Lack of disease recognition, and also of the risk factors, presentation, and cause, were and are major obstacles to good outcome and recovery.After the successful treatment of the first person, the Florida Department of Health was able to trace  the origin of the outbreak to Apalachicola Bay oysters and their harvesting in water prone to excessive growth of the organism. This contamination was due to warmth of the water and change in freshwater dilution because of a change in flow of the Chattahoochee River into the Apalachicola River, and in turn into Apalachicola Bay. A similar situation occurred after Hurricane Katrina in New Orleans. Further treatment research
While the treatment for V. vulnificus can be as straightforward as making the rapid choice of appropriate antibiotics, there have been cases in which the genes mutated, thus rendering antibiotics ineffective. While looking for an answer to this problem, researchers found that one way to stop the infection from spreading is to again mutate the bacteria. This mutation happens on the flagellum of the bacteria. When injected with flgC and flgE (two genes in the flagella that cause the mutation), the flagellum no longer function properly. When unable to move normally, the bacteria is no longer able to spread toxins through the body, thus decreasing the effect that V. vulnificus has on the body systemically. History
The pathogen was first isolated in 1976 from a series of blood culture samples submitted to the CDC in Atlanta. It was  described as a "lactose-positive vibrio".
This means that two copies of the mutated gene are required to cause the disease, so two unaffected parents, each of whom carries one mutant allele, can have an affected child if that child inherits the mutant allele from both parents.75 to 80 percent of Leigh syndrome is caused by mutations in nuclear DNA; mutations affecting the function or assembly of the fourth complex involved in oxidative phosphorylation, cytochrome c oxidase (COX), cause most cases of Leigh disease. Mutations in a gene called SURF1 (surfeit1) are the most common cause of this subtype of Leigh syndrome. The protein that SURF1 codes for is terminated early and therefore cannot perform its function, shepherding the subunits of COX together into a functional protein complex. This results in a deficit of COX protein, reducing the amount of energy produced by mitochondria. SURF1 is located on the long arm of chromosome 9. Another nuclear DNA mutation that causes Leigh syndrome affects another protein complex in the mitochondria, pyruvate dehydrogenase, which is an enzyme in the Link reaction pathway. Some types of SURF1 mutations cause a subtype of Leigh syndrome that has a particularly late onset but similarly variable clinical course.Other nuclear genes associated with Leigh syndrome are located on chromosome 2 (BCS1L and NDUFA10); chromosome 5 (SDHA, NDUFS4, NDUFAF2, and NDUFA2); chromosome 8 (NDUFAF6), chromosome 10 (COX15); chromosome 11 (NDUFS3, NDUFS8, and FOXRED1); chromosome 12 (NDUFA9 and NDUFA12); and chromosome 19 (NDUFS7). Many of these genes affect the first oxidative phosphorylation complex.