that Lurie used for natural airborne infection. Thirty commercial rabbits, many of which were shedding virulent bovine-type tubercle bacilli (Ravenel) in their urine, were distributed into the three rabbit runs (rear of the diagram). As the rabbits moved throughout the runs, they caused tubercle bacilli in the urine-dampened bedding to become airborne.
Noninfected inbred resistant and susceptible rabbits were placed in 30 cages (front of the diagram). These rabbits inhaled occasional tubercle bacilli over a period of many months. The cages were moved daily, so that during the course of 30 days, each cage resided in each position for 1 day. Reproduced with permission from reference 2.
Citation:
Dannenberg, Jr. A.
2006.
Natural Airborne Infection,
p 215-229.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch12
/content/10.1128/9781555815684.ch12.ch12fig02
FIGURE 2
Resistance to attack (the preallergic period) and resistance to the progress (duration) of tuberculosis in the resistant A and susceptible C and F strains of rabbits. The graph on the left shows the average time (in months) in which these rabbits converted their tuberculin reactions. The graph on the right shows the average time (in months) that these rabbits lived after they became tuberculin positive.
The difference in the preallergic period between the resistant A strain and the susceptible F strain was highly significant, but that between the A strain and the susceptible C strain was not (3). However, the duration of the disease in the resistant A strain was always significantly longer than that in both susceptible strains (C and F) (3).
Experiments were performed with relatively low, medium, and high numbers of tubercle bacilli in the air of the room. This figure represents data from the experiment with the highest number of tubercle bacilli. Reproduced with permission from reference 3.
The difference in the preallergic period between the resistant A strain and the susceptible F strain was highly significant, but that between the A strain and the susceptible C strain was not (3). However, the duration of the disease in the resistant A strain was always significantly longer than that in both susceptible strains (C and F) (3).
Experiments were performed with relatively low, medium, and high numbers of tubercle bacilli in the air of the room. This figure represents data from the experiment with the highest number of tubercle bacilli. Reproduced with permission from reference 3.
10.1128/9781555815684/f0220-01_thmb.gif
10.1128/9781555815684/f0220-01.gif
FIGURE 2
Resistance to attack (the preallergic period) and resistance to the progress (duration) of tuberculosis in the resistant A and susceptible C and F strains of rabbits. The graph on the left shows the average time (in months) in which these rabbits converted their tuberculin reactions. The graph on the right shows the average time (in months) that these rabbits lived after they became tuberculin positive.
The difference in the preallergic period between the resistant A strain and the susceptible F strain was highly significant, but that between the A strain and the susceptible C strain was not (3). However, the duration of the disease in the resistant A strain was always significantly longer than that in both susceptible strains (C and F) (3).
Experiments were performed with relatively low, medium, and high numbers of tubercle bacilli in the air of the room. This figure represents data from the experiment with the highest number of tubercle bacilli. Reproduced with permission from reference 3.
Citation:
Dannenberg, Jr. A.
2006.
Natural Airborne Infection,
p 215-229.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch12
/content/10.1128/9781555815684.ch12.ch12fig03
FIGURE 3
Lungs and other organs of resistant rabbit A2-6. It converted its tuberculin reaction at 9 months and died of tuberculosis 9 months later. The primary lesion was the single (well-encapsulated) cavity in the right lung. There was tuberculosis of the larynx and intestines, as well as a tuberculous ulcer of the colon—all from the spread of large numbers of virulent bovine-type tubercle bacilli up the bronchial tree and then into the alimentary canal. The hilar and mesenteric lymph nodes were grossly normal, as were the kidneys. Several nonprogressive tubercles of hematogenous origin were present in both lungs. Reproduced with permission from reference 2.
10.1128/9781555815684/f0221-01_thmb.gif
10.1128/9781555815684/f0221-01.gif
FIGURE 3
Lungs and other organs of resistant rabbit A2-6. It converted its tuberculin reaction at 9 months and died of tuberculosis 9 months later. The primary lesion was the single (well-encapsulated) cavity in the right lung. There was tuberculosis of the larynx and intestines, as well as a tuberculous ulcer of the colon—all from the spread of large numbers of virulent bovine-type tubercle bacilli up the bronchial tree and then into the alimentary canal. The hilar and mesenteric lymph nodes were grossly normal, as were the kidneys. Several nonprogressive tubercles of hematogenous origin were present in both lungs. Reproduced with permission from reference 2.
Citation:
Dannenberg, Jr. A.
2006.
Natural Airborne Infection,
p 215-229.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch12
/content/10.1128/9781555815684.ch12.ch12fig04
FIGURE 4
Lungs and other organs of susceptible rabbit F4-33. It converted its tuberculin reaction at 6.2 months and died of tuberculosis 3.0 months later (Table 1). The primary lesion is the large, completely caseous lesion in the middle of the left lung. The caseum in this lesion did not liquefy, so no cavity formed. The homolateral draining hilar lymph nodes show extensive enlargement and massive caseation. Numerous large progressive caseous tubercles of hematogenous origin are present in both lungs. The kidneys, pleura, and knee joint show rapidly progressive caseous lesions. Reproduced with permission from reference 2.
