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1 V. vulnificus infections were reported to the Centers fo
2 V. vulnificus inoculated into iron dextran-treated mice
3 V. vulnificus is a gram-negative bacterium, considered o
4 V. vulnificus is able to use host iron sources such as h
5 V. vulnificus strains containing pGTR902 were inoculated
6 V. vulnificus-associated diseases are noted for the rapi
8 the rtxA1 gene that encodes MARTX(Vv) in 40 V. vulnificus Biotype 1 strains and found four distinct
9 In a survey of the 16S rRNA genotype in 67 V. vulnificus human clinical and nonclinical strains, we
11 thal factor or when naturally delivered as a V. vulnificus MARTX toxin led to loss of mitochondrial m
12 is study, we have cloned and characterized a V. vulnificus type IV pilin (PilA) that shares extensive
13 lated outer membrane protein purified from a V. vulnificus fur mutant had 53% homology with the first
14 Using TnphoA mutagenesis, we identified a V. vulnificus CPS locus, which included an upstream ops
15 sults discussed here confirmed homology of a V. vulnificus CPS locus to the group 1 CPS operon in Esc
18 bacteriophages as therapeutic agents against V. vulnificus in an iron-dextran-treated mouse model of
19 hat estrogen is providing protection against V. vulnificus lipopolysaccharide-induced endotoxic shock
23 antibiotic-resistant V. parahaemolyticus and V. vulnificus, including V. parahaemolyticus pandemic st
24 ains), V. parahaemolyticus (30 strains), and V. vulnificus (10 strains) to determine the accuracy of
27 t hospitalizations and deaths were caused by V. vulnificus infection, and most patients were white me
28 inflammation-mediated septic shock caused by V. vulnificus is strongly associated with liver disease,
32 septicemia in humans, secretes a PFT called V. vulnificus hemolysin (VVH), which contains a single C
33 hages were effective against three different V. vulnificus strains with various degrees of virulence,
35 road exopeptidase activity which may enhance V. vulnificus invasiveness by altering peptides involved
36 tant, containing the transposon and flanking V. vulnificus DNA was cloned, and a probe complementary
39 n of fatty acid metabolism are essential for V. vulnificus to be able to cause disease in mammalian h
41 Using the rat, we have developed a model for V. vulnificus endotoxic shock that mimics the sexually d
43 , TcdA, TcnA, and TcsL; putative toxins from V. vulnificus, Yersinia sp., Photorhabdus sp., and Xenor
44 ransport genes are regulated by iron, and in V. vulnificus, transcriptional regulation by iron depend
46 hat a wide variety of capsular carbotypes in V. vulnificus may be readily distinguished by the HPAE f
47 ociated with both CPS and rEPS expression in V. vulnificus, designated the wcr (capsular and rugose p
49 that the HlyU protein, a virulence factor in V. vulnificus CMCP6, up-regulates the expression of VV20
52 and the extracytoplasmic stress response in V. vulnificus, mutants with defined mutations in rseB an
55 onfirm that phase variation and virulence in V. vulnificus correlate with the amount of CPS expressed
57 experiments in a murine model of intravenous V. vulnificus infection demonstrated that expression of
58 ences in virulence among naturally occurring V. vulnificus can be explained by diverse abilities to r
60 Inactivation of pilA reduces the ability of V. vulnificus to form biofilms and significantly decreas
61 ed a genome-wide transcriptional analysis of V. vulnificus growing at three different iron concentrat
62 ar typing systems have shown associations of V. vulnificus genotypes and the environmental or clinica
66 cutaneously with 10 times the lethal dose of V. vulnificus and injected intravenously, either simulta
67 2 X 10(9) colony-forming unit (high dose) of V. vulnificus was administered through a mini-laparotomy
69 dicate that an important virulence factor of V. vulnificus is undergoing significant genetic rearrang
72 ines the growing international importance of V. vulnificus, particularly in the context of coastal wa
73 sertion mutagenesis in a clinical isolate of V. vulnificus to find genes necessary for virulence, and
74 olved to facilitate the aquatic lifestyle of V. vulnificus but that their emergence also resulted in
75 les are present on the lipopolysaccharide of V. vulnificus, are required for full motility and biofil
76 ge of human-derived peptides by PGI-LysAP of V. vulnificus using three approaches: (i) a quantitative
77 oculated iron dextran-treated mouse model of V. vulnificus disease, was hypersensitive to the fatty a
80 We previously constructed a fur mutant of V. vulnificus which constitutively expresses at least tw
82 variants and genetically defined mutants of V. vulnificus M06-24/O was examined by using a CPS-speci
86 hich may contribute both to pathogenicity of V. vulnificus and to its survival under adverse environm
87 pulsed-field gel electrophoresis profiles of V. vulnificus strains isolated from blood and oysters as
93 saccharide of a related pathogenic strain of V. vulnificus (MO6-24) the structure of which was recent
94 accharide purified from a virulent strain of V. vulnificus 6353 did not show cross reactivity with an
97 pimerase is common to at least 10 strains of V. vulnificus that each express a serologically distinct
98 lar polysaccharides of pathogenic strains of V. vulnificus, there are distinct differences in the det
103 asize the importance of CPS for virulence of V. vulnificus and establish a correlation between CPS ex
104 nd septicemia in humans and the virulence of V. vulnificus has been strongly associated with encapsul
105 ng that in addition to capsule, virulence of V. vulnificus requires type IV pili and/or extracellular
106 mes cannot strictly predict the virulence of V. vulnificus strains and further investigation is neede
110 ted Vibrio species were V. parahaemolyticus, V. vulnificus, and V. alginolyticus; both surveillance s
114 prevalence of total Vibrio parahaemolyticus, V. vulnificus and V. cholerae and select genes associate
117 ated with human infections and that a single V. vulnificus strain, evidenced by pulsed-field gel elec
119 d that V. sinaloensis grew more rapidly than V. vulnificus in seawater at temperatures </= 30 degrees
124 ence of the 77-kDa protein purified from the V. vulnificus fur mutant had 67% homology with the first
127 ablished that the MARTXVv toxin is linked to V. vulnificus dependent induction of apoptosis, but the
128 tood; however, its phenotypic resemblance to V. vulnificus and the possibility that it could outcompe
129 ecrosis factor alpha elicited in response to V. vulnificus and measured in cell supernatants were not
134 t common rtxA1 gene variant in clinical-type V. vulnificus encodes a toxin with reduced potency and i
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