Abstract
Vibrio alginolyticus is a halophilic, Gram-negative marine bacterium that has emerged as a significant opportunistic pathogen affecting both marine animals and humans. As one of the most abundant vibrios in coastal and estuarine environments worldwide, V. alginolyticus causes substantial economic losses in aquaculture through vibriosis in fish, shrimp, and shellfish, while also being responsible for wound infections, otitis externa, and occasionally gastroenteritis in humans following seawater exposure or seafood consumption. The pathogenesis of V. alginolyticus is multifactorial, involving an arsenal of virulence determinants including secretion systems (type III, type VI, and type II), haemolysins, adhesins, biofilm formation, quorum sensing-regulated factors, and the recently recognized contributions of non-coding RNAs and outer membrane vesicles. Recent genomic analyses have revealed considerable genetic diversity among isolates and identified a ubiquitous presence of β-lactam resistance genes, raising concerns about natural resistance and the potential for horizontal gene transfer. The interplay between rising seawater temperatures, intensive aquaculture practices, and increasing antimicrobial resistance has positioned V. alginolyticus as an emerging pathogen of growing concern. This Review synthesizes current knowledge on the epidemiology, genomics, virulence mechanisms, host interactions, and control strategies of V. alginolyticus, with an emphasis on the molecular determinants of pathogenesis, including the regulatory networks governing adhesion, biofilm formation, and metabolic adaptation, and the challenges posed by antimicrobial resistance. We also discuss promising alternative control approaches, including phage therapy, vaccination, and probiotic strategies, and identify key knowledge gaps that warrant future investigation.
1 Introduction
The genus Vibrio encompasses a diverse group of Gram-negative, facultatively anaerobic bacteria that are ubiquitous in aquatic environments. Among the more than 100 recognized Vibrio species, a subset has gained prominence as human and animal pathogens, including Vibrio cholerae, Vibrio parahaemolyticus, and Vibrio vulnificus (). Vibrio alginolyticus, historically classified as biotype 2 of V. parahaemolyticus, has long been considered primarily an environmental organism with modest pathogenic potential. This perception is changing.
V. alginolyticus is now recognized as one of the most common Vibrio species in seawater and seafood, and its association with disease outbreaks in both aquaculture settings and human clinical cases has intensified over the past two decades (). In aquaculture, V. alginolyticus causes vibriosis in a wide range of commercially important species, including gilthead seabream (Sparus aurata), orange-spotted grouper (Epinephelus coioides), Pacific white shrimp (Penaeus vannamei), and kuruma prawn (Penaeus japonicus). The disease manifests as haemorrhagic septicaemia, skin ulcerations, and high mortality rates, leading to substantial economic losses (). In humans, V. alginolyticus is most frequently associated with wound infections and otitis externa following exposure to marine environments, though cases of gastroenteritis and, rarely, septicaemia have also been documented (, ).
Several converging factors have contributed to the rising prominence of V. alginolyticus as a pathogen. Climate change has led to warming of coastal waters, expanding the geographic range and seasonal window of Vibrio proliferation (). The expansion and intensification of aquaculture have created densely populated rearing conditions that facilitate pathogen transmission (). Meanwhile, the widespread use of antibiotics in aquaculture has selected for resistant strains, complicating treatment options (). These developments underscore the need for a comprehensive understanding of V. alginolyticus biology, pathogenesis, and epidemiology to inform effective surveillance and control strategies.
This Review provides a synthesis of the current state of knowledge on V. alginolyticus. We begin by examining its environmental distribution, ecological niches, and epidemiological patterns. We then discuss genomic features and population structure, followed by a detailed analysis of the molecular mechanisms underlying its pathogenicity, including the hierarchical regulatory networks that govern adhesion, flagellar assembly, chemotaxis, and metabolic adaptation. The host immune response, detection methods, and control strategies are subsequently addressed. We also highlight the emerging roles of non-coding RNAs and outer membrane vesicles in virulence regulation. We conclude by identifying priority areas for future research.
2 Environmental distribution and epidemiology
2.1 Ecological niche and environmental drivers
V. alginolyticus is an autochthonous member of marine and estuarine microbial communities, distributed globally in temperate, subtropical, and tropical coastal waters. The bacterium exhibits a marked preference for warm, moderately saline environments, with its abundance strongly correlated with water temperature and salinity (). Seasonal patterns of V. alginolyticus prevalence are well documented, with peak concentrations occurring during warmer months when water temperatures exceed 15–20 °C. Detection rates in environmental samples vary considerably by region: studies in Asia have reported V. alginolyticus in more than 80% of water samples, whereas detection rates in US and European shellfish at harvest range between 5 and 50% ().
The ecological success of V. alginolyticus can be attributed to several physiological adaptations. As a halophilic organism, it requires sodium chloride for growth and can tolerate salinities ranging from brackish to fully marine conditions. It forms large, yellow (sucrose-fermenting) colonies on thiosulfate-citrate-bile salts-sucrose (TCBS) agar and exhibits pronounced swarming on non-selective solid media (). The bacterium is capable of both planktonic and biofilm-associated lifestyles, with the latter providing enhanced survival under environmental stress ().
Integrated surveillance in mariculture-impacted coastal ecosystems, such as Dongshan Bay in southern China, has provided critical insights into the seasonal dynamics of Vibrio populations. Annual Vibrio abundance in such semi-enclosed bays ranges from 20 to 11,600 CFU mL−1, with temperature identified as the most significant positive correlate (). Community composition shifts markedly across seasons: V. campbellii dominates in summer, V. fortis in autumn, and species richness peaks in spring, while pathogenic vibrios are rarely isolated in winter (, ). These findings underscore the pronounced seasonality of Vibrio abundance and composition, with important implications for aquaculture disease forecasting.
