| Vibrio vulnificus | |
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| False-colorSEM image ofVibrio vulnificus | |
Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Pseudomonadati |
| Phylum: | Pseudomonadota |
| Class: | Gammaproteobacteria |
| Order: | Vibrionales |
| Family: | Vibrionaceae |
| Genus: | Vibrio |
| Species: | V. vulnificus |
| Binomial name | |
| Vibrio vulnificus | |
| Synonyms | |
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Vibrio vulnificus is a species ofGram-negative, motile, curved rod-shaped (vibrio), pathogenicbacteria of the genusVibrio. Present in marine environments such asestuaries, brackish ponds, or coastal areas,V. vulnificus is related toV. cholerae, the causative agent ofcholera.[3] At least one strain ofV. vulnificus isbioluminescent.[4]Increasing seasonal ocean temperatures and low-salt marine environments like estuaries favor a greater concentration ofVibrio within filter-feeding shellfish;V. vulnificus infections in the Eastern United States have increased eightfold from 1988–2018.
Infection withV. vulnificus leads to rapidly expanding skin infections by entering a wound causingcellulitis or evensepsis.[5]: 279 V. vulnificus is also a source of foodborne illness. It was first isolated as a source of disease in 1976.[6]
Vibrio vulnificus is a species ofgram-negative, motile, curved rod-shaped (bacillus), pathogenicbacteria of the genusVibrio. Present in marine environments such asestuaries, brackish ponds, or coastal areas,V. vulnificus is related toV. cholerae, the causative agent ofcholera.[7]The most harmful strains ofV. vulnificus documented have been observed in three different forms. The first is when there is a layer of protective sugar molecules surrounding the bacteria called a anti-phagocytic polysaccharide capsule. By encapsulating the bacteria, phagocytosis andopsonization can not occur, thus allowing the bacteria to continue throughout the organism it is in. The second way thatV. vulnificus has been most harmful is with some of the toxins that it creates. These toxins are not part of the infection thatV. vulnificus causes but instead they are part of a secondary infection in the gastrointestinal tract that most certainly will lead to systemic infection. Lastly,V. vulnificus has been seen to cause more harm in patients who have higher levels of iron.[8]
The genome size ofV. vulnificus is approximately 5.3Mbp. The genome is organized into two circular replicons, similar to that ofV. cholerae, which also has a large and a small chromosome. However, the genome ofV. vulnificus is at least one megabase bigger.[9][10][11][12]
Natural transformation is abacterial adaptation forDNA transfer between individual cells.V. vulnificus was found to become naturally transformable during growth onchitin in the form of crab shells.[13] The ability to now carry out transformation experiments in the laboratory should facilitatemolecular genetic analysis of this opportunisticpathogen.[13]
V. vulnificus has at least 3 biotypes. Biotype 1, which was the first to be isolated, is the biotype responsible for virtually all human infections. Within biotype 1, two distinctgenotypes have been isolated, the C-genotype (clinical) and the E-genotype (environmental). The C-genotype is associated with human clinical cases, and carries specific genes that increase virulence and resistance to serum killing. The E-genotype has been isolated from oysters and water, and possesses unique genes associated with enhanced environmental survival. This discovery has led to the proposal thatV. vulnificus exists as two divergentecotypes.[14][15]
Biotype 2, which has rarely been isolated in humans, primarily infects farm-raised eels, causing a fatalsepticemia. Biotype 3 is thought to be a hybrid of biotypes 1 and 2, and has only been isolated in human wound infections after an outbreak in an Israeli tilapia aquaculture in 1996.[14]
V. vulnificus has acapsule, made of polysaccharides, and is thought to protect againstphagocytosis.[16] The capsule also aids the bacteria in escapingopsonization.[17] Different strains of the bacteria are capable of shifting through the unencapsulated and encapsulated forms. Mouse models have shown that the unencapsulated forms are avirulent. These same strains, however, are more likely to be in their encapsulated form when taken up by oysters.[18]Varying levels of oxygen determine the amount of capsular production. Oxygen levels increase the amount of capsule the bacteria can make. Out of the two genotypes the strain commonly found in the environment showed a higher level of capsular production than the one found in human infections. In low oxygen conditions the capsule appears thin and translucent, while it is normally supposed to be thicker and more opaque.[19]
V. vulnificus creates lessbiofilm under anaerobic conditions, when in most bacteria the opposite is the case. Genotypes that are found more in the environment show this correlation more than the genotypes found in human infection. Environmental strains such as temperature change also play a role in the formation of biofilms, with lower temperatures increasing the production. Strains found in human infection showed more biofilm formation at temperatures of 24 °C than environmental strains, showing these strains are adapted for their environments.[20]
