Chapter 1 : Overview of the Bacterial Pathogens

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This chapter summarizes the most important findings on bacterial virulence factors and mechanisms of infection. Gastric infection by the gram-negative bacterium is associated with a number of clinical outcomes including gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue lymphoma, and adenocarcinoma of the stomach. A number of gram-negative pathogenic bacteria have evolved specialized systems for the delivery of virulence factors directly into the host cytosol. One such system is the type III secretion system, in which bacterial proteins lacking a typical signal sequence are secreted directly from the bacteria into the cytosol of infected cells. Recent studies of the role of the locus for enterocyte effacement (LEE)-encoded secreted proteins in enteropathogenic (EPEC) pathogenesis have demonstrated the potential involvement of EspA, EspB, and EspD as structural components of the secretion apparatus. The invasion plasmid antigens (Ipa proteins) orchestrate the cytoskeletal rearrangements necessary for bacterial entry. These proteins also direct many of the other virulence properties of , including escape from the phagocytic vacuole and induction of apoptosis of macrophages and resulting inflammation. Apoptosis is normally viewed as an immunologically silent cell death process unaccompanied by inflammation. However, this is clearly not the case for the caspase-1-dependent apoptosis induced by . Obligate intracellular bacterial pathogens like , , and species are less well characterized than facultative intracellular pathogens. Finally, the chapter discusses recent progress in understanding the cell biology of infections.

Citation: Kuhn M, Goebel W, Philpott D, Sansonetti P. 2002. Overview of the Bacterial Pathogens, p 3-23. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch1

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Figure 1

Model of type IV-mediated secretion of the virulence protein, CagA, into the eukaryotic cytosol by . (A and B) CagA is translocated into the host cytosol by the type IV secretion system (A), where it becomes phosphorylated on tyrosine residues by a host tyrosine kinase (B). (C) Phosphorylated CagA triggers cytoskeletal rearrangements, leading to pedestal formation. Reproduced from with permission of the National Academy of Sciences.

Citation: Kuhn M, Goebel W, Philpott D, Sansonetti P. 2002. Overview of the Bacterial Pathogens, p 3-23. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch1
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Image of Figure 2
Figure 2

Electron micrograph of the type III secretion apparatus from . A negative stain of osmotically shocked is shown. Arrows point to type III secretons on the surface of the bacteria. The inset shows an individual secreton at higher magnification, revealing the tripartite nature of the apparatus: needle, neck, and bulb domains are clearly visible. Adapted from with permission of The Rockefeller University Press.

Citation: Kuhn M, Goebel W, Philpott D, Sansonetti P. 2002. Overview of the Bacterial Pathogens, p 3-23. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch1
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Figure 3

The intracellular life cycle (A) and virulence gene cluster (B) of (A) enters mammalian cells through interaction of the surface proteins InlA, InlB, and p60 with mammalian cell receptors. The phagosome is lysed by the action of the pore-forming cytolysin LLO and a phosphatidylinositol-specific phospholipase C (PlcA), and the cytosolic bacteria induce the polymerization of host cell actin filaments by their surface protein ActA. Moving bacteria induce the formation of protrusions, which invade neighboring cells. The secondary vacuole is lysed by the action of LLO and a lecithinase (PlcB). (B) Virulence gene cluster, containing the genes (encoding the positive regulatory factor A), (PlcA), (LLO), (encoding a metalloprotease involved in PlcB maturation), (ActA), and (PlcB). Reproduced from with permission of Plenum Press.

Citation: Kuhn M, Goebel W, Philpott D, Sansonetti P. 2002. Overview of the Bacterial Pathogens, p 3-23. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch1
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Figure 4

phagosome maturation arrest. Accumulation of Rab5 and TfR demonstrates the early endosomal characteristic of the vacuole. The late endosomal markers Rab7, Lamp-1, Lamp-2, and M6PR are largely absent from the vacuole. Delivery of the proton pumping ATPase to the vacuole is also inhibited. Rab proteins control membrane trafficking within endosomal compartments. Rab5, endocytosis and fusion between early endosomes; Rab7, late endosome and mature phagosomes; Mtb, ; TfR, transferrin receptor; Lamp-1/2, glycoproteins; M6PR, mannose-6-phosphate receptor.

Citation: Kuhn M, Goebel W, Philpott D, Sansonetti P. 2002. Overview of the Bacterial Pathogens, p 3-23. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch1
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Figure 5

Model for the molecular basis of interaction with Schwann cells. binds to the LNα2G domain of laminin-2. α-Dystroglycan forms a bridge between laminin-2 and the membrane protein β-dystroglycan, which could act as a signaling receptor by its connections to the actin cytoskeleton. Reproduced from with permission of Elsevier Science.

Citation: Kuhn M, Goebel W, Philpott D, Sansonetti P. 2002. Overview of the Bacterial Pathogens, p 3-23. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch1
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Figure 6

Diagram of the developmental cycle of . The small, dark structures represent infectious elementary bodies (EBs). The larger, grey structures represent replicative reticulate bodies (RBs). Reproduced from with permission of Elsevier Science.

Citation: Kuhn M, Goebel W, Philpott D, Sansonetti P. 2002. Overview of the Bacterial Pathogens, p 3-23. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch1
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Generic image for table
Table 1

Some characteristics of gram-negative human pathogens

Citation: Kuhn M, Goebel W, Philpott D, Sansonetti P. 2002. Overview of the Bacterial Pathogens, p 3-23. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch1
Generic image for table
Table 2

Some characteristics of gram-positive human pathogens

Citation: Kuhn M, Goebel W, Philpott D, Sansonetti P. 2002. Overview of the Bacterial Pathogens, p 3-23. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch1
Generic image for table
Table 3

Some characteristics of spirochetal human pathogens

Citation: Kuhn M, Goebel W, Philpott D, Sansonetti P. 2002. Overview of the Bacterial Pathogens, p 3-23. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch1

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