2.2 Aquaculture impact
The economic impact of V. alginolyticus on aquaculture is substantial and growing. Disease outbreaks in Mediterranean aquaculture have become increasingly frequent, driven by the semi-enclosed nature of the Mediterranean Sea, rising seawater temperatures, and intensive farming practices (). Affected species include finfish (gilthead seabream, European seabass, groupers), crustaceans (shrimp, prawns), and bivalve molluscs (oysters, clams). In Pacific oyster (Crassostrea gigas) larvae, V. alginolyticus strain CG-1 induced dose-dependent mortality with an LD50 of 5.04 × 106 CFU/mL, with clinical symptoms comparable to those caused by the well-known oyster pathogen V. coralliilyticus (). The global expansion of aquaculture production, now supplying nearly half of all fish consumed worldwide, has created favorable conditions for the dissemination of V. alginolyticus and other Vibrio pathogens ().
2.3 Transmission and human disease
Human infections with V. alginolyticus are overwhelmingly associated with exposure to seawater or consumption of contaminated seafood. Wound infections typically occur when an individual with an open cut or abrasion wades or swims in coastal waters harboring the bacterium. The resulting cellulitis is generally mild, characterized by localized inflammation and seropurulent exudate, though more severe infections can occur in immunocompromised individuals. Otitis externa, or swimmer's ear, is another common presentation, particularly among individuals with prolonged water exposure. Gastroenteritis following ingestion of raw or undercooked seafood has been reported but is less common than infections caused by V. parahaemolyticus (, ). Immunocompromised patients and those with underlying chronic conditions are at increased risk of more severe outcomes, including bacteraemia ().
3 Genomics diversity and population structure
A comprehensive comparative genomic analysis of 184 V. alginolyticus isolates has revealed substantial genetic diversity and a complex population structure (). The population can be divided into three major lineages (L1, L2, and L3), each of which can be further subdivided into sublineages. Accessory genes, those not shared by all members of the species, are nonuniformly distributed among isolates and contribute to genomic differentiation. Importantly, the spread of certain post-evolutionary isolates (predominantly L3 strains from Chinese territorial seas) appears to be closely linked to human activities, whereas more ancestral strains (L1 and L2) tend to be locally endemic and form clonal complex groups ().
This population structure has implications for both pathogenesis and epidemiology. The uneven distribution of accessory genes, many of which are located on mobile genetic elements, facilitates the acquisition of virulence determinants and antibiotic resistance genes (). A study of 55 V. alginolyticus isolates from seafood and freshwater products in China identified 34 distinct sequence types (STs) by multilocus sequence typing, with ST421, ST166, ST523, ST516, and ST507 being the most prevalent (). This considerable genetic diversity underscores the adaptive capacity of V. alginolyticus and the challenges it poses for surveillance and control.
4 Virulence mechanisms
4.1 Virulence-associated genes
The genome of V. alginolyticus encodes a diverse array of virulence-associated genes (). These include components of the type III secretion system (T3SS), extracellular enzymes, motility and chemotaxis regulators, outer membrane proteins, iron acquisition systems, and antibiotic resistance genes. A genome-wide analysis of potential virulence factors identified genes associated with toxin production, adherence, motility, chemotaxis, and the T3SS as the most prominent (). The presence of these genes varies among isolates, contributing to differences in pathogenic potential.
4.2 Secretion systems
Secretion systems are central to the virulence of V. alginolyticus, enabling the delivery of effector proteins into host cells or the extracellular environment (Figure 1). The bacterium possesses at least three distinct secretion systems: type III secretion system (T3SS), type VI secretion system (T6SS), and type II secretion system (T2SS) ().
Figure 1
The T3SS is an essential virulence determinant. V. alginolyticus encodes a T3SS that translocates effector proteins directly into host cells, subverting host signaling pathways and promoting cell death. To date, four T3SS effectors have been identified in V. alginolyticus: VopQ, VopR, VopS, and VPA0450 (). VopR, a 317-amino-acid protein encoded by a 954-bp gene, binds directly to phosphatidic acid, PtdIns (3,5)P2, and PtdIns (4,5)P2 on the host cell membrane. This binding activates the host ubiquitination system and induces apoptosis through the MKK (mitogen-activated protein kinase kinase) signaling pathway (). VopS functions as a metabolic disruptor that promotes host cell ferroptosis by enhancing the synthesis of adrenic acid, depleting cellular glutathione, and increasing the accumulation of ferrous iron (). The deletion of vopS reduces the ability of V. alginolyticus to secrete extracellular proteases and attenuates virulence ().
The T6SS is a widespread protein secretion apparatus used by Gram-negative bacteria to deliver toxic effector proteins into adjacent bacterial or host cells (). V. alginolyticus possesses two complete T6SS gene clusters, designated T6SS1 and T6SS2 (). Both systems are active at 30 °C, but only T6SS2 is also active at 37 °C, suggesting distinct roles in environmental versus host-associated contexts (). The T6SS mediates interbacterial competition; V. alginolyticus can kill Escherichia coli in a T6SS-dependent manner (). The haemolysin-coregulated protein Hcp2, a hallmark of T6SS2, has been implicated in motility, adhesive capacity, and pathogenicity (). The T6SS is regulated by quorum sensing and the alternative sigma factor RpoN (), and a complex regulatory connection exists between T6SS, quorum sensing, and c-di-GMP signaling through the phosphatase PppA encoded within the T6SS gene cluster (, ).
The T2SS also contributes to V. alginolyticus virulence. Components of the general secretory pathway, including SecA, SecD, SecF, YajC, and YidC, play critical roles in adhesion regulation. Gene silencing of secA, secD, secF, yajC, and yidC significantly reduces adhesion to fish mucus, with secA-RNAi and yidC-RNAi showing the most pronounced effects (35). The expression of these T2SS genes is sensitive to environmental factors including temperature, salinity, pH, and starvation, suggesting that the T2SS mediates adhesion regulation in response to environmental cues (35).
