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Chapter 18 : Chronic Bacterial Pathogens: Mechanisms of Persistence

Authors: Mariana X. Byndloss1, Renee M. Tsolis2
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Affiliations: 1: Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, Sacramento, CA 95817; 2: Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, Sacramento, CA 95817
Content Type: Monograph
Publication Year: 2016
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Abstract:

Persistent bacterial infections such as brucellosis and typhoid fever are characterized by a long incubation period that leads to chronic, sometimes lifelong, debilitating disease with serious clinical manifestations ( ). Therefore, chronic bacterial diseases have a significant impact on public health, due to the utilization of resources for long-term treatment of patients ( ). Additionally, chronic infections affect the ability of the ill to provide for their families, resulting in a significant socioeconomic burden in affected countries ( ).

Citation: Byndloss M, Tsolis R. 2016. Chronic Bacterial Pathogens: Mechanisms of Persistence, p 515-528. In Kudva I, Cornick N, Plummer P, Zhang Q, Nicholson T, Bannantine J, Bellaire B (ed),

Virulence Mechanisms of Bacterial Pathogens, Fifth Edition

. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.VMBF-0020-2015
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Chronic Bacterial Pathogens: Mechanisms of Persistence
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Citation: Byndloss M, Tsolis R. 2016. Chronic Bacterial Pathogens: Mechanisms of Persistence, p 515-528. In Kudva I, Cornick N, Plummer P, Zhang Q, Nicholson T, Bannantine J, Bellaire B (ed),

Virulence Mechanisms of Bacterial Pathogens, Fifth Edition

. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.VMBF-0020-2015
/content/10.1128/9781555819286.chap18.fig18-1
Figure 1

Microgranuloma formation in spleen of -infected mice. Fully developed microgranuloma (black arrow) at 30 days postinfection. Granuloma is composed of epithelioid macrophages surrounded by lymphocytes. Hematoxylin and eosin stain, 400x magnification. Immunolabeling of within microgranulomas in spleen at 30 days postinfection. Note the presence of bacteria inside macrophages (black arrow). Immunohistochemistry, 400x magnification.

10.1128/9781555819286/fig18-1_thmb.gif
10.1128/9781555819286/fig18-1.gif
Image of Figure 1
Figure 1

Microgranuloma formation in spleen of -infected mice. Fully developed microgranuloma (black arrow) at 30 days postinfection. Granuloma is composed of epithelioid macrophages surrounded by lymphocytes. Hematoxylin and eosin stain, 400x magnification. Immunolabeling of within microgranulomas in spleen at 30 days postinfection. Note the presence of bacteria inside macrophages (black arrow). Immunohistochemistry, 400x magnification.

Citation: Byndloss M, Tsolis R. 2016. Chronic Bacterial Pathogens: Mechanisms of Persistence, p 515-528. In Kudva I, Cornick N, Plummer P, Zhang Q, Nicholson T, Bannantine J, Bellaire B (ed),

Virulence Mechanisms of Bacterial Pathogens, Fifth Edition

. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.VMBF-0020-2015
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Figure 2

Macrophage metabolism during infection. During the acute phase of infection (left), interferon-γ (IFN-γ) is transiently produced, resulting in a predominance of classically activated macrophages (CAMs). In these cells, oxygen is consumed by NADPH oxidase (Phox) to generate superoxide radicals, and energy is produced by anaerobic glycolysis. Since anaerobic glycolysis yields only 2ATP, the cell has to consume more glucose to meet its energy needs. In contrast, during the chronic infection phase (right), IFN-γ is absent, but interleukin-4 (IL-4) and IL-13 signal via STAT6 to induce the alternatively activated macrophage (AAM) phenotype. Activation of STAT6 increases the expression and activation of peroxisome proliferator-activated receptor gamma (PPARγ), which in turn upregulates genes controlling β-oxidation, thereby shifting cellular physiology toward oxidative pathways. As a result, less glucose is consumed for cellular metabolism, and the intracellular glucose concentration increases. This glucose can be utilized by for growth within infected macrophages.

10.1128/9781555819286/fig18-2_thmb.gif
10.1128/9781555819286/fig18-2.gif
Image of Figure 2
Figure 2

Macrophage metabolism during infection. During the acute phase of infection (left), interferon-γ (IFN-γ) is transiently produced, resulting in a predominance of classically activated macrophages (CAMs). In these cells, oxygen is consumed by NADPH oxidase (Phox) to generate superoxide radicals, and energy is produced by anaerobic glycolysis. Since anaerobic glycolysis yields only 2ATP, the cell has to consume more glucose to meet its energy needs. In contrast, during the chronic infection phase (right), IFN-γ is absent, but interleukin-4 (IL-4) and IL-13 signal via STAT6 to induce the alternatively activated macrophage (AAM) phenotype. Activation of STAT6 increases the expression and activation of peroxisome proliferator-activated receptor gamma (PPARγ), which in turn upregulates genes controlling β-oxidation, thereby shifting cellular physiology toward oxidative pathways. As a result, less glucose is consumed for cellular metabolism, and the intracellular glucose concentration increases. This glucose can be utilized by for growth within infected macrophages.

Citation: Byndloss M, Tsolis R. 2016. Chronic Bacterial Pathogens: Mechanisms of Persistence, p 515-528. In Kudva I, Cornick N, Plummer P, Zhang Q, Nicholson T, Bannantine J, Bellaire B (ed),

Virulence Mechanisms of Bacterial Pathogens, Fifth Edition

. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.VMBF-0020-2015
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Tables

Chronic Bacterial Pathogens: Mechanisms of Persistence
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Citation: Byndloss M, Tsolis R. 2016. Chronic Bacterial Pathogens: Mechanisms of Persistence, p 515-528. In Kudva I, Cornick N, Plummer P, Zhang Q, Nicholson T, Bannantine J, Bellaire B (ed),

Virulence Mechanisms of Bacterial Pathogens, Fifth Edition

. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.VMBF-0020-2015
/content/10.1128/9781555819286.chap18.tab18-1
TABLE 1

Strategies for persistence

Generic image for table
TABLE 1

Strategies for persistence

Citation: Byndloss M, Tsolis R. 2016. Chronic Bacterial Pathogens: Mechanisms of Persistence, p 515-528. In Kudva I, Cornick N, Plummer P, Zhang Q, Nicholson T, Bannantine J, Bellaire B (ed),

Virulence Mechanisms of Bacterial Pathogens, Fifth Edition

. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.VMBF-0020-2015

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