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Like allgram-negative bacteria,V. vulnificus has LPS (lipopolysaccharide) as the major component of its outer membrane. However, the LPS the bacteria produces isn't as efficient at triggering the immune system's release oftumor necrosis factor (TNF) alpha and other cytokines that produce shock syndromes. The capsular proteins the bacteria express, however, are capable of producing an immune response contributing to shock syndrome.[21]
V. vulnificus produces a number of extracellular toxins such asmetalloprotease VvpE,cytolysin/hemolysin VvhA, and themultifunctional autoprocessing repeats-in-toxins (MARTX) toxin.[22] These exotoxins are released to promote damage of host tissue, aid the spread of bacteria through the body, and evade immune defenses.[23]
Most prominently, MARTX toxin attaches to the cell membrane of host cells and injects effector domains which cause a cascade of effectors that aid the bacteria's binding ability, discontinue maintenance of cell skeleton, block autophagy, and disrupt internal cell signaling. Another exotoxin, PlpA breaks down host cell membranes and works with MARTX to cause necrotic damage. Two exotoxins, VvhA and VvpE are not essential in the pathogens ability to cause disease, but in combination with MARTX they are able to drastically worsen the infection. VvhA creates pores in cells to promote apoptosis, inflammation, and cytokine storms while VvpE breaks down proteins making colonization easier.[23]
These exotoxins collaborate to maximize infection, tissue damage and immune disruption. Different strains can have a different combination of exotoxins and MARTX effectors, explaining how the severity of infection and symptoms can differ.[23] While the VvhA and MARTX toxin are factors in the bacteria's virulence, in vivo studies in mice suggest that the MARTX toxin is more responsible for bacterial dissemination from the intestine to produce sepsis.[22][24]
Growth ofV. vulnificus is dependent on the amount of iron that is accessible to the bacteria.[25][26][27][28] The observed association of the infection with liver disease (associated with increased serum iron) might be due to the capability of more virulent strains to capture iron bound totransferrin.[16]
V. vulnificus is a motile bacterium that uses a polarflagellum to swim. The flagellum allows the bacterium to move to more favorable conditions. Motility also contributes to pathogenesis as it facilitates adhesion to host cells, biofilm formation, and colonization. Experimental studies have shown that mutants lacking a functional flagellum exhibit reduced movement, decreased adherence to epithelial cells, impaired biofilm formation, and lower virulence in animal models.[29]
V. vulnificus has genes that encode for the biosynthesis of atype IV pilus. These genes have been located on the large chromosome and may helpV. vulnificus adhere to host cells and with motility.[9]
V. vulnificus uses aquorum-sensing (QS) system in communication and virulence gene regulation. The QS system controls SmcR, which is the principal protein that regulates the expression of virulence genes, including CPS-related genes that promote capsular polysaccharide synthesis and the metalloproteinase gene vvpE. The QS system ofV. vulnificus is also related to a regulation of bacterial biofilm formation and plays a role in activation and suppression of toxins and enzymes that are key to the pathogenesis of the bacteria. At a low cell density, the QS communicates to suppress the expression of SmcR, effectively inactivating virulence genes, and at high cell density, the QS system works to signal the expression of SmcR, thus activating virulence genes.[30]
V. vulnificus requires many specific nutrients in order to grow and proliferate. The proliferation ofV. vulnificus is significantly higher during algal blooms, when an excess of nutrients from runoff or temperature changes occur.[31][32] This bacteria is classified as a facultative anaerobe and a chemoorganoheterotroph, which means it gets its energy from chemical compounds and uses organic molecules for electron and carbon sources. It uses various organic molecules, which become more abundant prior to an algal bloom.V. vulnificus processes glucose and many other carbohydrates through theEmbden-Meyerhof Parnas (EMP) pathway for glycolysis. Pyruvate generated from this pathway and others contribute to thetricarboxylic acid (TCA) cycle that produces electron sources for the bacterium'selectron transport chain.[33]V. vulnificus is usually found in brackish waters, like estuaries, where freshwater mixes with ocean saltwater. However, with the increase of nutrients that bring algal blooms,V. vulnificus proliferates in the same conditions. In fact, the phytoplankton that form an algal bloom produce a gas, Dimethylsulfoniopropionate (DMSP) that bacteria can utilize as an osmoprotectant.[31] The combination of increased nutrients and ability to protect itself from high salinity is what drivesV. vulnificus growth in the ocean.
