Answers are grounded in this paper and cite their sources.
Bacterial capsules, in general, are composed of polypeptides or polysaccharides and have been implicated in the virulence of a number of bacterial pathogens [1]. Neisseria meningitidis does not elaborate a capsule which can be observed readily as a cellular organelle, however, the various serogroups do elaborate group-specific polysaccharide [2]. This polysaccharide is a homopolymer of N-acetylneuraminic acid linked a (2 ~ 8), in the case of the serogroup B strains. Rough and smooth variants from a given strain have been observed and it has been suggested that the presence of polysaccharide on smooth variants could be associated with virulence [3]. However, the biosynthetic pathways for polysaccharide production, their regulation, and the role that polysaccharide plays in virulence of N. meningitidis remain obscure. Spontaneous isogenic mutants of serogroup B N. meningitidis strain M986, which were deficient in polysaccharide production and release, were examined for their virulence for mice. The loss of polysaccharide biosynthetic capability in the mutants resulted in a dramatic loss in virulence for mice, which was regained upon reversion to the wild-type phenotype.
No takes yet. Share an insight, caveat, or question.
Masson et al. (1982) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: