Abstract
Vibrio vulnificus populates coastal waters around the world, where it exists freely or becomes concentrated in filter feeding mollusks. It also causes rapid and life-threatening sepsis and wound infections in humans. Of its many virulence factors, it is the V. vulnificus capsule, composed of capsular polysaccharide (CPS), that plays a critical role in evasion of the host innate immune system by conferring antiphagocytic ability and resistance to complement-mediated killing. CPS may also provoke a portion of the host inflammatory cytokine response to this bacterium. CPS production is biochemically and genetically diverse among strains of V. vulnificus, and the carbohydrate diversity of CPS is likely affected by horizontal gene transfer events that result in new combinations of biosynthetic genes. Phase variation between virulent encapsulated opaque colonial variants and attenuated translucent colonial variants, which have little or no CPS, is a common phenotype among strains of this species. One mechanism for generating acapsular variants likely involves homologous recombination between repeat sequences flanking the wzb phosphatase gene within the Group 1 CPS biosynthetic and transport operon. A considerable number of environmental, genetic, and regulatory factors have now been identified that affect CPS gene expression and CPS production in this pathogen.
Highlights
Vibrio vulnificus is a natural inhabitant of estuarine and other coastal marine environments where it exists free living or becomes concentrated in filter-feeding molluscan shellfish, such as oysters
nuclear magnetic resonance (NMR) and high-performance anion-exchange chromatography (HPAEC) analyses of purified capsular polysaccharide (CPS) from a subset of strains revealed most had distinct sugar composition and structure [19]. Such preliminary studies led to the development of a chemotyping method for V. vulnificus CPS, which involved HPAEC analysis coupled with electrochemical detection and computer automation
As with other Gram-negative pathogens, outer membrane vesicles (OMVs) may contribute to pathogenicity of V. vulnificus, a hypothesis supported by the finding that OMVs of this species induced death of epithelial cells by delivery of the cytolysin-hemolysin VvhA [29]
Summary
Vibrio vulnificus is a natural inhabitant of estuarine and other coastal marine environments where it exists free living or becomes concentrated in filter-feeding molluscan shellfish, such as oysters. The increased proportion of stained cells correlated with increased virulence in mice and to resistance to the bacteriocidal action of normal human serum (NHS). These authors referred to this surface polysaccharide as a capsule [8]. Compared to the opaque clinical isolate MO6-24/O (Table 1), two translucent transposon mutant derivatives appeared acapsular in carbohydrate staining procedures and were attenuated by several orders of magnitude for virulence in mice [11]. A spontaneous translucent variant of MO6-24/O, strain MO6-24/T (Table 1), which showed reduced CPS on its cell surface, was attenuated for virulence though not to the same magnitude as the acapsular transposon mutants. Attenuation of virulence was a common property seen for acapsular transposon mutants of V. vulnificus in other studies as well [12,13,14]
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