Vibrio vulnificus, a coastal marine bacterium and opportunistic pathogen, poses increasing health risks due to rising sea water temperatures. While it harbors diverse virulence factors, its disease mechanisms remain poorly understood. To address this, we sequenced 82 environmental isolates from the Baltic Sea and combined them with 325 published genomes (clinical and environmental) for comparative analysis. Phylogenetic reconstruction revealed four major lineages, with Baltic strains restricted to L2 and L4. Clinical and environmental strains were found across all lineages, suggesting phylogeny reflects environmental adaptation more than pathogenicity. Using our newly developed PhyloBOTL pipeline, we identified 128 orthologs enriched in clinical isolates, grouped into 36 co-localization clusters. These include both known and novel virulence candidates, such as chaperone-usher pili, type VI secretion effectors, and spermidine synthases. Some clusters showed convergent loss across clades, implying niche-specific evolution. We also designed PCR primers targeting these genes to aid in the surveillance of pathogenic V. vulnificus strains.IMPORTANCEVibrio vulnificus is a naturally occurring marine bacterium that can cause life-threatening infections, with incidence increasing as coastal waters warm due to climate change. Determining which environmental strains pose the greatest risk remains a major challenge for public health surveillance. By analyzing hundreds of genomes from globally distributed strains, including extensive sampling from the rapidly warming Baltic Sea, this study shows that pathogenic potential is not restricted to specific evolutionary lineages but is instead associated with distinct sets of genes enriched in clinical strains. To support pathogen detection, we developed PCR primers targeting a subset of these clinically associated genes. Together, these findings provide new insight into the molecular basis of V. vulnificus infections and offer practical tools for improved detection, monitoring, and risk assessment of harmful strains in coastal waters and seafood under ongoing climate change.

Vibrio vulnificus (V. vulnificus) is a highly virulent marine pathogen responsible for severe infections, including necrotizing fasciitis and life-threatening sepsis, particularly in immunocompromised individuals. This review synthesizes current knowledge on V. vulnificus pathogenesis, focusing on key virulence factors such as cytolysins (VvhA and MARTX), iron acquisition systems, and immune evasion strategies. The bacterium's ability to induce rapid tissue damage, endothelial dysfunction, and systemic inflammation-mediated through cytokine storms and necroptosis-underpins V. vulnificus high mortality rates. Risk factors include chronic liver disease, diabetes, and environmental exposure to seafood harboring V. vulnificus or brackish water. Clinical management hinges on early diagnosis, prompt antibiotic therapy (e.g., doxycycline combined with third-generation cephalosporins), and surgical intervention for necrotizing infections. Despite advances, challenges persist, including antibiotic resistance and delayed diagnosis. Future directions emphasize novel therapeutics targeting virulence mechanisms, rapid diagnostics, and climate-adaptive public health strategies to curb the rising incidence of V. vulnificus infections in warming coastal ecosystems. This review underscores the urgent need for multidisciplinary approaches to mitigate the global burden of this formidable pathogen.

Vibrio vulnificus is a rapidly progressive, life-threatening pathogen endemic to coastal environments, yet clinical data from Southeast Asia remain limited despite substantial environmental contamination. We conducted a 6.5-year multicenter retrospective cohort study at two tertiary-care hospitals in Eastern Thailand to describe clinical characteristics, antimicrobial susceptibility, treatment practices, and factors associated with early mortality among adults with culture-confirmed V. vulnificus infection. Forty-nine patients were identified, most of whom presented with severe illness; 83.7% had bacteremia, 61.2% required mechanical ventilation, and 75.5% required vasopressor support. Skin and soft tissue infection was the most common syndrome, with necrotizing soft-tissue infection accounting for approximately two-thirds of cases. Antimicrobial susceptibility was uniformly high for fluoroquinolones, carbapenems, and third-generation cephalosporins, although susceptibility to doxycycline was unavailable. Despite high rates of empirical antimicrobial therapy (91.8%), mortality remained substantially high: 42.9% died within 48 hours, and 7-day mortality reached 49.0%. In multivariable analysis, elevated serum lactate and lack of surgical treatment were associated with early mortality, while chronic alcohol use and vasopressor requirement showed nonsignificant trends toward increased mortality. These findings highlight the fulminant nature of V. vulnificus infection and the narrow therapeutic window for effective intervention. In settings where necrotizing soft-tissue infection is common and patients present with advanced disease, early recognition, aggressive resuscitation, timely surgical management, and prompt initiation of antimicrobial therapy remain essential. This study provides region-specific epidemiologic and clinical insights that may inform clinical management and public health strategies in coastal communities at risk.

