Journal of The Showa Medical Association
Online ISSN : 2185-0976
Print ISSN : 0037-4342
ISSN-L : 0037-4342
SELECTION OF NON-MUCOID VAR. FROM MUCOID VAR. ORIGINATED IN THE MUTABILE-TYPE VAR. (MURASE) OF ENTERIC BACTERIA BY USING SODIUM SULFITE
Masami Yamagishi
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1965 Volume 25 Issue 3 Pages 101-116

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Abstract
The growth of mucoid-type M and mucoid-type RT, originated in the Mutabile-type var. (Murase) is inhibited by the addition of 1 % sodium sulfite. This phenomenon is common to the variants of Salm. typhi-murium, Salm, enteritidis and E. coli.
The effective concentration of sodium sulfite was 0.5 %-1 % when estimated by so-called streak plate cup method.
Of their growths wild strains, RT and M (Mutabile-type var.) were not inhibited.
Usually a few smooth type colonies can be seen on the plate, when a large dosis of mucoid-type M or mucoid-type RT is streaked and cultured on the 1 % sodium sulfite agar. They corespond to the colonies of M in case of mucoid-type M or RT in case of mucoid-type RT. So it may be said that the M or the RT colonies are those in which only their mucoid character was lost from the respective mucoid-type ones.
The ratio of mucoid-type M to M is roughly estimated to be 3.3×102-7.0×104: 1 in case of Salm, typhi-murium, 1.8×105 -5.0×105: 1 in case of Salm, enteritidis and 3.6×104-3.6×105 : 1 in case of E, coli and that of mucoid-type RT to RT 8.6×102-5.6×105: 1 in case of Salm. typhi-murium, and 3.5×104-1.4×105: 1 in case of E. coli.
It was very difficult to discover mucoid-type RT directly from the mucoid-type M probably because of its low mutation rate.
Two different routes are conceivable through which so-called backmutation from nonpathogenic M or mucoid-type M to pathogenic RT might occur in experimental animals. One is the course of mucoid type M to M and then to RT and the other is mucoid-type M to mucoid-type RT and to RT.
Whichever course it may take it is necessary that the starting mutant and the intermediate variant multiply in a sufficient amount to permit further mutaion suggesting that this mutation does not necssarily take place in the living host which possesses an inhibitory power not to allow a weak variant to multiply in the tissue.
From the above experiments, it is very likely that the mutation of the organism, its in-heritability to the offspring and the resistance of the host form a trio which will theoretically result in the extreme diminution of so-called backmutation of the mucoid-type M to its original form.
This phenomenon is highly desirable for a live vaccine for the prophylaxis of typhoid disease.
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