4.3 Haemolysins and toxins
Toxins constitute the most frequently identified category of virulence factors in V. alginolyticus, accounting for more than 50% of virulence-related keywords in bibliometric analyses (36). Haemolysins are the predominant toxins and function as pore-forming exotoxins that lyse erythrocytes and other mammalian cell membranes. V. alginolyticus produces three types of haemolysins: thermostable direct haemolysin (TDH), TDH-related haemolysin (TRH), and thermolabile haemolysin (TLH) (37). TLH is notable for its strong phospholipase activity rather than pore-forming activity, and it has been implicated in the induction of apoptosis through membrane damage (38). In addition to haemolysins, V. alginolyticus produces exfoliative toxins and microbial collagenase (39). The presence of tdh and trh genes, which are well-characterized virulence determinants in V. parahaemolyticus, has been documented in some V. alginolyticus strains (40). Surveillance studies in mariculture-impacted ecosystems have detected tdh in 6.32% and trh in 15.52% of atypical Vibrio isolates, indicating horizontal gene transfer of these virulence determinants across species boundaries () (Figure 1).
4.4 Adhesion, biofilm, and motility
Adhesion to host surfaces is a critical early step in infection, and V. alginolyticus employs multiple adhesins for this purpose. The toxin-coregulated pilus has been identified as a major motility-related virulence factor (41). Mannose-sensitive haemagglutinin type IV pili (MSHA) are also involved in adhesion and biofilm formation (42).
The hierarchical regulatory network governing adhesion involves multiple interconnected pathways. The flagellar assembly pathway, particularly genes encoding the filament (FliC), filament cap (FliD), L-ring (FlgH), and chaperone (FliS), plays an essential role in adhesion. Silencing of fliC, fliD, flgH, and fliS significantly impairs both motility and adhesion, though motility is not the sole mechanism through which the flagellar assembly pathway affects adhesion (43). The two-component regulatory system FlrA-FlrB-FlrC, which controls flagellar synthesis, directly regulates adhesion by modulating the expression of critical downstream genes including fliA, flgH, fliS, fliD, cheR, cheV, and the c-di-GMP-related gene V12G01_22158. Notably, silencing of flrB results in the most pronounced inhibition of flagellar assembly and adhesion, while silencing of flrA and flrC leads to upregulation of virulence genes including toxT, ctxB, and hlyA, suggesting that FlrA and FlrC repress certain virulence factors under normal conditions (44).
The chemotaxis pathway constitutes another critical regulatory layer. Genes encoding methyl-accepting chemotaxis proteins (MCPs), aerotaxis transducer (Aer), methylesterase (CheB), and methyltransferase (CheV) are essential for adhesion. Silencing of mcp, aer, cheB, and cheV not only reduces adhesion but also impairs chemotaxis, flagellar assembly, and motility. The expression of these genes is sensitive to temperature, pH, salinity, and starvation, indicating that environmental factors modulate adhesion through the chemotaxis pathway (45). Chemotaxis genes cheA, cheB, cheR, cheV, and cheY have also been shown to regulate adhesion in the related pathogen V. harveyi by affecting motility (46).
The RstB-RstA two-component system represents an additional regulatory node in the adhesion network. Silencing of rstA and rstB reduces adhesion, biofilm production, motility, haemolysis, and virulence, and their expression is responsive to temperature, pH, and starvation (47). Similarly, the general stress response sigma factor RpoS regulates multiple virulence phenotypes including adhesion, growth, haemolysis, biofilm production, motility, and virulence. RpoS modulates adhesion in response to temperature, pH, and starvation, but not salinity, suggesting pathway-specific environmental sensitivity (48).
Biofilm formation is a central feature of V. alginolyticus pathogenesis, providing protection against environmental stresses, antimicrobial agents, and host immune defenses (49). The biofilm matrix is composed primarily of extracellular polysaccharides, proteins, and nucleic acids. Vibrio exopolysaccharide (VPS) plays multiple roles, functioning both as a molecular glue for cell-cell and cell-surface adhesion and as a structural component of biofilms (50). The vps gene cluster, which is responsible for VPS production, is directly controlled by the alternative sigma factor RpoN. RpoN mediates biofilm formation by directly controlling the vps gene cluster and c-di-GMP synthetic metabolism (51). The stringent response regulators RelA and SpoT, which synthesize the alarmone (p)ppGpp, are involved in regulating cell motility, exopolysaccharide production, and biofilm formation (52, 53). The small non-coding RNA MicX has emerged as a critical regulator of biofilm formation; a ΔmicX mutant exhibits reduced exopolysaccharide synthesis, biofilm formation, and alkaline serine protease production. Proteomic analysis of the ΔmicX mutant identified 900 differentially expressed proteins, with downregulated proteins primarily engaged in biofilm formation, cellular communication, and transmembrane transport (54).
Motility, mediated by flagella, is another important virulence attribute. V. alginolyticus possesses a single polar flagellum that enables swimming motility in liquid environments and swarming over surfaces. The flagellum also contributes to adhesion and biofilm formation (55). Studies using real-time fluorescent imaging have revealed length-dependent flagellar growth in V. alginolyticus (56) (Figure 1).
4.5 Iron acquisition
Iron is an essential nutrient for bacterial growth, and V. alginolyticus has evolved multiple strategies to acquire iron from the host environment. The genome encodes iron acquisition systems, including siderophore-mediated uptake pathways (57). The biosynthetic gene clusters for the siderophore vibrioferrin exhibit genetic and structural variations across Vibrio species, including V. alginolyticus (58). These iron acquisition systems are critical for survival and proliferation within the host, where iron is sequestered by host proteins such as transferrin and lactoferrin.
