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Chapter 8 : Microvascular Density in Tuberculous Lesions

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Abstract:

The microvasculature plays an important role in the pathogenesis of tuberculous lesions. Blood vessels bring in the host defense cells, and vascular thrombosis is a major cause of caseous necrosis. This chapter describes the study of microvascular density in tissue sections of developing and healing dermal BCG lesions and in 48-h dermal tuberculin reactions. Rabbits were placed under deep terminal anesthesia, and their entire vasculature was perfused (via the aorta) with a gelatin-colloidal carbon suspension. Then, serial 250-µm thick tissue sections of the dermal BCG lesions were prepared, and the total length of the microvasculature in the whole BCG lesion was calculated from measurements made with a microscope containing an ocular grid. By 3 days, the vascular density in BCG lesions had increased to roughly 1.6 times that found in normal skin. It remained at this level for at least 6 to 7 weeks. The vascular density in tuberculin reactions showed a similar increase. It was concluded that the local microvasculature increases relatively little during the course of this slowly healing infection. A greater blood flow through existing capillaries evidently provides most of the nourishment needed by the infiltrating cells. These studies also demonstrated that microvascular thrombosis is a major cause of the caseous necrosis that occurs during the course of this disease.

Citation: Dannenberg, Jr. A. 2006. Microvascular Density in Tuberculous Lesions, p 161-169. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch8
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Figures

Image of FIGURE 1
FIGURE 1

Capillary density in the BCG lesions of Experiment II and in the normal skin nearby. In this experiment, the skin of each of the six rabbits contained 3-, 15-, 35-, and 49-day BCG lesions when they were perfused with the gelatin-colloidal carbon suspension. The means and their standard errors are depicted.

The capillary density of BCG lesions (in lengths per mm2) was increased as early as 3 days. This density was highest at 15 days, when tuberculin sensitivity was developing, and decreased relatively little as the lesions healed. Reproduced with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Microvascular Density in Tuberculous Lesions, p 161-169. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch8
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Image of FIGURE 2
FIGURE 2

Dermal BCG lesion, 3 days of age. An increased number of vessels are present in the subpapillary vascular plexus surrounding the hair follicles (sometimes called the peritrichous plexus). In the center and on the right of the photograph, the hair follicles were damaged by microabscesses developing between them. In the lower part of the photograph, the deep cutaneous vascular plexus is prominent. It supplies the intrinsic muscles of the skin and helps regulate body heat. Gelatin-colloidal carbon perfusion, counterstained with hematoxylin. Magnification, ×16. Reproduced with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Microvascular Density in Tuberculous Lesions, p 161-169. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch8
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Image of FIGURE 3
FIGURE 3

Dermal BCG lesion, 15 days of age, cut near the edge of the necrotic center. At this location, the vessels of the subpapillary vascular plexus form a rich anastomosing network with the vessels of the deep cutaneous vascular plexus. Magnification, ×23.

We used an ocular grid to count (at 44× magnification) the lengths of capillaries within grid squares, each measuring 0.45 by 0.45 mm. In the grid square shown centrally in the inset, the 23 pieces of microvasculature totaled 8.3 grid widths. Gelatin-colloidal carbon perfusion, counterstained with hematoxylin. Magnification, ×3.7. Reproduced with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Microvascular Density in Tuberculous Lesions, p 161-169. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch8
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Image of FIGURE 4
FIGURE 4

Dermal BCG lesion, 35 days of age. This section was cut from the outer regions of the caseous necrotic center (but more central than that in Fig. 3). Here, the cellular infiltrate is not completely necrotic, and the capillaries are still patent or only partly thrombosed. Gelatin-colloidal carbon perfusion, counterstained with hematoxylin. Magnification, ×22. Reproduced with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Microvascular Density in Tuberculous Lesions, p 161-169. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch8
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Image of FIGURE 5
FIGURE 5

Dermal BCG lesion, about 21 days of age. This section was cut through the caseous necrotic center. The intact epidermis is shown above. The liquefied caseous necrotic center is shown below. Part of this center fell out during the preparation of this tissue section.

Note that in the necrotic area the capillaries were not perfused with carbon, which indicates that thrombosis and the resulting ischemia are major causes of tissue necrosis. Gelatin-colloidal carbon perfusion, counterstained with hematoxylin. Magnification, ×23.

Citation: Dannenberg, Jr. A. 2006. Microvascular Density in Tuberculous Lesions, p 161-169. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch8
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Image of FIGURE 6
FIGURE 6

Dermal BCG lesion, 15 days of age, with ulceration and discharge of some of the necrotic material. The vascular plexus at the base of the ulcer is richly developed. Some leakage of the colloidal carbon into the necrotic area is evident. Gelatin-colloidal carbon perfusion, counterstained with hematoxylin. Magnification, ×20. Reproduced with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Microvascular Density in Tuberculous Lesions, p 161-169. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch8
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Image of FIGURE 7
FIGURE 7

Healing dermal BCG lesion, 49 days of age. The total vascular network has decreased, and most of the necrotic material has been discharged or absorbed. Fibroblasts, producing new collagen fibers and ground substance, are present. The intrinsic muscles of the skin (the panniculus carnosis) can be seen at the bottom of the photograph. Gelatin-colloidal carbon perfusion, counterstained with hematoxylin. Magnification, ×17. Reproduced with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Microvascular Density in Tuberculous Lesions, p 161-169. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch8
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Image of FIGURE 8
FIGURE 8

A positive 2-day tuberculin reaction. The subpapillary vascular plexus surrounding the hair follicles has proliferated, but no necrosis is present. Gelatin-colloidal carbon perfusion, counterstained with hematoxylin. Magnification, ×23. Reproduced with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Microvascular Density in Tuberculous Lesions, p 161-169. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch8
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References

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