ObjectiveTo compare the epidemiological, clinical, and laboratory data of patients with confirmed and suspected Vibrio vulnificus infection in Chaoshan District, Guangdong.MethodsThis retrospective study analyzed 25 confirmed cases and 23 suspected cases of V. vulnificus infection at the First Affiliated Hospital of Shantou University Medical College from January 2014 to December 2025. A confirmed case was defined by the presence of a positive result from culture and/or mNGS and a suspected case by the experience of a clear marine trauma followed by rapidly progressive soft tissue manifestations, but without etiological confirmation of V. vulnificus infection after exclusion of other infectious etiologies. The epidemiological history, early clinical manifestations, routine blood parameters, and in-hospital outcomes of the two groups were compared.ResultsThe confirmed group had a greater severity of soft tissue infection (84.0% vs 26.0%, P<0.01) and more involved sites (88.0% vs 47.8%, P<0.01). The laboratory data indicated the confirmed group had more abnormalities in markers of tissue injury (creatinine kinase, lactate dehydrogenase), coagulation function (platelets, prothrombin time, international normalized ratio), liver function (aspartate transaminase, total bilirubin), renal function (serum creatinine), and lipid and nutritional markers (all P<0.05). The confirmed group also had significantly higher rates of in-hospital mortality (32.0% vs 0%), multi-organ dysfunction syndrome (36.0% vs 0%), and surgical intervention (60.0% vs 30.4%), and a greater economic burden (all P<0.001).ConclusionThere are significant differences in the early clinical manifestations, routine blood parameters, and in-hospital outcomes for patients with confirmed and suspected V. vulnificus infection.

Vibrio vulnificus is an opportunistic marine pathogen that causes severe wound-associated and systemic infections. Following entry into the host, the bacterium must rapidly adapt to host-associated stresses that differ substantially from those encountered in aquatic environments. However, the physiological functions supporting bacterial fitness during infection remain incompletely understood. Previously, we applied signature-tagged mutagenesis (STM) to identify genes required for V. vulnificus survival during host infection, revealing numerous loci that did not correspond to classical toxin-encoding genes. In the present study, we extended this genome-wide screen by linking STM-identified mutations to observable fitness-related phenotypes. Functional annotation revealed enrichment of genes associated with chemotaxis, flagellar motility, regulation, metabolism, and poorly characterized functions. Phenotypic analyses showed that many STM-derived mutants exhibited defects in swimming motility and altered colony surface properties. Bioluminescence imaging further revealed distinct patterns of impaired persistence and dissemination within host tissues, while several mutants displayed increased susceptibility to phagocytic stress in an HL-60-derived neutrophil model. Notably, some regulatory mutants affecting global signaling pathways exhibited impaired tissue dissemination despite retaining resistance to phagocytic stress, indicating the presence of fitness determinants that operate independently of classical surface-associated or cytotoxic traits. Together, these findings demonstrate that V. vulnificus fitness during infection depends on diverse physiological pathways beyond classical virulence factors, highlighting the value of phenotype-centered analyses for understanding bacterial adaptation in host-associated environments.IMPORTANCEVibrio vulnificus causes rapidly progressive wound infections and septicemia, yet the bacterial functions that support fitness within host environments remain incompletely defined. While substantial effort has focused on canonical virulence factors and regulation, increasing evidence suggests that successful infection also depends on broader physiological adaptation. In this study, we link signature-tagged mutagenesis with systematic phenotypic analyses to define physiological determinants of V. vulnificus fitness during host-associated infection. Our results demonstrate that genes involved in motility, regulatory signaling, metabolism, and stress tolerance collectively shape bacterial persistence and dissemination in host tissues. Notably, we identify regulatory and metabolic determinants that influence fitness independently of classical surface-associated or cytotoxic traits, highlighting noncanonical pathways that contribute to pathogenic success. By integrating genome-wide screening with phenotype-centered analyses, this work advances understanding of how physiological adaptation underpins V. vulnificus infection and provides a framework for studying bacterial fitness alongside established concepts of bacterial virulence.

