26
D. E. MAHONY
(1978) and in this Chapter further demonstrates the typability of C. perfringens using bacteriocins. One is cautioned, however, that this methodology has not been widely tested and that the concentration of bacteriocin
and the number of indicator cells used are critical aspects of this test. The
technique is simple and, if proved to be completely reliable and of suitable specificity through extensive trials, would make typing of virtually all
strains of C. perfringens a relatively easy task. This high degree of typability is not yet possible with serological tests involving a large battery of
antisera, although the proposed international typing system would seem to
show considerable promise (Stringer et al., 1976).
With respect to C. botulinum, phage typing has not been performed, but
phage host ranges seem to be restricted to non-proteolytic types B, E and
F and non-toxigenic type E (Sugiyama and King, 1972). Bacteriocins seem
to have a variety of host ranges: those active only on non-proteolytic strains
(Anastasio et al., 1971; Lau, 1974); those active only on proteolytic strains
(Ueda and Takagi, 1972); and those which do not seem to be restricted to
one class or the other (Beerens and Tahon, 1967). A potential typing
system resides in the work of Beerens and Tahon (1967).
Not enough is known about phages of C. novyi or C. tetani to predict
whether phage typing of these organisms is feasible. The rare occurrence
of many anaerobic infections or intoxications may discourage development
of bacteriocin or bacteriophage typing methodology and this may well
explain why the frequently encountered C. perfringens has received most
attention from an epidemiological viewpoint.
ACKNOWLEDGEMENTS
The author wishes to thank D r S. Hirano, D r A. Sasarman and Dr M. Sebald
for correspondence, literature and expression of opinions with regard to bacteriocins and bacteriophages of clostridia and Dr R. Lewis for his contribution to the
literature search of bacteriocins as presented in his doctoral thesis “Characterisation
of a Bacteriocin of Clostridiurn perfringens”, Dalhousie University, 1972.
REFERENCES
Ackerman, H. W. (1974). Path. Biol. 22, 909-917.
Anastasio, K. L., Soucheck, J. A. and Sugiyama, H. (1971).J. Bact. 107, 143-149.
Batty, I. and Walker, P. D. (1965).J. appl. Bact. 28, 112-118.
Beerens, H. and Tahon, M. M. (1967). In “Botulism 1966” (Eds M. Ingram and
T. A. Roberts), pp. 424-428. Chapman and Hill, London.
Betz, J. V. (1968) Virology 36, 9-19.
Betz, J. V. and Anderson, K. E. (1964). J . Bact. 87, 4084115.
Bradley, D. E. and Hoeniger, J. F. M. (1971). Can. J . Microbiol. 17, 397-402.
Bychkov, K. Ya. (1964). J . Microbiol. Epidcm. Irnmmobiol. 41, 39-41.
Cherniak, R. and Henderson, B. G. (1972). Inject. Immun. 6, 32-37.
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