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Vibrio vulnificus, a marine bacerium, causes serious wound
infection and septicemia with a high mortality rate in persons
with underlying diseases that result in immunocompromised
conditions and/or high serum iron levels, such as chronic
cirrohosis and hemochromatosis. It is important to understand
the pathogenesis of this bacterium in order to be able to
properly prevent and treat its infectious diseases. Most V.
vulnificus are encapsulated. To study the role of the capsular
polysaccharide in the pathogenesis of this microorganism,
spontaneous or U.V mutagenized translucent (morphology of
acapsular strains) mutants were isolated from three clinical
isolates and characterized for their virulence in mice and
properties relating to pathogenesis. It was shown that the LD50
of acapsular mulants is higher than their parental strains by 3
logs or more, either by intraperitoneal injection or force
feeding, in the mice pretreated with iron or CCl4. This result
indicates that the capsule is an important virulence factor of
V. vulnificus in susceptible hosts. The growth rates of
acapsular mutants were similar to their parental strains, in
either rich or iron-limitng media. Adherence of the acapsular
mutans to an epithelial cell line HEp-2 was less efficient, but
the hemagglutination ability was slightly higher than their
parental strains indicating that the capsule but not the
hemagglutinin(s) is involved in adherence to the epithelial
cells. The ability of the acapsular mutants to resist killing
by human serum was also reduced in two of the three strains.
The third one, although exhibited equal resistance to human
serum with its parental strain, was rapidly cleared from the
blood of an infected mouse, suggesting that the capsule may
protect the bacteria from other host defense mechanisms, such
as phagocytosis. In another study, we tried to develop
transposon mutagenesis in V. vulnificus. We used two transposon
(Tn5 or TnphoA)-containing plasmids to mutagenize this
bacterium.
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