Vibrio vulnificus , a major human-pathogenic Vibrio species, causes foodborne or wound-related infections with a globally rising incidence. The study aimed to characterize the molecular characteristics of V. vulnificus to support the prevention, control, and clinical treatment of its infection. A total of 63 V. vulnificus isolates from seafood and patients in Wenzhou were subjected to sequencing, bioinformatic analysis, and antimicrobial susceptibility testing. Single nucleotide polymorphism and multilocus sequence typing analysis of 100 isolates (63 from this study, 37 from the NCBI database) were performed to assess genetic characteristics. Nine key virulence genes, associated with adhesion, RTX toxin, and T6SS, and eight antimicrobial resistant genes (ARGs) were identified. All isolates were resistant to colistin (CT), with 74.6%, 58.7%, and 3.2% resistance to streptomycin, amikacin, and nalidixic acid, respectively, and were susceptible to 12 other tested antimicrobials. V. vulnificus infection cases in this study showed a significant demographic skew toward males aged ≥50 years. The isolates exhibited genetic diversity while sharing virulence genes and ARGs. In silico detected ARGs could not accurately predict in vitro antimicrobial resistance phenotypes, so extreme caution is required when using ARGs detection results to guide clinical anti-infective medication. This study provides basic genomic and phenotypic data of local V. vulnificus isolates, which may serve as a reference for local surveillance and clinical empirical treatment of V. vulnificus infection.

The injury site of severe acute polytrauma complicated by Vibrio vulnificus infection determines clinical outcomes in Beagle models.

Role of Rab5b in the defense of Cynoglossus semilaevis against Vibrio vulnificus infection.

A 65-year-old man on maintenance hemodialysis for chronic renal failure and hepatitis C-related liver cirrhosis developed Vibrio vulnificus bacteremia after consuming raw seafood, including sashimi. Initial contrast-enhanced CT showed no obvious signs of inflammation, but due to persistent fever and bilateral lower-limb pain, gallium-67 scintigraphy was subsequently performed. SPECT/CT imaging showed multiple intramuscular abscesses, particularly in the gastrocnemius muscles. Follow-up CT confirmed abscess formation, prompting ultrasound-guided percutaneous drainage along with targeted antibiotic therapy. Gradual clinical improvement was observed. This case highlights the utility of gallium-67 SPECT/CT for detecting deep soft-tissue infections, allowing early diagnosis and timely intervention in high-risk patients.

Vibrio vulnificus is one of the most lethal marine pathogens, causing wound infections, septicemia, and necrotizing soft tissue infection with case fatality rates exceeding 20%–50%. In Northern Europe, incidence is rising alongside warming coastal waters. The genomic relatedness between environmental and clinical isolates and the long-term persistence of virulent clades in temperate waters remains poorly defined. An analysis of 117 V. vulnificus genomes, including 60 newly sequenced (36 environmental isolates and 24 clinical isolates from Denmark, 1994–2023), 27 publicly available Nordic clinical genomes, and 30 comparative reference public genomes were analysed. Comparative genomics, virulence gene profiling, pangenome analysis, and core-genome SNP (Single Nucleotide Polymorphism) phylogeny were used to define clade structure, persistence, and genetic determinants of pathogenicity. Four major clades were identified; three (C2–C4) persisted for up to three decades and contained both clinical and environmental isolates. Clonal pairs (≤40 SNPs) linked environmental and clinical sources across up to 8 years and multiple countries. The virulence gene repertoire including the major virulence factors MARTX toxin genes (rtxA/B/C/D), chiRP (chitin-regulated pilus), flp2/tad2 pili (fimbrial low-molecular-weight protein/tight adherence pili), ilpA (immunogenic lipoprotein A), and ompU (outer membrane porin), and vvhA (V. vulnificus hemolysin).) were present in both environmental and clinical isolates. All isolates carried the tetracycline resistance gene tet(34). We report that environmental aquatic reservoirs harbor fully virulent V. vulnificus lineages, making human infections exposure-driven rather than the result of emerging novel lineages.

