Cholera is a devastating disease, the epidemics of which, until 1992, were caused by Vibrio cholerae serogroup O1 biotype classical or El Tor. The classical biotype is believed to have caused the first six pandemics, which occurred in the Indian subcontinent and subsequently in other areas of the world between 1817 and 1923 (9, 27). V. cholerae O1 biotype El Tor was first reported in 1905 (30). However, it was not until the early 1960s that V. cholerae biotype El Tor displaced the sixth-pandemic V. cholerae O1 classical biotype (11,32). The emergence in 1992 of a V. cholerae non-O1 serovar, designated V. cholerae synonym O139 Bengal, in Bangladesh (2, 4) and India (28) and its subsequent appearance in Southeast Asia, displacing V. cholerae O1 El Tor, was considered a significant point in the history of cholera (33). V. cholerae O1 El Tor reemerged in 1994 to 1995, but V. cholerae O139 continues to coexist with V. cholerae O1 as indicated by its temporal quiescence and subsequent reemergence in 1997, 1999, and 2002 (11, 15). Of all of these outbreaks, the resurgence of V. cholerae O139 in a major outbreak, resulting in an estimated 30,000 cases in Dhaka, Bangladesh, caused more cases than the number attributed to V. cholerae O1 El Tor within a very short time (11,30). Since then, V. cholerae serogroup O139 has continued to cause a small number of cases of cholera in the subcentral parts of Bangladesh and southern Bangladesh (34). Despite its significance as a causal agent of cholera, little is known about the geographic distribution of V. cholerae O139 in the coastal areas of the Bay of Bengal.Despite being autochthonous to the aquatic environment (6, 7), toxigenic strains of V. cholerae O1 are only infrequently isolated from surface waters by culture methods (7,21) and are rarely isolated during interepidemic periods (18). It was when fluorescent-antibody (FA) and molecular-based detection methods were used that the presence of V. cholerae O1 in the environment was unequivocally demonstrated (3, 18) and its viable but not culturable state was discovered (5,7,18,29). V. cholerae O139 has been shown to behave similarly to V. cholerae O1, since detection and isolation of V. cholerae O139 from water samples were negative by culture methods between epidemics (19, 21).The correlation of sea surface temperature and sea surface height in the Bay of Bengal with the occurrence of cholera in Bangladesh has been established (8). Field studies in Bakerganj, which is located 70 km north of the Bay of Bengal coast, showed correlation of selected environmental parameters with the ecology and epidemiology of V. cholerae and cholera, respectively (19). In 1992, V. cholerae serogroup O139 was first isolated in Bangladesh in the vicinity of the Bay of Bengal. With the resurgence of V. cholerae O139 in 2002, the number of cholera cases caused by this serogroup surpassed the number caused by V. cholerae O1 in Bangladesh. This phenomenon is believed to have been the result of rapid genetic changes in
A mismatch amplification mutation PCR assay was developed and validated for rapid detection of the biotype specific cholera toxin B subunit of V. cholerae O1. This assay will enable easy monitoring of the spread of a new emerging variant of the El Tor biotype of V. cholerae O1.
PCR surveillance of the rstR genes of CTX phages in Vibrio cholerae O1 and O139 showed no relationship between the incidence of disease and changes in the rstR but showed variations in their presence in O1 and O139 strains and the occurrence of multiple types in a few strains.Of the 209 currently recognized serogroups of Vibrio cholerae, only strains belonging to serogroups O1 and O139 can cause cholera. Two major virulence gene clusters are now known to carry key virulence genes that are essential for the pathogenicity of V. cholerae O1 and O139. These gene clusters include the CTX prophage (14), which carries the ctxA and ctxB genes (the genes that encode cholera toxin [CT], which is responsible for severe diarrhea), and the toxin-coregulated pilus (TCP) pathogenicity island, which carries genes for the biosynthesis of the TCP, required for colonization of the small intestinal epithelium (7).The approximately 7-kb CTX genome consists of the core and the RS2 region. The core region encodes proteins needed for the assembly and secretion of viral particles (Psh, Cep, pIII CTX , Ace, and Zot) and also encodes CT, which is not necessary for phage morphogenesis (3), while the RS2 region represents a site-specific recombination system that allows lysogenic phage to integrate at a specific site on the host chromosome (14). The RS2 region of CTX prophage encodes proteins required for replication (RstA), phage integration (RstB), and regulation (RstR) of the lysogeny of CTX (14). An antirepressor, rstC, is carried by a satellite phage, RS1, often present adjacent to the CTX prophage in toxigenic V. cholerae O1 El Tor and O139 strains (1, 5).Diversity of the CTX phage repressor rstR has been described previously, and this diversity constitutes heteroimmunity among diverse CTX phages (8, 2). The difference in the rstR gene is also the only known genetic difference between any two different CTX phage types. The existence of at least four different rstR genes carried by different CTX phages, namely, CTX ET , CTX class , CTX Calc , and CTX Env , has been recognized (8, 2, 10). The epidemiological significance of the diversity of CTX phages is not clearly known, but at least two periods of explosive resurgence of cholera have been associated with strains showing changes in the rstR type of CTX phages. The first was the resurgence of V. cholerae O139 in August 1996 in Calcutta, India, which continued for a year (8, 9, 13), and the second was the resurgence of strain O139 in March to April of 2002 in Dhaka, Bangladesh (6). On the basis of their rstR genes and other phenotypic traits, genetic hybrids of classical and El Tor biotypes that cause cholera have been shown to exist, and these hybrids have been designated the Matlab variants of V. cholerae (11). To further document the distribution and temporal changes in the CTX phage contents of epidemic strains, we conducted a surveillance of CTX phage types by analyzing the types of rstR genes carried by a large collection of toxigenic V. cholerae strains.We selected every 10th con...
Based on this first report in Peru of such strains, we recommend including V. parahaemolyticus in the differential diagnosis of the etiologic agents for diarrhea in this part of the world.
Vibrio cholerae O1 biotype El Tor (ET), the cause of the current 7th pandemic, has recently been replaced in Asia and Africa by an altered ET biotype possessing cholera toxin (CTX) of the classical (CL) biotype that originally caused the first six pandemics before becoming extinct in the 1980s. Until recently, the ET prototype was the biotype circulating in Peru; a detailed understanding of the evolutionary trend of V. cholerae causing endemic cholera in Latin America is lacking. The present retrospective microbiological, molecular, and phylogenetic study of V. cholerae isolates recovered in Mexico (n ؍ 91; 1983 to 1997) shows the existence of the pre-1991 CL biotype and the ET and CL biotypes together with the altered ET biotype in both epidemic and endemic cholera between 1991 and 1997. According to sero-and biotyping data, the altered ET, which has shown predominance in Mexico since 1991, emerged locally from ET and CL progenitors that were found coexisting until 1997. In Latin America, ET and CL variants shared a variable number of phenotypic markers, while the altered ET strains had genes encoding the CL CTX (CTX CL ) prophage, ctxB CL and rstR CL , in addition to resident rstR ET , as the underlying regional signature. The distinct regional fingerprints for ET in Mexico and Peru and their divergence from ET in Asia and Africa, as confirmed by subclustering patterns in a pulsed-field gel electrophoresis (NotI)-based dendrogram, suggest that the Mexico epidemic in 1991 may have been a local event and not an extension of the epidemics occurring in Asia and South America. Finally, the CL biotype reservoir in Mexico is unprecedented and must have contributed to the changing epidemiology of global cholera in ways that need to be understood.
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