enteric bacteria in human, because human carriers or
patients are the source of S. typhi infection. We,
therefore, were interested in searching for the
probable origin of the R-plasmid conferring ACCoT-
resistance in S. typhi. We explained, performing in
vitro conjugation experiments, the possibility of
acquisition of R-factor from various intestinal flora
like E. coli, P. vulgaris, K. pneumoniae isolated from
different clinical cases. In vitro and in vivo acquisitions
of R-plasmids from common bacterial flora of
intestine by S. typhi have been reported earlier. The
phenomenon of acquisition of R-plasmid can be
explained based on the facts described by Datta et al.
(24), who before antibiotic therapy isolated plasmid-
less antibiotic sensitive S. typhi strain from enteric
fever case. The strain, however, acquired, after
antibiotic therapy, the ACCo-resistance in the bowel
of a patient from Klebsiella aerogenes, which was
originally resistant to A, C, Co. Both S. typhi and K.
aerogenes were found to contain similar plasmids.
Ridley (25) also reported about the acquisition of R-
plasmids by S. typhi, in the bowel of patient with
enteric fever. Schwalbe et al (26), by studying the
plasmid profile, demonstrated the transfer of drug
resistance from the intestinal flora, viz, E. coli and K.
pneumoniae to S. typhi. In vitro intergenic conjugation
experiments demonstrated transfer of drug resistance
between intestinal MDR E. coli and S. typhi strains.(27)
Thus, one or more S. typhi clones in the patients’
intestine acquired resistance plasmids by transfer
from the resistant commensal bacteria, and the
resistant clone replaced the original sensitive S. typhi
as a result of the antibacterial therapy. Two factors
play role in the fact of acquisition of R-plasmids: the
capacity of the antibiotic resistance transposon to
spread between plasmids (28), and the selection
exerted antibiotic treatment of enteric fever.(24, 29)
In this study, it was considered that the commensal
bacteria like E. coli, P. vulgaris, K. pneumoniae might be
the source of dissemination of the plasmid conferring
resistance to A, C, Co and T in S. typhi, based on the
fact that most of these isolates (E. coli, P. vulgaris, K.
pneumoniae) in between 1995 and 2001 showed a
common resistance pattern (ACCoT), and that the
resistance pattern was transferred to the drug
sensitive S. typhi, obtained in between 1992 and 2001
(22), with the same degree of resistance. In addition,
plasmids contained in the E. coli, P. vulgaris, K.
pneumoniae strains as well as in their corresponding
transconjugants comigrated with that contained in S.
typhi isolates having ACCoT-resistance pattern. Thus
the present findings suggest that the MDR S. typhi
may arise from sensitive isolates by acquisition of
multidrug resistance plasmid from antibiotic-resistant
enteric bacteria. However, additional investigations
are needed to ascertain the role of plasmid in the
mediation of multidrug resistance among enteric
bacteria.
Acknowledgements
Authors are thankful to Dr. P. K. Saha, Chairman,
Department of Botany, Bose Institute, Kolkata for
extending help regarding gel documentation of
plasmid DNAs. We also acknowledge the help of Dr.
B. L. Sarkar, Assistant Director, NICED, Kolkata, for
providing the E. coli V517 strain.
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