Cutaneous Injury and<i>Vibrio vulnificus</i>Infection

Chung, P.H.; Chuang, S.K.; Tsang, T.; Wai-man, Lai; Yung, Raymond; Lo, Janice Y.C.

doi:10.3201/eid1708.051495

Cited by 6 publications

(4 citation statements)

References 6 publications

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“…The casefatality rate was 7.6% for the entire study population and 10.6 % for patients with laboratory-confi rmed infection. These characteristics concur with prior reports of wound infection syndrome caused by non-biotype 3 V. vulnifi cus (9,10,23,24,(27)(28)(29)(30).…”

Section: Discussionsupporting

confidence: 92%

“…Patients with primary bacteremia caused by non-biotype 3 strains are more likely to have predisposing conditions, particularly liver diseases in >80% of patients (7-9), whereas patients with wound infection are more likely to be previously healthy and have a more favorable outcome (9,10,23,24,(28)(29)(30). The death rate may exceed 50% in the most seriously ill patients (7-9,23).…”

Section: Discussionmentioning

confidence: 95%

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Clinical Characteristics and Molecular Subtyping ofVibrio vulnificusIllnesses, Israel

Zaidenstein¹,

Sadik²,

Lerner³

et al. 2008

Emerg. Infect. Dis.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 95%

Clinical Characteristics and Molecular Subtyping ofVibrio vulnificusIllnesses, Israel

Zaidenstein¹,

Sadik²,

Lerner³

et al. 2008

Emerg. Infect. Dis.

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“…(Jones & Oliver, 2009). Additionally, in healthy individuals, as well as individuals with underlying medical conditions, V. vulnificus can cause serious wound infection that may lead to secondary septicemia (Oliver, 2005; Chung et al , 2006). Even with antibiotic treatment, mortality rates can exceed 50% for primary septicemia and 25% for wound infection (Gulig et al , 2005; Jones & Oliver, 2009).…”

Section: Introductionmentioning

confidence: 99%

Role of TLR4 in the host response toVibrio vulnificus, an emerging pathogen

Stamm¹

2010

FEMS Immunol Med Microbiol

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The incidence of infection with Vibrio vulnificus is increasing due to changing ecologic and demographic factors. Most fatal cases are caused by septic shock that results from dysregulation of proinflammatory cytokines such as tumor necrosis factor-alpha (TNFalpha), presumably due to interaction of V. vulnificus components with Toll-like receptors (TLRs). The goal of this study was to investigate the role of TLR4 in the host response to V. vulnificus. Results obtained using V. vulnificus type strain ATCC 27562 showed that (1) TLR4 signaling is myeloid differentiation factor 88 dependent and plays a key role in TNFalpha production by mouse blood and splenocytes stimulated ex vivo with inactivated V. vulnificus cells, (2) TLR4 signaling is deleterious in a mouse model of V. vulnificus infection, (3) signaling by TLR(s), exclusive of TLR4, is needed to eradicate infection, and (4) the TLR-mediated TNFalpha response plays a critical role in determining the outcome of infection. These results suggest that blockade of the harmful TLR4-mediated inflammatory response could be a useful adjunct to antibiotics for treatment of severe V. vulnificus infection.

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“…V. vulnificus infections affect many people due to the intake of contaminated seafood (Chung et al, 2006). Large amounts of bile salt are distributed in the human intestinal environment, and the gastrointestinal tract is one of the most important ways for V. vulnificus to enter the human body.…”

Section: Discussionmentioning

confidence: 99%

TolCV1 Has Multifaceted Roles During Vibrio vulnificus Infection

Gong

Guo

Rhee

et al. 2021

Front. Cell. Infect. Microbiol.

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RtxA1 is a major cytotoxin of Vibrio vulnificus (V. vulnificus) causing fatal septicemia and necrotic wound infections. Our previous work has shown that RpoS regulates the expression and secretion of V. vulnificus RtxA1 toxin. This study was conducted to further investigate the potential mechanisms of RpoS on RtxA1 secretion. First, V. vulnificus TolCV1 and TolCV2 proteins, two Escherichia coli TolC homologs, were measured at various time points by Western blotting. The expression of TolCV1 was increased time-dependently, whereas that of TolCV2 was decreased. Expression of both TolCV1 and TolCV2 was significantly downregulated in an rpoS deletion mutation. Subsequently, we explored the roles of TolCV1 and TolCV2 in V. vulnificus pathogenesis. Western blot analysis showed that RtxA1 toxin was exported by TolCV1, not TolCV2, which was consistent with the cytotoxicity results. Furthermore, the expression of TolCV1 and TolCV2 was increased after treatment of the host signal bile salt and the growth of tolCV1 mutant was totally abolished in the presence of bile salt. A tolCV1 mutation resulted in significant reduction of V. vulnificus induced-virulence in mice. Taken together, TolCV1 plays key roles in RtxA1 secretion, bile salt resistance, and mice lethality of V. vulnificus, suggesting that TolCV1 could be an attractive target for the design of new medicines to treat V. vulnificus infections.

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Cutaneous Injury andVibrio vulnificusInfection

Cited by 6 publications

References 6 publications

Clinical Characteristics and Molecular Subtyping ofVibrio vulnificusIllnesses, Israel

Clinical Characteristics and Molecular Subtyping ofVibrio vulnificusIllnesses, Israel

Role of TLR4 in the host response toVibrio vulnificus, an emerging pathogen

TolCV1 Has Multifaceted Roles During Vibrio vulnificus Infection

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