It was subsequently given the name Beneckea vulnifica, and finally Vibrio vulnificus by Farmer in 1979.Increasing seasonal temperatures and decreasing coastal salinity levels seem to favor a greater concentration of  Vibrio within filter-feeding shellfish of the US Atlantic seaboard and the Gulf of Mexico, especially oysters (Crassostrea virginica). Scientists have frequently demonstrated the presence of V. 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 from V. vulnificus became ill after they ate raw oysters; most of these cases have been men.In 2005, health officials clearly identified strains of V. vulnificus infections among evacuees from New Orleans due to the flooding there caused by Hurricane Katrina.In 2015 in Florida, eight cases of V. vulnificus infection with two resulting in death were reported. Natural transformation
Natural transformation is a bacterial adaptation for DNA transfer between individual cells. V. vulnificus was found to become naturally transformable during growth on chitin in the form of crab shells. The ability to now carry out transformation experiments in the laboratory should facilitate molecular genetic analysis of this opportunistic pathogen. References
External links
Large and detailed article on V. vulnificus at Todars Online Textbook of Bacteriology
CNN video on vibrio vulnificus
Type strain of Vibrio vulnificus at BacDive -  the Bacterial Diversity Metadatabase
This causes the number of repeats to change in successive generations, such that an unaffected parent with an "intermediate" number of repeats (28–35), or "reduced penetrance" (36–40), may pass on a copy of the gene with an increase in the number of repeats that produces fully penetrant HD. The earlier age of onset and greater severity of disease in successive generations due to increases in the number of repeats is known as genetic anticipation. Instability is greater in spermatogenesis than oogenesis; maternally inherited alleles are usually of a similar repeat length, whereas paternally inherited ones have a higher chance of increasing in length. Rarely is Huntingtons disease caused by a new mutation, where neither parent has over 36 CAG repeats.In the rare situations where both parents have an expanded HD gene, the risk increases to 75%, and when either parent has two expanded copies, the risk is 100% (all children will be affected). Individuals with both genes affected are rare. For some time, HD was thought to be the only disease for which possession of a second mutated gene did not affect symptoms and progression, but it has since been found that it can affect the phenotype and the rate of progression. Mechanisms
Huntingtin protein interacts with over 100 other proteins, and appears to have multiple functions. The behavior of the mutated protein (mHtt) is not completely understood, but it is toxic to certain cell types, particularly brain cells.