Wounds caused by Vibrio vulnificus (V. vulnificus) infection often exhibit delayed healing and are prone to complications, making them a significant challenge in clinical treatment. Current conventional treatments, such as antibiotics and gauze dressings, have limited effectiveness. To address this, this study developed a multifunctional fiber membrane using electrospinning technology. Micron- or nano-sized Haliotidis Concha (HC) and eugenol (Eu) were loaded onto the membrane to promote healing in V. vulnificus-infected wounds. The prepared fiber membranes exhibited diameters of approximately 0.35 ± 0.01 μm. Membranes loaded with nano-HC demonstrated significant antibacterial efficacy, achieving a 96.2% inhibition rate against V. vulnificus, which was markedly superior to the micron-HC group (p < 0.05). Notably, the nano-HC/Eu membranes exhibited exceptionally high flexibility with an elongation at break of 878.1 ± 35.3%, while maintaining a tensile strength of approximately 2.2 MPa. Furthermore, these membranes exhibited excellent biocompatibility, with cell viability exceeding 85% for fibroblasts, and demonstrated good hemocompatibility. They also effectively promoted cell migration, indicating their potential as wound scaffold materials. In a V. vulnificus-infected skin wound model, the nano-HC/Eu fiber membrane accelerated collagen deposition and promoted wound healing, achieving a wound closure rate of 94.7 ± 1.1% on day 15. In summary, this study developed a multifunctional fiber membrane with antibacterial, antioxidant, and wound healing properties, offering a novel dressing for treating V. vulnificus infections.

ObjectivesThis study investigates the potential source and transmission routes of a confirmed Vibrio vulnificus infection reported in the Republic of Korea in 2025 through epidemiological surveys. The findings provide evidence to support future prevention and management strategies for vibriosis.MethodsThe Central Epidemiological Investigation Team of the Korea Disease Control and Prevention Agency, in collaboration with local governments, established a joint investigation team. The team interviewed the patient and conducted on-site epidemiological assessments. Environmental samples were collected and analyzed through laboratory testing to culture and identify Vibrio vulnificus bacteria. Genetic analysis using pulsed-field gel electrophoresis (PFGE) was conducted on the isolates to determine their genetic relatedness.ResultsThe investigation indicated that the patient’s clinical symptoms and incubation period were consistent with major symptoms of vibriosis. Laboratory testing identified Vibrio vulnificus in both human and clam samples; however, PFGE showed that the strains were not genetically related, making it difficult to designate the clams as the definitive source of infection.ConclusionsTo prevent vibriosis, frozen seafood should be thoroughly heat treatment before consumption. Proper hygiene practices, such as washing hands after handling raw seafood and storing raw seafood separately from other foods, are also essential. High-risk individuals, particularly those with underlying conditions such as chronic liver disease, should strictly adhere to these prevention guidelines to reduce the risk of infection.

We report the first case of Vibrio vulnificus sepsis in a patient with vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic (VEXAS) syndrome. A 76-year-old man was diagnosed with VEXAS and myelodysplastic syndromes. He was treated with tocilizumab, oral prednisolone, and regular blood transfusions. The patient presented with fever, chills, and vomiting and was subsequently diagnosed with sepsis. A blood culture confirmed V. vulnificus infection, which resolved after tazobactam/piperacillin treatment. V. vulnificus infections can be facilitated by iron overload resulting from frequent blood transfusions. Since patients with VEXAS syndrome often require regular transfusions, clinicians should monitor for this potentially fatal infection.

Copper-based nanozyme-doped fiber-catalytic membranes mediate reactive oxygen species and tissue regeneration-promoting functions against marine Vibrio vulnificus infections.