The copper tolerance system CusS-CusR-CusCFBA exemplifies the intersection of metal homeostasis and virulence regulation. Copper stress, which arises from nutritional immunity during infection, activates the CusS-CusR two-component system, inducing expression of the cusCFBA efflux complex. Unexpectedly, activation of CusS-CusR by copper stress reduces adhesion, haemolysis, biofilm formation, motility, and overall virulence, despite conferring copper tolerance. This suggests that V. alginolyticus prioritizes copper homeostasis over virulence expression when facing metal stress, possibly as an energy-conservation strategy (59). Promoter region analysis, EMSA, and LacZ reporter assays confirmed that CusR directly regulates multiple virulence-related genes including pilN, ompA, lptC, pykF, pflD, and feoA, establishing a direct link between metal-sensing two-component systems and virulence gene regulation (59) (Figure 1).
5 Virulence regulatory mechanisms
Virulence in V. alginolyticus is coordinated by multilayered regulatory networks. Among these, quorum sensing and non-coding RNAs provide major cell-density-dependent and post-transcriptional regulatory mechanisms, respectively.
5.1 Quorum sensing
Quorum sensing (QS) is a cell-density-dependent regulatory mechanism that orchestrates many bacterial behaviors, including virulence and biofilm formation (60). In V. alginolyticus, QS tightly regulates pathogenicity. The QS circuit involves the production and detection of signaling molecules, predominantly N-acyl homoserine lactones (AHLs) (61). AphA, a master activator of the QS system at low cell density, can initiate the virulence cascade by positively regulating the expression of secretion systems, flagellar systems, and biofilm formation (62). At high cell density, LuxR becomes the dominant regulator. The small RNA MicX modulates QS by affecting the expression levels of LuxR and AphA (54) (Figure 1).
An intriguing and potentially clinically relevant finding is that QS positively regulates capsular polysaccharide (CPS)-dependent phage infection. QS upregulates the expression of the ugd gene, leading to increased synthesis of Autographiviridae phage receptor CPS. While this QS-mediated increase in phage susceptibility represents a trade-off, it also results in the upregulation of virulence factors, promoting biofilm development and enhanced capsular polysaccharide production. This observation has important implications for phage therapy, as inhibiting QS may reduce the therapeutic efficacy of CPS-specific phages (63).
5.2 Non-coding RNAs
Recent systematic screens have identified numerous non-coding RNAs (ncRNAs) that function as critical post-transcriptional regulators of virulence in V. alginolyticus. High-throughput sequencing combined with bioinformatics analysis revealed 32 ncRNAs commonly altered under adhesion-reducing stress conditions (Cu2+, Pb2+, Hg2+, and low pH) (64). Among these, seven ncRNAs, Candidate_103, Candidate_283, Candidate_424, Candidate_438, Candidate_442, Candidate_448, and Candidate_635, negatively regulate adhesion by targeting genes encoding type IV pilus assembly proteins (PilQ, PilM), chemotaxis proteins (MotB), and flagellar motor switch proteins (FliM) (65). Stable overexpression of these ncRNAs significantly reduced both target gene expression and adhesion ability, confirming their regulatory roles (65).
The ncRNA Vvrr1 (Vibrio virulence regulatory RNA 1) has been characterized as a key regulator of virulence. Overexpression of Vvrr1 reduces adhesion, biofilm formation, and virulence in V. alginolyticus. Proteomic analysis identified pyruvate kinase I (PykF) as a primary target of Vvrr1. GFP reporter gene analysis confirmed that Vvrr1 interacts with pykF mRNA, and silencing of pykF phenocopies the effects of Vvrr1 overexpression, reducing adhesion, biofilm formation, and virulence, while downregulating downstream genes including ndk, eno, sdhB, glpF, and cysH (66). The Vvrr1-PykF axis thus represents a critical regulatory node linking metabolism and virulence.
Furthermore, the ncRNA Vvrr1 has been shown to modulate the VarS/VarA-Csr system via the transcriptional regulator LeuO. Vvrr1 post-transcriptionally represses LeuO by targeting leuO mRNA and accelerating its decay. LeuO, in turn, directly represses varS transcription by binding to a conserved motif (ATTGGTGTTCAT) in the varS promoter. This repression alleviates inhibition of the Csr sRNAs (CsrB, CsrC, CsrD), which sequester the global regulator CsrA, leading to derepression of LuxO and subsequent modulation of exopolysaccharide biosynthesis and biofilm architecture (67). This multilayered regulatory circuit, from sRNA to transcription factor to two-component system to small RNA cascade, exemplifies the sophisticated integration of post-transcriptional and transcriptional control mechanisms in V. alginolyticus pathogenesis.
Building on this work, the ncRNA Vvrr2 has been shown to regulate biofilm formation through multiple target genes. Overexpression of Vvrr2 reduces adhesion, motility, biofilm formation, and virulence. Raman spectroscopy and confocal laser scanning microscopy revealed that Vvrr2 overexpression alters both the chemical composition and three-dimensional structure of biofilms, reducing extracellular polysaccharide, protein, and nucleic acid content (68). GFP reporter assays confirmed that Vvrr2 directly targets fliG (flagellar rotor protein), cheV (chemotaxis signal transduction protein), and lps (lipopolysaccharide synthesis), which are essential for motility, adhesion, and biofilm formation, respectively (68).
The oligopeptide permease (Opp) system, while not an ncRNA itself, functions within the broader regulatory network of adhesion. The oppABCDF gene cluster contributes to multiple steps of pathogenesis, including adhesion, biofilm production, and haemolytic activity. Silencing of oppA, oppB, oppC, oppD, and oppF reduces adhesion, peptide internalization, biofilm formation, haemolytic activity, and virulence, while expression of oppABCDF is sensitive to temperature, pH, and starvation (69) (Figure 1).
6 Outer membrane vesicles
Outer membrane vesicles (OMVs) have emerged as important mediators of V. alginolyticus pathogenesis and intercellular communication. V. alginolyticus produces OMVs with typical characteristics, spherical, membrane-bound structures ranging from 10 to 400 nm in diameter, containing the outer membrane protein OmpC (70). These OMVs carry a high abundance of small RNAs (sRNAs), which are protected from RNase degradation by the lipid membrane, indicating that OMVs serve as vehicles for sRNA delivery (70).
