Jansen W H, Gielen H, Rijpkema S G, Guinée P A
National Institute of Public Health and Environmental Protection, Bilthoven, The Netherlands.
Microb Pathog. 1988 Jan;4(1):21-6. doi: 10.1016/0882-4010(88)90044-7.
Cholera disease can be induced in the rabbit by ligation of the cecum (C) followed by duodenal inoculation (DI) of virulent Vibrio cholerae organisms (DIC model). When the cecum is not ligated, DI does not induce disease. In contrast, the animals are primed which becomes apparent upon challenge with live V. cholerae in the DIC model. Such animals are vibriocidally protected. This protection is characterized by absence of disease symptoms, rapid disappearance of V. cholerae from the feces and presence of high levels of anti-lipopolysaccharide Immunoglobulin A in the bile. The present study shows that primed rabbits can also be boosted by duodenal administration of killed, smooth V. cholerae cells. On the other hand, killed cells cannot prime. The minimal lethal dose of a rough derivative of a smooth strain C5, designated R5 and lacking the O antigen part of the LPS, was 100,000 times higher than that of its parent strain C5, in the DIC model. Rabbits which had been duodenally immunized with strain R5 and were subsequently challenged with the smooth strain C5, all developed diarrhea and two out of eight died. This result supports an earlier observation that the specific O antigen part of the V. cholerae LPS is an essential prerequisite for the induction of protective immunity in the rabbit.