Vibrio vulnificus is notorious for inducing rapidly progressive infections with high lethality and significant morbidity. Macrophages, being essential components of the innate immune system, play a vital role in combating infections, and their activation and effector functions are closely intertwined with metabolic reprogramming processes. However, the mechanisms governing macrophage glycolytic metabolism in response to V. vulnificus infection remain poorly elucidated. Based on our current data, we propose that NOD-like receptor 3 (NLRP3) could potentially contribute to the regulation of glycolytic metabolism in macrophages infected with V. vulnificus, though further validation is needed to confirm this relationship in both in vivo and in vitro. Upon V. vulnificus infection, NLRP3 was shown to augment glucose uptake, upregulate the aerobic glycolytic pathway, facilitate lactate release, and enhance reactive oxygen species (ROS) production. Notably, these metabolic alterations were abolished in NLRP3 knockout (KO) macrophages, as observed in both NLRP3-deficient macrophage cell lines and primary cells. We also found that the abundances of fructose 1,6-bisphosphate and 3-phosphoglyceric acid in glycolytic metabolism were decreased in V. vulnificus-infected NLRP3 KO macrophages by non-targeted metabolic flux analysis, which might be due to the reduction of PFKL that converts fructose 6-phosphate to fructose 1,6-bisphosphate in V. vulnificus-infected NLRP3 KO macrophage. These findings suggest that NLRP3 may promote inflammation in macrophages during V. vulnificus infection by driving glycolysis and increasing ROS production. The absence of these metabolic changes in NLRP3 KO macrophages underlines the crucial role of NLRP3 in modulating the immunometabolic response to V. vulnificus infection.IMPORTANCEThe results of this study demonstrate that NOD-like receptor 3 (NLRP3) is critical for metabolic reprogramming in macrophages during Vibrio vulnificus infection. NLRP3 enhances glucose uptake, upregulates glycolysis, reprograms metabolic flux, and promotes reactive oxygen species production. These findings are significant, as they reveal a previously unrecognized role of NLRP3 in regulating immune function in V. vulnificus-infected macrophages. This study identifies NLRP3 as a central mediator linking immune cell metabolism to defense against infections, providing novel insights into how innate immunity controls pathogenic bacteria and suggesting potential strategies for improving treatment or prevention of severe infections. However, further research is required to fully elucidate its impact on macrophage glycolysis in V. vulnificus-induced sepsis.

Climate change has led to a rise in Vibrio vulnificus infections, while the global obesity epidemic has increased susceptibility to severe bacterial infections. Obesity and high-fat diet (HFD) consumption promote systemic inflammation and immune dysregulation, which may exacerbate sepsis and its complications, including acute kidney injury (AKI). This study investigates the mechanistic role of HFD-induced metabolic dysfunction in V. vulnificus sepsis-associated AKI. Adult C57BL/6J mice were placed on a standard CHOW diet or a 60% kcal HFD for 6 wk before infection. V. vulnificus infection was induced via intragastric administration by oral gavage of 108 colony-forming units of V. vulnificus suspended in PBS. Kidney function was assessed, and kidney tissues were analyzed for markers of inflammation, oxidative stress, and necrosis. Systemic Th17/Treg ratios were determined. In vitro, renal proximal tubular epithelial cells were treated with leptin and IL-17A with/without an IL-17 receptor antagonist to confirm the role of IL-17 signaling in renal epithelial cell pathology. A proinflammatory Th17/Treg imbalance, along with a marked increase in renal TLR4 activation, inflammation, and necrosis, was observed in the HFD + Vibrio vulnificus infection group. In vitro studies confirmed that IL-17 and leptin synergistically activate the NF-κB pathway, promoting inflammatory cytokine release. These findings indicate that HFD-induced metabolic stress exacerbates V. vulnificus sepsis-associated AKI. The interplay between IL-17 signaling and leptin may further amplify renal injury, underscoring the need for targeted interventions. Strategies to modulate IL-17 signaling and metabolic inflammation may offer novel therapeutic approaches to reduce AKI severity in obese individuals with bacterial sepsis.NEW & NOTEWORTHY This study reveals that high-fat diet (HFD)-induced metabolic dysfunction exacerbates Vibrio vulnificus sepsis-associated acute kidney injury (AKI) via TLR4-driven inflammation, oxidative stress, and systemic Th17/Treg imbalance. Novel in vitro findings show that IL-17 and leptin synergistically activate NF-κB signaling in renal epithelial cells, amplifying inflammation, which is mitigated by IL-17 receptor blockade. These results highlight IL-17 signaling as a potential therapeutic target for reducing AKI severity in obese individuals with bacterial sepsis.