RNA sequencing of OMV-associated sRNAs identified 180 distinct sRNA sequences, with the ten most abundant sRNAs predicted to regulate genes involved in quorum sensing, secretion systems, two-component signal transduction, biofilm formation, and amino acid and carbohydrate metabolism (70). Two of these sRNAs, Va.OMV_R1 and Va.OMV_R8, were functionally characterized. Deletion of Va.OMV_R1 or Va.OMV_R8 reduced motility, extracellular matrix production, and biofilm formation by 52.7% and 58.7%, respectively. qRT-PCR validation confirmed that Va.OMV_R1 regulates target genes including yscT, tkt1, aroB, and ygiP, while Va.OMV_R8 regulates clpV1, gcvA, mraY, and oppD (70).
Crucially, OMVs from wild-type V. alginolyticus promote biofilm formation in a dose-dependent manner, accelerating biofilm development and increasing biomass. However, OMVs from Va.OMV_R1 or Va.OMV_R8 knockout strains exhibit diminished biofilm-promoting activity. GFP reporter assays and rifampicin chase experiments confirmed that Va.OMV_R1 promotes yscT expression while Va.OMV_R8 represses gcvA translation, establishing direct sRNA-mRNA interactions (70). These findings demonstrate that OMVs deliver functional sRNAs to recipient bacterial cells, modulating gene expression and biofilm formation through intercellular communication, a mechanism with significant implications for bacterial community behavior and pathogenesis (Figure 1).
The major virulence factors discussed above, including secretion systems, haemolysins, adhesins, motility apparatus, iron acquisition systems, regulatory circuits (quorum sensing, two-component systems, sigma factors, non-coding RNAs), and outer membrane vesicles, are summarized in Table 1 with their respective functions and key references.
Table 1
| Virulence factor category | Specific factors | Function |
|---|---|---|
| Secretion systems | T3SS (effectors VopQ, VopR, VopS, VPA0450) | Translocation of effectors into host cells; VopR induces apoptosis via MKK pathway (); VopS induces ferroptosis () |
| T6SS1 and T6SS2 | Interbacterial competition; delivery of toxic effectors; T6SS2 active at 37 °C (, ) | |
| T2SS (SecA, SecD, SecF, YajC, YidC) | Secretion of extracellular enzymes; adhesion regulation (35) | |
| Haemolysins and toxins | TDH, TRH, TLH | Pore-forming and phospholipase activities; cytolysis; apoptosis induction (37, 38) |
| Exfoliative toxins, collagenase | Tissue damage (39) | |
| Adhesion and biofilm | VPS (Vibrio exopolysaccharide) | Biofilm matrix component; cell-cell and cell-surface adhesion (50) |
| MSHA pili | Adhesion; biofilm formation (42) | |
| Toxin-coregulated pilus | Motility-related virulence (41) | |
| Motility | Polar flagellum | Swimming and swarming motility; adhesion (55) |
| Iron acquisition | Vibrioferrin siderophore | Iron acquisition from host (57, 58) |
| CusS-CusR-CusCFBA | Copper tolerance; negatively regulates virulence under copper stress (59) | |
| Regulation | Quorum sensing (AphA, LuxR) | Cell-density-dependent regulation of virulence; biofilm formation (60–62) |
| sRNA MicX | Post-transcriptional regulation of biofilm and QS (54) | |
| RpoN | Regulation of vps cluster and biofilm formation (51) | |
| FlrA-FlrB-FlrC | Flagellar synthesis; adhesion regulation via downstream genes (44) | |
| RstB-RstA | Adhesion, biofilm, motility, haemolysis regulation (47) | |
| RpoS | Stress response; adhesion, growth, haemolysis, biofilm, motility, virulence (48) | |
| sRNA Vvrr1 | Represses adhesion, biofilm, virulence via PykF and LeuO-VarS-Csr cascade (66, 67) | |
| sRNA Vvrr2 | Represses biofilm formation via FliG, CheV, Lps (68) | |
| Outer membrane vesicles | OMV-associated sRNAs (Va.OMV_R1, Va.OMV_R8) | Intercellular sRNA delivery; biofilm regulation (70) |
| Nutrient acquisition | OppABCDF | Oligopeptide transport; adhesion, biofilm, haemolysis, virulence (69) |
Major virulence factors of Vibrio alginolyticus.
T2SS, type II secretion system; T3SS, type III secretion system; T6SS, type VI secretion system; Vop, Vibrio outer protein; MKK, mitogen-activated protein kinase kinase; TDH, thermostable direct haemolysin; TRH, TDH-related haemolysin; TLH, thermolabile haemolysin; VPS, Vibrio exopolysaccharide; MSHA, mannose-sensitive hemagglutinin; QS, quorum sensing; sRNA, small regulatory RNA; OMV, outer membrane vesicle.
7 Host-pathogen interactions and immune response
The interaction between V. alginolyticus and its hosts involves complex molecular crosstalk that determines the outcome of infection (Figure 2). In aquatic organisms, the innate immune system provides the primary defense against Vibrio infections. Transcriptomic studies in bivalves have revealed that the response to V. alginolyticus infection involves coordinated regulation of pathogen recognition, oxidative stress, inflammatory signaling, apoptosis, and antimicrobial defense. In the clam Mactra veneriformis, infection triggers significant changes in multiple signaling pathways, including those involved in lysosomes, apoptosis, amino acid metabolism, and endocytosis (71).
Figure 2
In fish, the immune response to V. alginolyticus involves both humoral and cellular components. Glutathione peroxidase homologs from teleosts, such as PoGPx-7 (glutathione peroxidase homolog 7 from Paralichthys olivaceus), exhibit bactericidal activity by binding to V. alginolyticus via lipopolysaccharide and peptidoglycan, and activate host immune cells (72). The anti-lipopolysaccharide factor ALF4 has been identified as a key immune regulator against V. alginolyticus in the mud crab Scylla paramamosain (73).
