Genomic Structure of Capsular Determinants

Abstract

The production of an extracellular polysaccharide capsule is a common feature of many bacteria (Whitfield and Valvano 1993). The capsule, which often constitutes the outermost layer of the cell, mediates the interaction between the bacterium and its immediate environment and plays a crucial role in the survival of bacteria in hostile environments. One such environment is the human host, where interactions between the capsule and the host’s immune system may be vital in deciding the outcome of an infection (Moxon and Kroll 1990). In the absence of specific antibody, a capsule offers protection against the nonspecific arm of the host’s immune system by conferring increased resistance to complement-mediated killing and complement-mediated opsonophagocytosis (Michalek et al. 1988; Moxon and Kroll 1990). A small set of capsular polysaccharides which resemble polysaccharide moieties present in host tissue are poorly immunogenic (Finne 1982; Lindahl et al. 1994). The Escherichia coli K1 and Neisseria meningitidis serogroup B capsules, both of which contain N-acetyl-neuraminic acid and the heparin-like E. coli K5 capsule, all elicit a poor antibody response in infected individuals (Jennings 1990) and confer some measure of resistance to the host’s adaptive humoral response. Aside from direct interactions with the host’s immune system, capsules may promote the formation of biofilms and the colonisation of a variety of ecological niches, including indwelling catheters, prostheses and the formation of alginate-rich biofilms in the lungs of cystic fibrosis patients (Roberts 1995). In such instances the polysaccharide may present a permeability barrier to antibiotics and hinder the effective eradication of the bacteria (Costerton et al. 1999).