The emergence and rapid rise to dominance of Vibrio cholerae 0139 in India and Bangladesh in 1992 led to the consideration that choleraphage might serve as both a selective mechanism and a means for horizontal transmission of genetic information. A filamentous phage '493' from 0139 strain AJ27-493 has been purified and partially characterized. The phage was inactive on classical biotype V. cholerae 01 but it was active on El Tor biotype strains isolated prior to 1994 when E l Tor re-emerged in Bangladesh. More recent E l Tor isolates were all resistant to the phage. The phage was also active on 0139 strains. Unlike the filamentous -4, the receptor for 493 is not TcpA. The phage genome was a 9 3 kb closed circular single-stranded molecule containing a 0.4 kb double-stranded stem supporting a 2 kb single-stranded loop. A 283 bp fragment was cloned and used as a probe in Southern hybridization, in parallel with total phage 493 DNA. These probes hybridized both chromosomally and extrachromosomally with most 0139 strains, but not with 01 strains. Infection of hybridization-negative E l Tor or 0139 strains resulted in the presence of hybridizing loci (both plasmid and chromosomal), in the appearance of an 18 kDa protein, and in marked alterations in colonial morphology. Phage 493 is clearly distinct from other 0139 choleraphages which have been described. Phage 493 DNA hybridized with an encapsulated non-01 (031) strain (NRT36S) which was isolated before 0139 was recognized. NRT36S also produces a phage which can infect El Tor strains with low efficiency. Further studies may reveal whether bacteriophage play a role in the emergence and the territoriality of new choleragenic vibrios.
We previously isolated from a 1994 isolate of Vibrio cholerae O139 a filamentous lysogenic bacteriophage, choleraphage 493, which inhibits pre-O139 but not post-O139 El Tor biotype V. cholerae strains in plaque assays. We investigated the role of the mannose-sensitive hemagglutinin (MSHA) type IV pilus as a receptor in phage 493 infection. Spontaneous, Tn5 insertion, andmshA deletion mutants are resistant to 493 infection. Susceptibility is restored by mshA complementation of deletion mutants. Additionally, the 493 phage titer is reduced by adsorption with MSHA-positive strains but not with a ΔmshA1 strain. Monoclonal antibody against MSHA inhibits plaque formation. We conclude that MSHA is the receptor for phage 493. The emergence and decline of O139 in India and Bangladesh are correlated with the susceptibility and resistance of El Tor strains to 493. However, mshA gene sequences of post-O139 strains are identical to those of susceptible pre-O139 isolates, indicating that phage resistance of El Tor is not due to a change in mshA. Classical biotype strains are (with rare exceptions) hemagglutinin negative and resistant to 493 in plaque assays. Nevertheless, they express the mshA pilin gene. They can be infected with 493 and produce low levels of phage DNA, like post-O139 El Tor strains. Resistance to 493 in plaque assays is thus not equivalent to resistance to infection. The ability of filamentous phages, such as 493, to transfer large amounts of DNA provides them, additionally, with the potential for quantum leaps in both identity and pathogenicity, such as the conversion of El Tor to O139.
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