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Indian J Med Res. 1996 Jul;104:14-27.

Epidemiology & molecular biology of Vibrio cholerae O139 Bengal.

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Laboratory Sciences Division, International Centre for Diarrhoeal Disease Research Bangladesh (ICDDR,B), Dhaka, Bangladesh.


The emergence of Vibrio cholerae O139 Bengal as the second aetiologic agent of epidemic cholera in October 1992 in the south Indian coastal city of Madras has shattered the long-held notion that only V. cholerae belonging to serogroup O1 are capable of causing epidemic (and pandemic) cholera. Within months of its appearance in Madras, V. cholerae O139 engulfed the entire Indian subcontinent in a series of outbreaks of cholera. It also spread to several neighbouring countries in Asia. Several western countries also reported imported cholera cases due to this organism. In the regions of the Indian subcontinent where cholera due to V. cholerae O1 is endemic, children are mostly susceptible because adults would have acquired at least some immunity due to earlier exposure. However, when V. cholerae O139 struck people in these areas, even though all age groups were affected, the disease was more prevalent in adults, which suggested that the disease is new in this population. As with O1 cholera, water and food seemed to be the vehicles of infection. Many family contracts of index cases of O139 cholera were found to be infected with V. cholerae O139, and in many of them, the infection was asymptomatic which is reminiscent of O1 EITor infection. Again as with O1 EITor infection, individuals of blood group O were more susceptible to O139 infection than those with other blood groups. In its molecular aspects, O139 vibrio resembles O1 EITor vibrio. The virulence genes encoding cholera toxin, zonula occludens toxin, accessory cholera enterotoxin and core-encoded pilin are present in a 4.5 kb 'virulence cassette' region of the chromosome as in EITor vibrios and the expression of these virulence factors, toxin coregulated pilus (TCP) and several outer membrane proteins are found to be under the control of the master regulator ToxR as in EITor vibrios. The iron-regulated genes involved in virulence are also found in the same locus as in EITor vibrios. However, the genes involved in the somatic antigen synthesis in O1 vibrios are found to be deleted in O139 vibrios and are replaced by a new region of chromosome which encodes the new surface antigen synthesis in O139 vibrios. When V. cholerae O139 emerged and caused outbreaks, the prevailing O1 EITor vibrios virtually disappeared from most of the areas. The disappearance of EITor vibrios, the rapid spread of O139 vibrios and the resemblance of O139 vibrios to EITor vibrios seemed to suggest that O139 vibrios might be the causative agent of the 'eighth' pandemic of cholera. However, after a year of its appearance, O139 vibrios are on the wane and O1 EITor vibrios have re-emerged as the predominant organism, in the Indian subcontinent. Thus, the immediate threat of a new cholera pandemic posed by V. cholerae O139 may not be as large as it first seemed. However, whether it will follow the pattern of EITor vibrio which took approximately 60 yr since its first isolation before emerging as the seventh pandemic strain of cholera, is not clear. The factor(s) contributing to the diminished isolation of O139 vibrios and the re-emergence of O1 EITor vibrios are not understood. The vibrios might have undergone changes that would have affected their ability to survive and compete in the environment.

[Indexed for MEDLINE]

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