Botulinum Neurotoxin and Tetanus Toxin by Lance L. Simpson

By Lance L. Simpson

Botulinum Neurotoxin and Tetanus Toxin

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Sei. 33, 81-86. , and Garmise, L. (1961). Phenotype alterations associated with the bacteriophage carrier state of Shigella dysenteriae. J. Gen. Microbiol. 24, 355-367. C. (1980). Plasmid-associated toxigenicity in Clostridium tetani. J. Infect. Dis. 142, 623. , Hardegree, M . P. (1981). Genetics of virulence plasmids of Clostridium tetani. In Int. Conf. Tetanus, (Proc), 6th, pp. 9-16. Lederberg, J. (1954). Genetic transduction. Am. Sei. 44, 264-280. L. (1984). Atypical strains of Clostridium botulinum isolated from specimens in infant botulism cases.

When biochemical, physiological, serological, and deoxyribonucleic-acid homologies are used to characterize the different strains of Clostridium botulinum, they can be divided into the following groups: Group I strains are proteolytic, saccharolytic, and produce types A, B, and F or combinations of A B , A F , B A , and B F neurotoxins; Group II strains are nonproteolytic, saccharolytic, psychotrophic, and produce types B, E, and F neurotoxins; Group III strains are also nonproteolytic and saccharolytic, produce types Ci and D neurotoxins, and C 2 binary toxin.

Habig phage-host relationship. With types C and D, the relationship of pseudolysogeny exists and phage-sensitive derivatives can routinely be isolated from the toxigenic parent culture. In contrast, with Groups I and II, this relationship is true lysogeny and phage-sensitive bacteria can seldom be isolated. Recently, a procedure was developed to cure the lysogenic strains of their prophages (Eklund and Poysky, unpublished data). In the first step, bacterial cells in the early log phase of growth are treated with mitomycin C, a DNA inhibitor.

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