Environmental stressors can modulate host susceptibility to V. alginolyticus infection. Low salinity stress does not significantly affect the proliferation or virulence of the bacterium but can significantly alter the microbial composition and immune response of infected oysters. The synergistic interaction between environmental stress and pathogen infection can cause mass mortalities by inducing host microflora imbalance and immune dysregulation (74). Understanding these environment–host–pathogen interactions is critical for predicting and managing disease outbreaks in aquaculture settings.
The metabolic interplay between host and pathogen represents another dimension of the host–pathogen interaction. The tricarboxylic acid (TCA) cycle plays a central role in this context. Genes encoding key TCA cycle enzymes, including phosphoenolpyruvate carboxylase (PckA), pyruvate dehydrogenase (PdhB), aconitate hydratase (AcnA), succinate dehydrogenase (SdhC), succinyl-CoA synthetase (SucC), and 2-oxoglutarate ferredoxin oxidoreductase (OorA), are downregulated under adhesion-reducing stress conditions (Cu2+, Pb2+, and low pH). Silencing of these genes reduces adhesion by 2.13- to 5.51-fold, with acnA showing the closest association with adhesion (75). Expression of TCA cycle genes is sensitive to pH and starvation, but not temperature, suggesting pathway-specific environmental responsiveness. The TCA pathway thus functions as an important metabolic sensor that links energy metabolism, precursor biosynthesis, and adhesion regulation (75).
Similarly, the oxidative phosphorylation pathway contributes to adhesion regulation. Six genes encoding subunits of cytochrome c oxidases, coxA, coxB, coxC (aa3-type) and ccoN, ccoO, ccoQ (cbb3-type), are downregulated under Cu2+, Pb2+, and low pH stress. Silencing of these genes reduces both cytochrome c oxidase activity and adhesion, with ccoQ showing the greatest impact on adhesion despite encoding a non-catalytic subunit (76). The expression of oxidative phosphorylation genes is sensitive to temperature, salinity, pH, and starvation, indicating that this pathway mediates adhesion regulation across diverse environmental conditions (76). These findings establish that central carbon and energy metabolism are integral components of the virulence regulatory network, not merely passive housekeeping functions.
7.1 Antimicrobial resistance
Antimicrobial resistance (AMR) in V. alginolyticus has emerged as a significant concern for both aquaculture and public health (77). The widespread use of antibiotics in aquaculture has contributed to the selection and dissemination of resistant strains ().
7.2 Resistance prevalence
Surveillance studies have documented high rates of antibiotic resistance among V. alginolyticus isolates. A study of isolates from seafood and freshwater products in China found that 122 out of 128 isolates (95.31%) were resistant to at least one antibiotic category, and 2 isolates (1.56%) exhibited multidrug resistance (resistance to at least three antibiotic categories) (). Similarly, V. alginolyticus isolates from aquaculture systems showed high resistance to ampicillin, erythromycin, cefotaxime, kanamycin, and doxycycline, with multiple antibiotic resistance (MAR) indices reaching 0.55–0.80 in isolates from the Hergla aquaculture farm (78). In Norwegian marine environments, resistance or reduced susceptibility to ampicillin was observed in 74% of V. alginolyticus isolates (79).
Seasonal surveillance in mariculture-impacted ecosystems reveals that the MAR index of environmental Vibrio isolates ranges from 0.01 to 0.03 across seasons, with three MAR strains detected (). Notably, resistance to neomycin (6.78%) and intermediate resistance to neomycin (81.4%) and ciprofloxacin (31.07%) were observed, suggesting that these antibiotics may be under selective pressure and that resistance could emerge more broadly (). The detection of MAR strains in spring, summer, and autumn indicates ongoing selection pressure in aquaculture environments.
7.3 Resistance mechanisms
Genomic analyses have identified five types of antibacterial drug resistance genes in V. alginolyticus (). The most striking finding is the universal presence of β-lactam resistance genes: their prevalence is 100% among isolates, indicating a potential risk of natural resistance to β-lactam drugs. The blaCARB gene, encoding a carbenicillin-hydrolysing class A β-lactamase, is particularly prevalent, with detection rates of 98.04% in some studies (, ). Other commonly detected resistance genes include tet (encoding tetracycline resistance, 97.06%) and fos (encoding fosfomycin resistance, 4.90%) (). Multidrug efflux pumps, such as the CRP-encoding efflux pump conferring resistance to fluoroquinolones and macrolides, have also been identified (80).
The discordance between genotypic and phenotypic resistance patterns has been noted; despite the ubiquitous presence of blaCARB genes in V. alginolyticus, both between- and within-species variations in ampicillin resistance are observed. This suggests that resistance gene carriage does not always translate to phenotypic resistance, possibly due to differences in gene expression or the presence of additional resistance mechanisms (81).
7.4 Implications
The high prevalence of AMR in V. alginolyticus has important implications. For aquaculture, antibiotic treatment options are becoming increasingly limited, necessitating the development of alternative control strategies. For public health, the potential for horizontal gene transfer of resistance determinants between V. alginolyticus and other Vibrio species, including human pathogens such as V. cholerae and V. parahaemolyticus, is a concern (80). The presence of mobile genetic elements in V. alginolyticus genomes facilitates such transfer (). Virulence genes also show evidence of horizontal transfer; tdh, trh, and hlyA are detected in atypical host strains at rates of 6.32%, 15.52%, and 11.30%, respectively, indicating that virulence determinants move across species boundaries within the Vibrio genus (). The antimicrobial resistance genes identified in V. alginolyticus, their prevalence rates, and their mechanisms of action are summarized in Table 2.
