Abstract
Vibrio vulnificus biotype 2 is subdivided into two main serovars, serovar E, able to infect fish and humans, and serovar A, only virulent for fish. Serovar E emerged in 1976 as the causative agent of a haemorrhagic septicaemia (warm‐water vibriosis) affecting eels cultured in brackish water. Serovar A emerged in 2000 in freshwater‐cultured eels vaccinated against serovar E, causing warm‐water vibriosis with fish showing a haemorrhagic intestine as the main differential sign. The aim of the present work was to compare the disease caused by both serovars in terms of transmission routes, portals of entry and host range. Results of bath, patch‐contact and oral‐anal challenges demonstrated that both serovars spread through water and infect healthy eels, serovar A entering mainly by the anus and serovar E by the gills. The course of the disease under laboratory conditions was similar for both serovars in terms of transmission and dependence of degree of virulence on water parameters (temperature and salinity). However, the decrease in degree of virulence in fresh water was significantly greater in serovar E than in serovar A. Finally, both serovars proved pathogenic for tilapia, sea bass and rainbow trout, but not for sea bream, with significant differences in degree of virulence only in rainbow trout. In conclusion, serovar A seems to represent a new antigenic form of V. vulnificus biotype 2 with an unusual portal of entry and is better adapted to fresh water than serovar E.