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Chicory leaves (Cichorium intybus) are widely consumed due to their health benefits. They are mainly consumed raw or without adequate washing, which has led to an increase in food-borne illness. This study investigated the taxonomic composition and diversity of chicory leaves collected at different sampling times and sites. The potential pathogenic genera (Sphingomonas, Pseudomonas, Pantoea, Staphylococcus, Escherichia, and Bacillus) were identified on the chicory leaves. We also evaluated the effects of various storage conditions (enterohemorrhagic E. coli contamination, washing treatment, and temperature) on the chicory leaves' microbiota. These results provide an understanding of the microbiota in chicory and could be used to prevent food-borne illnesses. [ABSTRACT FROM AUTHOR]

The Vibrio vulnificus aphB mutant was significantly less virulent than the wild type and was impaired in motility and adherence to host cells. Microarray analysis revealed that AphB of V. vulnificus ([AphB.sub.Vv]) influences the expression of over 10% of the V. vulnificus genome. The combined results indicated that [AphB.sub.Vv] is a global regulator contributing to the pathogenesis of V. vulnificus.

A mutant of Vibrio vulnificus that was more sensitive to low pH was screened from a library of mutants constructed by random transposon mutagenesis. By use of a transposon-tagging method, an open reading frame encoding a LysR homologue, AphB, was identified and cloned from V. vulnificus. The deduced amino acid sequence of AphB from V. vulnificus was 80% identical to that reported from V. cholerae. A mutational analysis demonstrated that the gene product of aphB contributes to acid tolerance of V. vulnificus. The lysine decarboxylase activity and cellular level of the cadA transcript were decreased in the aphB mutant, indicating that AphB exerts its effect on the acid tolerance of V. vulnificus by enhancing the expression of cadBA. Western blot analyses demonstrated that the cellular level of CadC, a transcription activator of the cadBA operon, was significantly reduced by aphB mutation, and a primer extension analysis revealed that the cadC promoter ([P.sub.cadC]) activity was under the positive control of AphB. A direct interaction between AphB and the [P.sub.cadC] DNA was demonstrated by gel mobility shift assays. The AphB binding site mapped by deletion analyses of the [P.sub.cadC] regulatory region and confirmed by a DNase I protection assay was centered at the 61.5 bp upstream of the transcription start site. Accordingly, these results demonstrate that AphB and CadC function sequentially in a regulatory cascade to activate cadBA expression and that AphB activates the expression of cadC by directly binding to an upstream region of [P.sub.cadC].

A correction is presented to the article "Additive Function of Vibrio vulnificus MARTX Vv and VvhA Cytolysins Promotes Rapid Growth and Epithelial Tissue Necrosis During Intestinal Infection" which appeared in the June 19, 2019 issue.

The glycogen branching enzyme from Vibrio vulnificus (VvGBE) transfers short side chains (DP 3–5) significantly greater than any other bacterial glycogen branching enzyme (GBE). To elucidate the role of the N-domain of VvGBE in the unique branching pattern, domain-truncated (N1 and N) and N1-domain-swapped (with VvGBE N1 replacing the counter part of Escherichia coli GBE) mutants were constructed. The truncation mutants synthesized branched products with a greatly reduced proportion of short chains. The swapping mutant exhibited a branching pattern of the short chain region similar to that of VvGBE. We conclude that the N1-domain of VvGBE has a crucial role in the determination of the branching pattern of glycogen. [ABSTRACT FROM AUTHOR]

Vibrio vulnificus is a pathogen that causes both severe necrotizing wound infections and life-threatening food-borne infections. Food-borne infection is particularly lethal as the infection can progress rapidly to primary septicemia resulting in death from septic shock and multiorgan failure. In this study, we use both bioluminescence whole animal imaging and V. vulnificus bacterial colonization of orally infected mice to demonstrate that the secreted multifunctional-autoprocessing RTX toxin (MARTXVv) and the cytolysin/hemolysin VvhA of clinical isolate CMCP6 have an important function in the gut to promote early in vivo growth and dissemination of this pathogen from the small intestine to other organs. Using histopathology, we find that both cytotoxins can cause villi disruption, epithelial necrosis, and inflammation in the mouse small intestine. A double mutant deleted of genes for both cytotoxins was essentially avirulent, did not cause intestinal epithelial tissue damage, and was cleared from infected mice by 36 hours by an effective immune response. Therefore, MARTXVv and VvhA seem to play an additive role for pathogenesis of CMCP6 causing intestinal tissue damage and inflammation that then promotes dissemination of the infecting bacteria to the bloodstream and other organs. In the absence of these two secreted factors, we propose that this bacterium is unable to cause intestinal infection in humans. [ABSTRACT FROM AUTHOR]

Proteomic analysis led to identification of the proteins of Vibrio vulnificus that were induced upon exposure to INT-407 cells, and 7 of which belong to the functional categories such as amino acid transport/metabolism, nucleotide transport/metabolism, posttranslational modification/protein turnover/chaperones, and translation. Among the genes encoding the host-induced proteins, disruption of purH, trpD, tsaA, and groEL2 resulted in reduced cytotoxicity. The purH, trpD, and tsaA mutants showed impaired growth in the INT-407 lysate; however, the growth rate of the groEL2 mutant was not significantly changed, indicating that the possible roles of the host-induced proteins in the virulence of V. vulnificus are rather versatile.