Table 2
| Resistance gene | Specific genes | Prevalence | Mechanism |
|---|---|---|---|
| β-Lactam resistance | blaCARB (class A β-lactamase) | 98%−100% (, ) | Hydrolysis of β-lactam antibiotics |
| Tetracycline resistance | tet (efflux) | 97.06% () | Tetracycline efflux |
| Fosfomycin resistance | fos | 4.90% () | Fosfomycin inactivation |
| Multidrug efflux | CRP-encoding efflux pump | Variable (80) | Efflux of fluoroquinolones and macrolides |
| Chloramphenicol resistance | Type B chloramphenicol O-acetyltransferase | Detected (106) | Chloramphenicol acetylation |
| Oxytetracycline resistance | Phosphoribosyltransferase | Detected (106) | Oxytetracycline modification |
Antimicrobial resistance genes and prevalence in Vibrio alginolyticus.
blaCARB, gene encoding a CARB-type class A β-lactamase; tet, tetracycline resistance gene family; fos, fosfomycin resistance gene family; CRP, cyclic AMP receptor protein.
8 Detection and diagnosis
Accurate and rapid detection of V. alginolyticus is essential for both clinical diagnosis and surveillance in aquaculture and food safety contexts. Traditional culture-based methods, while reliable, are time-consuming and require expertise in species identification. Molecular methods have largely supplanted culture for many applications.
Several PCR-based approaches have been developed for V. alginolyticus detection. Real-time PCR (qPCR) targeting the groEL gene has been employed for detection and quantification (82). Multiplex real-time PCR assays using TaqMan probes have been developed for the simultaneous detection of multiple Vibrio species, including V. alginolyticus (83). A triple PCR method targeting the blaCARB-17 gene of V. parahaemolyticus and the gyrB gene of V. alginolyticus enables simultaneous detection of V. parahaemolyticus, V. alginolyticus, and V. cholerae in aquatic foods (84). Digital PCR-based methods using microfluidic chambers offer quantitative detection with high sensitivity (85). To differentiate between viable and non-viable cells, propidium monoazide (PMA) has been coupled with multiplex real-time PCR (86). The limit of detection for some RT-PCR methods can be as low as 0.88 pg of DNA per reaction or 2 CFU per reaction (87).
9 Control strategies
The increasing prevalence of antimicrobial-resistant V. alginolyticus strains has spurred interest in alternative control strategies. These include phage therapy, vaccination, and probiotic approaches (88).
9.1 Phage therapy
Bacteriophages offer a promising alternative to antibiotics for controlling V. alginolyticus infections. Numerous lytic phages have been isolated and characterized. Phage R12Z, a broad-spectrum vibriophage, infects at least three Vibrio species, including seven strains of V. alginolyticus, and shows effective protection of shrimp postlarvae (89). Application of a V. alginolyticus phage to seabream resulted in a 93% decrease in the Vibrio population (90). Phage R23Z, a lytic siphovirus, significantly enhanced shrimp survival rates (>16%) during V. alginolyticus infection (91). The jumbo vibriophage pVa-22 possesses antivirulence activity and therapeutic potential (92). Importantly, phages can inhibit biofilm formation and eradicate mature biofilms (93).
However, phage therapy faces challenges, including the development of phage resistance. V. alginolyticus can acquire resistance through mutations in genes involved in the biosynthesis of phage receptors (94). The finding that QS positively regulates CPS-dependent phage infection suggests that inhibiting QS may inadvertently reduce phage therapy efficacy (63).
9.2 Vaccination
Vaccination represents another important control strategy for aquaculture. Several vaccine candidates have been developed against V. alginolyticus (88). Live-attenuated vaccines (LAVs) have shown particular promise. An attenuated live strain of the HY9901 mutant Δgr provided protection against V. alginolyticus in pearl gentian grouper (95). Similarly, LAV candidates ΔcpxA and ΔcpxR have been evaluated (96). A hop (T3SS effector) mutant has been constructed and evaluated as a potential LAV in orange-spotted grouper (97). Subunit vaccines targeting flagellin proteins FlaD and FlaF, combined with the Montanide™ ISA 763B VG adjuvant, have induced protective immune responses in pearl gentian grouper (98). Autogenous vaccines, formulated from locally prevalent strains, can reduce antibiotic dependence (99). The Hfq mutant has also been proposed as a live attenuated vaccine candidate, given its role in stress adaptation and virulence (100).
9.3 Probiotics
Probiotics offer a sustainable and eco-friendly alternative to antibiotics for disease prevention in aquaculture, functioning through multiple mechanisms that collectively enhance host resistance while suppressing pathogen proliferation. The protective effects of probiotics are mediated through several complementary pathways: competitive exclusion of pathogens for adhesion sites and nutrients, secretion of antimicrobial compounds that directly inhibit Vibrio growth, interference with bacterial quorum sensing systems that coordinate virulence gene expression, and modulation of the host's innate immune responses (). These mechanisms work synergistically to improve larval survival, enhance digestive enzyme activities, stabilize gut microbial communities, and maintain water quality in aquaculture systems (, 101).
Among the most extensively studied probiotic genera in the context of V. alginolyticus control are Bacillus, Lactobacillus, and Pseudoalteromonas. In vitro antagonistic assays have demonstrated that Lacticaseibacillus paracasei and Bacillus amyloliquefaciens significantly inhibit the growth of V. alginolyticus and V. vulnificus in white shrimp (Litopenaeus vannamei) culture, with treated groups showing markedly lower Vibrio counts and ammonia levels compared to controls (101). Lactobacillus plantarum strains isolated from kefir have been shown to enhance non-specific immunity and immune-related gene expression in white shrimp; feeding with strain MRS18 at 109 CFU/g for 14 days significantly improved survival rates following V. alginolyticus challenge (102).
Beyond Bacillus and Lactobacillus, other probiotic candidates have shown promise. Pseudoalteromonas piscicida strain SW-1, isolated from seawater in a clam farm, inhibits the growth of V. alginolyticus in vitro and improves clam survival following challenge. Mortality was only 11% when clams were simultaneously exposed to Pseudoalteromonas SW-1 and the pathogen, compared to 100% mortality in the pathogen-only group (103). Strains of Bacillus licheniformis YB-1 and Bacillus megaterium YB-2, isolated as potential probiotics for sea cucumber aquaculture, demonstrate strong antibacterial activity against V. alginolyticus in vitro, and the optimal combination achieved a 55% survival rate after pathogen challenge (104).