When preferred carbon sources are limited,Vibrio vulnificus is able to use a broad range of alternative carbon sources which contributes to its success in survival and growth in its environments. Recent studies have found thatV. vulnificus's use of alternative carbon sources, namelyglycerol,mannitol,pyruvate,maltose,trehalose, andpropylene glycol, influences the expression of virulence genes. Specifically, mannitol and propylene glycol were found to strongly reduce thetranscription of virulence-related genes.[34]
In the United States,Vibrio vulnificus is responsible for 95% of all seafood-related mortalities.Vibrio vulnificus infections have a 33% mortality rate, which is the highest mortality rate of all food-borne illnesses in the United States. The infection can lead to many diseases, includinggastroenteritis,cellulitis,necrotizing fasciitis, andsepsis.[35]
Vibrio vulnificus typically breeds in warm coastal waters. Infection generally arises from the consumption ofV. vulnificus contaminated seafood or exposure of open wounds to contaminated seawater. The bacteria has been observed in oysters, crabs, clams, shrimp, mussels, mullets, and seabass; however, oysters consumption has historically been the most common source of infection. Infection via consumption typically occurs with inoculation of at least 1 millionV. vulnificus bacteria.[35]
Vibrio vulnificus is an extremely virulent bacterium that can cause three types of infections:
Among healthy people, ingestion ofV. vulnificus can cause vomiting, diarrhea, and abdominal pain. In someone with a compromised immune system, particularly those with chronicliver disease, it can infect the bloodstream, causing a severe and life-threatening illness characterized by fever and chills, decreased blood pressure (septic shock), and blistering skin lesions. While men have been shown to be more at risk from this infection than women, co-morbidities such as alcoholic cirrhosis and diseases affecting the endocrine system (diabetes, rheumatoid arthritis, etc.) put a person far more at risk of developing an infection fromV. vulnificus.[8]
Vibrio vulnificus wound infections have a mortality rate of around 25%. In people in whom the infection worsens into sepsis, typically following ingestion, the mortality rate rises to 50%. The majority of these people die within the first 48 hours of infection. The optimal treatment is not known, but in one retrospective study of 93 people in Taiwan, the use of a third-generationcephalosporin and atetracycline (e.g.,ceftriaxone anddoxycycline, respectively) was associated with an improved outcome.[39] Prospective clinical trials are needed to confirm this finding, butin vitro data support the suggestion that this combination issynergistic againstV. vulnificus. Likewise, theAmerican Medical Association and theCenters for Disease Control and Prevention (CDC) recommend treating the person with aquinolone orintravenous doxycycline withceftazidime. The first successful documented treatment offulminantV. vulnificussepsis was in 1995. Treatment was ceftazidime and intravenous (IV)ciprofloxacin and IV doxycycline, which proved successful. Prevention of secondary infections fromrespiratory failure andacute renal failure is crucial. Key to the diagnosis and treatment were the early recognition ofbullae in an immunocompromised person withliver cirrhosis and oyster ingestion within the previous 48 hours, and the request by the physician forSTATGram staining andblood cultures forV. vulnificus.[40] Amputation of limbs may be required.[41]Vibrio vulnificus often causes large, disfiguringulcers that require extensivedebridement or even amputation.[42]
Vibrio vulnificus is the most common cause of death due to seafood in the United States, causing over 95% of deaths that are known to have occurred due to ingested seafood. If treatment with tetracycline or other cephalosporin antibiotics is initiated at the onset of symptoms and the full course followed, patients generally experience no long-term effects.[43]
The worst prognosis is in those people arriving at the hospital in a state ofshock. Total mortality in treated people (ingestion and wound) is around 33%.[39]
People especially vulnerable are those with liver disease (especiallycirrhosis andhepatitis) orimmunocompromised states (some kinds ofcancer, bone marrow suppression,HIV,diabetes, etc.). In these cases,V. vulnificus usually enters the bloodstream, where it may cause fever and chills, septic shock (with sharply decreased blood pressure), and blistering skin lesions.[44] About half of those who contract blood infections die.
