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Chapter 2 : Bacterial Pathogenesis

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Bacterial Pathogenesis, Page 1 of 2

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Abstract:

This chapter serves as an introduction of some of the most relevant points and highlights features that are particularly essential for an understanding of bacterial invasion of eukaryotic cells, immunity to extracellular and intracellular bacteria, evasion of immune mechanisms by extracellular and intracellular bacteria, antibacterial mechanisms of action, and bacterial resistance to antibacterial agents. The chapter provides definitions of some important terms in bacterial pathogenesis such as bacterial pathogen, virulence factors, chaperone, lectins and enterotoxins. Adhesins are assembled into pili or fimbriae that extend from the bacterial surface. Alternatively, the adhesins are directly associated with the microbial cell surface. These adhesions can be performed by the afimbrial adhesins (also called nonfimbrial adhesins). The observation that culture supernatant free from bacteria fully reproduced the symptoms of diseases such as diphtheria, tetanus, cholera, and botulism led to the conclusion that in these instances, bacterial toxins were the only factors needed by bacteria to cause a disease. In the chapter, various aspects of bacterial pathogenicity have been presented from the point of view that these microorganisms exist as isolated single cells suspended in an aqueous environment (i.e., the planktonic mode); however, most in vivo populations of bacteria grow as adherent bacterial biofilms. Inhibition of virulence factors is one potential therapeutic strategy in the search for novel targets for new antivirulence drugs such as vaccines and inhibitors of bacterial adhesion and of LPS synthesis.

Citation: Mascaretti O. 2003. Bacterial Pathogenesis, p 33-42. In Bacteria versus Antibacterial Agents. ASM Press, Washington, DC. doi: 10.1128/9781555817794.ch2
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Figures

Image of Figure 2.2
Figure 2.2

Model of P-pilus biogenesis and PapG recognition of three Gal-(α1→4)-Galcontaining receptors. Reprinted from S. J. Hultgren, S. Abraham, M. Caparon, P. Falk, J. W. St Geme, and S. Normark, Cell 73:887–901, 1993, with permission from the publisher.

Citation: Mascaretti O. 2003. Bacterial Pathogenesis, p 33-42. In Bacteria versus Antibacterial Agents. ASM Press, Washington, DC. doi: 10.1128/9781555817794.ch2
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Image of Figure 2.3
Figure 2.3

Saccharides of the globoseries glycolipids.

Citation: Mascaretti O. 2003. Bacterial Pathogenesis, p 33-42. In Bacteria versus Antibacterial Agents. ASM Press, Washington, DC. doi: 10.1128/9781555817794.ch2
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Image of Figure 2.1
Figure 2.1

Diagrammatic representation of the steps in bacterial invasion of a human cell.

Citation: Mascaretti O. 2003. Bacterial Pathogenesis, p 33-42. In Bacteria versus Antibacterial Agents. ASM Press, Washington, DC. doi: 10.1128/9781555817794.ch2
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Figure 2.4

Schematic representation of the four groups of bacterial toxins. Reprinted from P. Cossart, P. Boquet, S. Normark, and R. Rappuoli (ed.), Cellular Microbiology (ASM Press, Washington, D.C., 2000), with permission from the American Society for Microbiology.

Citation: Mascaretti O. 2003. Bacterial Pathogenesis, p 33-42. In Bacteria versus Antibacterial Agents. ASM Press, Washington, DC. doi: 10.1128/9781555817794.ch2
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References

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Tables

Generic image for table
Table 2.1

Selected examples of bacterial pathogenesis and their location with respect to eukaryotic cells a

Citation: Mascaretti O. 2003. Bacterial Pathogenesis, p 33-42. In Bacteria versus Antibacterial Agents. ASM Press, Washington, DC. doi: 10.1128/9781555817794.ch2
Generic image for table
Table 2.2

Some examples of common diseases caused by bacterial toxins a

Citation: Mascaretti O. 2003. Bacterial Pathogenesis, p 33-42. In Bacteria versus Antibacterial Agents. ASM Press, Washington, DC. doi: 10.1128/9781555817794.ch2

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