10.1128/9781555815684/f0222-01_thmb.gif
10.1128/9781555815684/f0222-01.gif
FIGURE 4
Lungs and other organs of susceptible rabbit F4-33. It converted its tuberculin reaction at 6.2 months and died of tuberculosis 3.0 months later (Table 1). The primary lesion is the large, completely caseous lesion in the middle of the left lung. The caseum in this lesion did not liquefy, so no cavity formed. The homolateral draining hilar lymph nodes show extensive enlargement and massive caseation. Numerous large progressive caseous tubercles of hematogenous origin are present in both lungs. The kidneys, pleura, and knee joint show rapidly progressive caseous lesions. Reproduced with permission from reference 2.
Citation:
Dannenberg, Jr. A.
2006.
Natural Airborne Infection,
p 215-229.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch12
References
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Dannenberg, A. M., Jr.,, M. S. Burstone,, P. C. Walter, and, J. W. Kinsley. 1963. A histochemical study of phagocytic and enzymatic functions of rabbit mononuclear and polymorphonuclear exu-date cells and alveolar macrophages. I. Survey and quantitation of enzymes, and states of cellular activation. J. Cell Biol. 17: 465– 486.
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Henderson, H. J.,, A. M. Dannenberg, Jr., and, M. B. Lurie. 1963. Phagocytosis of tubercle bacilli by rabbit pulmonary alveolar macrophages and its relation to native resistance to tuberculosis. J. Immunol. 91: 553– 556.
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Lurie, M. B. 1932. The correlation between the histological changes and the fate of living tubercle bacilli in the organs of tuberculous rabbits. J. Exp. Med. 55: 31– 54.
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Dannenberg, A. M., Jr.,, O. T. Meyer,, J. R. Esterly, and, T. Kambara. 1968. The local nature of immunity in tuberculosis, illustrated histochemically in dermal BCG lesions. J. Immunol. 100: 931– 941.
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Dannenberg, A. M., Jr. 1968. Cellular hyper-sensitivity and cellular immunity in the pathogenesis of tuberculosis: specificity, systemic and local nature, and associated macrophage enzymes. Bacteriol. Rev. 32: 85– 102.
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Ando, M.,, A. M. Dannenberg, Jr.,, M. Sugimoto, and, B. S. Tepper. 1977. Histochemical studies relating the activation of macrophages to the intracellular destruction of tubercle bacilli. Am. J. Pathol. 86: 623– 634.
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Rich, A. R. 1951. The Pathogenesis of Tuberculosis, 2nd ed. Charles C Thomas Publisher, Springfield, Ill.
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Dannenberg, A. M., Jr., and, J. F. Tomashefski, Jr. 1998. Pathogenesis of pulmonary tuberculosis, p. 2447– 2471. 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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Riley, R. L.,, C. C. Mills,, F. O’Grady,, L. U. Sultan,, F. Wittstadt, and, D. N. Shivpuri. 1962. Infectiousness of air from a tuberculosis ward. Ultra-violet irradiation of infected air: comparative infectiousness of different patients. Am. Rev. Respir. Dis. 85: 511– 525.
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Lurie, M. B.,, S. Abramson, and, A. G. Heppleston. 1952. On the response of genetically resistant and susceptible rabbits to the quantitative inhalation of human-type tubercle bacilli and the nature of resistance to tuberculosis. J. Exp. Med. 95: 119– 134.
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Dannenberg, A. M., Jr.,, W. R. Bishai,, N. Parrish,, R. Ruiz,, W. Johnson,, B. C. Zook,, J. W. Boles, and, L. M. Pitt. 2001. Efficacies of BCG and vole bacillus ( Mycobacterium microti) vaccines in preventing clinically apparent pulmonary tuberculosis in rabbits: a preliminary report. Vaccine 19: 796– 800.
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Tables
Natural Airborne Infection
Citation:
Dannenberg, Jr. A.
2006.
Natural Airborne Infection,
p 215-229.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch12
/content/10.1128/9781555815684.ch12.ch12tab01
TABLE 1
Resistance to the establishment of tuberculosis and resistance to its progress with a natural airborne contagion of virulent bovine-type tubercle bacilli
a
TABLE 1
Resistance to the establishment of tuberculosis and resistance to its progress with a natural airborne contagion of virulent bovine-type tubercle bacilli a
Citation:
Dannenberg, Jr. A.
2006.
Natural Airborne Infection,
p 215-229.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch12
/content/10.1128/9781555815684.ch12.ch12tab02
TABLE 2
Effect of the intensity of natural airborne contagion on tuberculosis acquired by rabbits of various levels of natural resistance
a
TABLE 2
Effect of the intensity of natural airborne contagion on tuberculosis acquired by rabbits of various levels of natural resistance a
Citation:
Dannenberg, Jr. A.
2006.
Natural Airborne Infection,
p 215-229.
In
Pathogenesis of Human Pulmonary Tuberculosis.
ASM Press, Washington, DC.
doi: 10.1128/9781555815684.ch12