The integration of probiotics with modern aquaculture practices, such as biofloc technology and zero-water-exchange systems, has further strengthened their disease management potential by creating stable microbial ecosystems that naturally suppress Vibrio proliferation (101).
Despite these promising outcomes, the large-scale application of probiotics in aquaculture faces several practical challenges. A major limitation is stability, as maintaining microbial viability during feed formulation, storage, and exposure to variable environmental conditions such as temperature, salinity, and pH remains difficult (). Many probiotic strains lose activity before reaching the host's gastrointestinal tract, thereby reducing their intended biological effects (). Another challenge concerns applicability and consistency, as probiotic performance varies according to host species, developmental stage, culture conditions, and local microbial communities (). Such strain-specific interactions necessitate customized formulations rather than universal “one-size-fits-all” solutions (). Economic feasibility is also a key constraint, as continuous application is often required to maintain optimal probiotic levels, and production, formulation, and quality-control expenses can limit adoption, especially among small- and medium-scale farms (). The lack of standardized regulatory frameworks and quality-assurance guidelines further complicates product evaluation and comparison across markets, leading to inconsistent performance of commercial formulations ().
Nevertheless, the growing body of evidence supporting the efficacy of probiotics, combined with increasing pressure to reduce antibiotic use in aquaculture, underscores their potential as essential tools for sustainable disease management (101). Future research should focus on strain selection and optimization, formulation technologies that enhance stability and delivery, and the integration of probiotics into comprehensive health management strategies that combine biosecurity, environmental monitoring, and targeted interventions (, 101).
10 Challenges and future research
Despite significant advances in understanding V. alginolyticus, several major challenges and priorities for future research remain. First, the molecular details of host–pathogen interactions, particularly the signaling pathways targeted by T3SS effectors and the mechanisms by which the bacterium evades host immune responses, warrant further investigation. The interplay between metabolic pathways (TCA cycle, oxidative phosphorylation) and virulence regulation represents a particularly promising area for future research (75, 76). Second, the ecological factors driving the emergence and dissemination of pathogenic and antibiotic-resistant strains are incompletely understood (). The role of mobile genetic elements in the horizontal transfer of virulence and resistance genes merits closer scrutiny, particularly given the evidence of horizontal gene transfer of tdh, trh, and hlyA across Vibrio species (). Third, the development of effective and practical control strategies for aquaculture settings requires continued research, particularly in the areas of phage therapy, vaccination, and probiotics (88). The complex interplay between QS, biofilm formation, and phage susceptibility highlights the need for integrated approaches that consider the multiple layers of regulation governing V. alginolyticus pathogenesis (63). Fourth, improved surveillance systems that integrate genomic, environmental, and clinical data are needed to detect emerging threats and inform public health interventions (). The spatial and seasonal heterogeneity of Vibrio communities in mariculture-impacted ecosystems underscores the importance of targeted monitoring in high-risk areas (, ). Finally, the impact of climate change on the distribution and virulence of V. alginolyticus, and on the broader Vibrio community, represents a critical area for future investigation (, 105). The emerging roles of ncRNAs and OMVs in virulence regulation (66–68, 70) open new avenues for therapeutic intervention, including RNA-based biopesticides and OMV-targeted strategies.
11 Conclusion
Vibrio alginolyticus has transitioned from a largely overlooked environmental organism to an emerging pathogen of significant concern in aquaculture and public health. Its success as a pathogen reflects a combination of factors: a versatile genome encoding diverse virulence determinants, sophisticated regulatory systems including quorum sensing, two-component systems, and non-coding RNAs, the capacity to form protective biofilms, the ability to deploy outer membrane vesicles for intercellular communication, and an expanding repertoire of antimicrobial resistance genes. The convergence of climate change, aquaculture intensification, and antimicrobial overuse has created conditions favorable for the continued emergence of V. alginolyticus as a threat to both aquatic animal health and human wellbeing. Addressing this threat will require an integrated, One Health approach that encompasses surveillance, basic research on pathogenesis, and the development of sustainable control strategies. Practical priorities include cross-sector sharing of surveillance data, improved aquaculture biosecurity and water-quality management, and stronger antimicrobial stewardship to reduce unnecessary antibiotic use and monitor resistance. These coordinated measures may support earlier outbreak detection and more sustainable control of V. alginolyticus.
Statements
Author contributions
SW: Investigation, Visualization, Funding acquisition, Conceptualization, Writing – original draft. JL: Visualization, Funding acquisition, Investigation, Writing – original draft. RX: Writing – original draft, Resources, Investigation, Funding acquisition. WX: Formal analysis, Writing – review & editing, Supervision, Project administration.
Funding
The author(s) declared that financial support was received for this work and/or its publication. This work was funded by Fujian Provincial Key Laboratory of Marine Physical and Geological Processes (grant number KLMPG-25-05), and the Natural Science Foundation of Xiamen, China (grant numbers: 3502Z202674013, 3502Z202374070).
Conflict of interest
WX was employed by Aquabrain Biotech (Xiamen) Co., Ltd.
The remaining author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Summary
Keywords
control strategies, environmental distribution, genomics, host-pathogen interactions, immune response, virulence mechanisms
Citation
Wei S, Lin J, Xue R and Xu W (2026) Vibrio alginolyticus: an emerging marine pathogen at the intersection of aquaculture, public health, and antimicrobial resistance. Front. Vet. Sci. 13:1965608. doi: 10.3389/fvets.2026.1965608
Received
12 August 2026
Revised
28 August 2026
Accepted
04 September 2026
Published
29 September 2026
Volume
13 - 2026
Edited by
Lixing Huang, Jimei University, China
Updates
Copyright
© 2026 Wei, Lin, Xue and Xu.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Wei Xu, xwkhj@163.com
Disclaimer
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