The consumption of contaminated raw oysters in those with chronic liver disease causes primarysepsis with a mortality rate of over 50%. Exposure of wounds to contaminated seawater or handling of contaminated seafood products causes infections with a mortality rate of about 25%.[9][45][46]
Vibrio vulnificus infections also disproportionately affect males; 85% of those developingendotoxic shock from the bacteria are male. Females having had anoophorectomy experienced increased mortality rates, asestrogen has been shown experimentally to have a protective effect againstV. vulnificus.[47]
Vibrio vulnificus is commonly found in theGulf of Mexico, where more than a dozen people have died from the infection since 1990.[48] Most deaths at that time were occurring due to fulminant sepsis, either in the area of oyster harvest and ingestion, or in tourists returning home. Lack of disease recognition, and also of the risk factors, presentation, and cause, were and are major obstacles to good outcome and recovery.[49]
Increasing seasonal temperatures and decreasingsalinity levels seem to favor a greater concentration ofVibrio within filter-feeding shellfish of the U.S. Atlantic seaboard and the Gulf of Mexico, especially oysters (Crassostrea virginica). Scientists have frequently demonstrated the presence ofV. vulnificus in the gut of oysters and other shellfish and in the intestines of fish that inhabit oyster reefs. The vast majority of people who develop sepsis fromV. vulnificus became ill after they ate raw oysters; most of these cases have been men.[50]
According to the CDC,V. vulnificus infections in the Eastern United States increased eightfold from 1988–2018 and the border of where these infections occur has migrated 48 km northward each year. In July–August 2023, Connecticut, New York, and North Carolina reported severe and fatalV. vulnificus infections. On August 8, 2025, aV. vulnificus infection was confirmed in a swimmer who had swum with an open wound at aFalmouth, Massachusetts beach.[51]
Vibrio vulnificus is heavily affected by climate change, which causes rising sea temperatures and more frequent severe weather events. These consequences of climate change have allowed all species ofVibrio to increase their population range into previous environments that were too cold, and a study has shown they were moving as far north as the Baltic Sea.[52]V. vulnificus in the United States used to only inhabit Gulf Coast states, but there have been deadly cases as far north as New York in recent years.[51]
Vibrio vulnificus also colonizes populations of marine filter feeders. Populations such as oysters, clams, and mussels feed by filtering ocean water, which can cause accumulation ofV. vulnificus. Increasing ocean temperatures have only increased the occurrence of vibrio in oysters, leading to more infections. This is why shellfish are an important vector of this bacterium, and regardless of their look or taste, the CDC highly advises against eating raw oysters.[53]
Unlike other strains ofVibrio,V. vulnificus can be transferred to humans through open wounds. This ability is concerning because one in five people die when they get this disease. Action like education and health alerts are needed in the summer months to reduce the cases.[54]Increased danger of this bacteria has led public health agencies to advise the danger of this disease especially after severe weather events to try and stop the growing number of infections.[55]
The pathogen was first isolated in 1976 from a series of blood culture samples submitted to the CDC inAtlanta.[6] It was described as a "lactose-positive vibrio".[6] It was initially given the nameBeneckea vulnifica,[1] and then finally the nameVibrio vulnificus by J. J. Farmer in 1979.[2]
In 2005, health officials identified strains ofV. vulnificus infections amongevacuees from New Orleans due to the flooding there caused by Hurricane Katrina.[56]
In 2015, eight cases ofV. vulnificus infection were reported in Florida, with two resulting in death.[57]
In 2022, followingHurricane Ian,Lee County, Florida, saw a sharp rise in infections and deaths fromV. vulnificus. By October 18, 2022, four deaths and 29 illnesses had been recorded since the landfall of the hurricane in late September.[58][59]
In 2023, it was reported that a 40-year-old woman from California had been infected byVibrio vulnificus after eating undercooked fish (tilapia). She had her four limbs removed to save her life.[60] However, upon further investigation, local public health officials reported no evidence ofV. vulnificus infection in her case.[61]
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