Chapter 20 : Abscesses

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This chapter examines (i) the predisposing conditions that lead to abscess formation, (ii) the bacteria that predominate in various abscesses and their contribution to abscess formation, and (iii) the host response to the invading organisms and why that response is usually ineffective in eradicating the infection. The formation of intra-abdominal abscesses is used throughout the chapter as a model. Due to the prevalence of intra-abdominal abscesses, much research has been conducted to examine the molecular interactions between the invading microorganisms and the host that lead to abscess formation. The chapter discusses other examples of abscesses such as renal, brain, lung and skin. Intra-abdominal infection is caused by the leakage of gastrointestinal contents laden with bacteria. Following bacterial spillage, the majority of organisms are removed by the diaphragmatic lymphatics. The best-studied system for understanding the molecular interactions between host and microorganism that lead to abscess formation is the induction of intra-abdominal abscesses by the capsular polysaccharide complex (CPC) of . Studies in which the purified capsular polysaccharide from induced abscesses in the absence of viable organisms demonstrated the importance of this virulence factor in abscess formation. The authors propose that abscessogenic bacteria produce the structural components that induce the formation of abscesses because these structures serve an important function in the organisms' normal niche rather than serving solely as a mechanism to enhance their persistence as pathogens.

Citation: Comstock L, Tzianabos A. 2000. Abscesses, p 397-408. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch20
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Image of FIGURE 1

Proposed model for the initiation of intra-abdominal-abscess formation by CPC. The CPC binds to the peritoneal mesothelium, allowing bacterial attachment. The CPC also stimulates various immune cells to secrete IL-8 and tumor necrosis factor alpha. These factors have been shown to upregulate the expression of ICAM-1 on the mesothehal cells and recruit and activate PMNs. The upregulation of ICAM-1 allows for enhanced binding of PMNs to the mesothelium. This localization of bacteria and immune cells is necessary for the development of an abscess. PMΦ, peritoneal macrophage.

Citation: Comstock L, Tzianabos A. 2000. Abscesses, p 397-408. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch20
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