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Salmonella typhimurium cob mutants are not hyper-virulent
J Björkman1, M Rhen, D I Anderson
1Department of Microbiology, Uppsala University, Biomedical Centre, Sweden.
FEMS Microbiology Letters
|June 1, 1996
Summary
Vitamin B12 (cobalamin) does not affect Salmonella typhimurium virulence. Previous studies showing increased virulence in cob mutants were due to an uncharacterized mutation in the wild-type strain, not the B12 deficiency.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Nutritional Biochemistry
Background:
- Salmonella typhimurium cob mutants, deficient in vitamin B12 biosynthesis, were previously reported as hyper-virulent in mice.
- This reported hyper-virulence suggested a role for vitamin B12 in regulating bacterial pathogenicity.
Purpose of the Study:
- To re-evaluate the virulence of Salmonella typhimurium cob mutants.
- To determine if vitamin B12 deficiency directly impacts S. typhimurium virulence in a mouse model.
Main Methods:
- Reconstruction of isogenic wild-type and cob mutant strains of Salmonella typhimurium LT2.
- Comparative analysis of the virulence and in vivo growth rates of reconstructed strains in a mouse model.
Main Results:
- The previously reported hyper-virulence of cob mutants was attributed to an uncharacterized mutation in the "wild type" strain used in prior studies.
- This mutation in the "wild type" strain likely attenuated its virulence, making the cob mutant appear hyper-virulent.
- Reconstructed isogenic strains demonstrated similar growth rates and virulence in mice, indicating no effect of vitamin B12 deficiency.
Conclusions:
- Vitamin B12 biosynthesis is not a determinant of Salmonella typhimurium LT2 virulence.
- The observed differences in virulence in previous studies were artifacts of non-isogenic strains and confounding mutations.