IgY antibodies as a non-antibiotic approach to combat Vibrio vulnificus infection and gut microbiota dysbiosis in zebrafish.

Background Vibrio vulnificus is a foodborne and waterborne pathogen causing substantial morbidity and mortality; however, its epidemiology remains poorly understood. To inform prevention and control efforts, we characterized U.S. V. vulnificus epidemiology and identified risk factors for mortality. Methods For all culture-confirmed V. vulnificus cases reported to the Cholera and Other Vibrio Illness Surveillance (COVIS) system from 2000 to 2022, patient characteristics and medical outcomes were described by foodborne vs. non-foodborne transmission routes. Risk factors for mortality were identified using multivariate logistic regression. Results Two thousand nine hundred and eighty-nine V. vulnificus cases were reported from 2000 to 2022, including 656 (22%) foodborne and 1,619 (54%) non-foodborne cases. Five-year case total increased 70% from 2000–2004 (n = 487) to 2018–2022 (n = 827). Most patients were male, older and White, with reported underlying health conditions; 2,493 (83%) patients were hospitalized and 692 (23%) died. Number of deaths (260 vs. 200) and fatality rate (40% vs. 12%) were higher among foodborne vs. non-foodborne cases. Mortality was associated with history of liver disease/alcoholism (odds ratio (OR) = 6.5, p < 0.001), age 45–59 (OR = 11.3, p = 0.001), foodborne transmission (OR = 1.3, p = 0.006), and Black (OR = 1.8, p = 0.03) or Asian (OR = 2.5, p = 0.009) race. Antibiotic use was protective (OR = 0.33, p = 0.001). Liver disease associated with diabetes had lower mortality than other forms of liver disease (interaction OR = 0.5, p = 0.04). Conclusions V. vulnificus infections confer a substantial and increasing public health burden in the United States. Non-foodborne transmission caused 2.5 times more cases, and foodborne transmission caused 30% more deaths and had >3 times higher fatality rate. Identifying risk factors for mortality can inform public health and medical interventions.

Vibrio vulnificus infections caused by aquatic product-related injuries pose severe clinical challenges due to their rapid progression and high morbidity and mortality. Early diagnosis and timely intervention are critical to improving patient outcomes, yet standardized diagnostic and treatment protocols remain limited. We conducted a retrospective descriptive case series of 14 patients with confirmed V vulnificus infection admitted between 2020 and 2023. Clinical data, including demographic characteristics, injury history, symptoms, laboratory results, diagnostic methods, treatment strategies, and outcomes, were collected and analyzed. Microbial culture and metagenomic next-generation sequencing (mNGS) were compared in terms of diagnostic timing. All 14 patients had a clear history of aquatic product-related trauma, with 85.7% (12/14) presenting within 24 hours of injury. The average time from injury to symptom onset was 13.11 ± 6.61 hours. All patients exhibited limb erythema, swelling, warmth, and pain; 11 patients (78.6%) developed complications such as sepsis (42.9%), compartment syndrome (35.7%), or multiple organ dysfunction syndrome (28.6%). Ten cases were confirmed by microbial culture (average time: 1.68 ± 0.63 days), and 4 by mNGS (average time: 1.00 day). The average time to diagnosis was shorter in patients diagnosed by culture than those requiring mNGS (1.86 ± 0.68 vs 4.82 ± 0.90 days). All patients received empirical combination antibiotic therapy upon admission; the average duration of intravenous antibiotic treatment was approximately 10 days. Six patients (42.9%) underwent amputation, and 2 (14.3%) died. Among the survivors, 50% achieved Brunnstrom stage V to VI hand function recovery at final follow-up. Early identification and aggressive treatment are essential in managing V vulnificus infections related to aquatic product injuries. mNGS plays an important supplementary role in diagnosis, especially in culture-negative cases. The proposed diagnostic and treatment protocol, based on real-world experience, may help improve clinical decision-making and reduce poor outcomes such as amputation and death.

Non-invasive vaccination enhances immune response and protects Asian seabass (Lates calcarifer) against Vibrio vulnificus infection