In an attempt to dissect the virulence regulatory mechanism in Vibrio vulnificus, we tried to identify the V. cholerae transmembrane virulence regulator toxRS (toxRS Vc ) homologs in V. vulnificus. By comparing the sequences of toxRS of V. cholerae and V. parahaemolyticus (toxRS Vp ), we designed a degenerate primer set targeting well-conserved sequences. Using the PCR product as an authentic probe for Southern blot hybridization, a 1.6-kb BglII-HindIII fragment and a 1. Vibrio vulnificus is a halophilic estuarine bacterium that causes fatal septicemia and necrotizing wound infections. Primary septicemia occurs following ingestion of raw seafood contaminated with V. vulnificus. V. vulnificus preferentially affects persons with underlying hepatic diseases, a heavy alcohol drinking habit, and other immunocompromised conditions. Primary septicemia shows a rapidly progressing and fulminant course, which results in a high mortality rate of over 50% despite aggressive antimicrobial and supportive shock therapies (38,39,48).The optimal natural habitat of V. vulnificus is an estuary. The bacterium normally flourishes in estuarine seawater, shellfish, and plankton during warm months (8,35,50,54). V. vulnificus is concentrated in oysters and probably in other shellfish as well (21, 49). V. vulnificus opportunistically causes primary septicemia when contaminated shellfish is eaten raw by susceptible patients. This opportunist should experience a very dramatic change in environmental parameters during the infection process. Successful infection by pathogenic bacteria, in general, is established by coordinate expression of various virulence factors in vivo. Expression of virulence factors is controlled by environmental cues. Pathogenic bacteria possess elegant regulatory systems that sense and react to fluctuations in environmental parameters such as temperature, osmolarity, pH, iron concentration, CO 2 concentration, etc. (12, 27).Many pathogens employ novel signal transduction systems in regulating the virulence gene expression (12). Toxigenic V. cholerae has the toxRS system for that purpose (30). The genes toxR and toxS are clustered in an operon and encode transmembrane proteins ToxR and ToxS, respectively (10,29,32). ToxR regulates expression of multiple V. cholerae virulence factors such as the cholera toxin (ctx), toxin-coregulated pilus (tcp), and accessory colonization factor (acf) genes (9, 47). The activity of ToxR is further enhanced by ToxS, which interacts with the former protein in the periplasmic space and is thought to stabilize it (10, 36). The toxRS system seems to play universally important roles in the survival and host-microorganism interaction of Vibrio species. V. parahaemolyticus and V. fischeri also have homologs of the V. cholerae toxRS (toxRS Vc ) system (25,43). In the present study, we identified the toxRS homolog in V. vulnificus and showed the functional homology of ToxRS Vv with ToxRS Vc . We also observed that ToxR Vv regulates the production of hemolysin, the most potent exotoxin produced ...

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BackgroundScrub typhus is an infectious disease caused by Orientia tsutsugamushi. The differences in virulence of O. tsutsugamushi prototypes in humans are still unknown. We investigated whether there are any differences in the clinical features of the Boryoung and Karp genotypes.Methodology/Principal FindingsPatients infected with O. tsutsugamushi, as Boryoung and Karp clusters, who had visited 6 different hospitals in southwestern Korea were prospectively compared for clinical features, complications, laboratory parameters, and treatment responses. Infected patients in the Boryoung cluster had significantly more generalized weakness, eschars, skin rashes, conjunctival injection, high albumin levels, and greater ESR and fibrinogen levels compared to the Karp cluster. The treatment response to current antibiotics was significantly slower in the Karp cluster as compared to the Boryoung cluster.ConclusionThe frequency of occurrence of eschars and rashes may depend on the genotype of O. tsutsugamushi.

The standard iron-chelator deferoxamine is known to prevent the growth of coagulase-negative staphylococci (CoNS) which are major pathogens in iron-overloaded patients. However, we found that deferoxamine rather promotes the growth of coagulase-positive Staphylococcus aureus. Accordingly, we tested whether deferiprone, a new clinically-available iron-chelator, can prevent the growth of S. aureus strains as well as CoNS. Deferiprone did not at least promote the growth of all S. aureus strains (n=26) and CoNS (n=27) at relatively low doses; moreover, it could significantly inhibit the growth of all staphylococci on non-transferrin-bound-iron and the growth of all CoNS on transferrin-bound iron at relatively high doses. At the same doses, it did not at least promote the growth of all S. aureus strains on transferrin-bound-iron. These findings indicate that deferiprone can be useful to prevent staphylococcal infections, as well as to improve iron overload, in iron-overloaded patients.