A new study has shown how Clostridium botulinum could potentially transfer their deadly neurotoxin genes to other bacteria. This highlights the need for constant vigilance in identifying new threats to food safety.

Clostridium botulinum and its spore (inset)
Jason Brunt, Kathryn Cross and Mary Parker

The botulinum neurotoxin is the most potent known, and has been much studied because of this, helping ensure it doesn’t get into our food supply. Seven different types of neurotoxin have been described. The Institute of Food Research has been studying the genetic variability of one of the types responsible for human botulism, type E. Many different strains of Clostridium botulinum produce type E neurotoxin. Intriguingly, a different species of bacteria, Clostridium butyricum has also been found to produce type E toxin and cause botulism.

To find clues about the mobility of the type E neurotoxin gene, Dr Andy Carter at IFR analysed the DNA of more than 150 different strains of C. botulinum producing type E toxin. In most strains, this gene was located at the same place on the chromosome, but in a small number of strains, this chromosomal location lacked the neurotoxin gene. Further analysis showed that the toxin gene was instead present on a large plasmid.

Plasmids are small circular DNA molecules that many bacteria possess, which replicate independently from the main chromosomes. They can also be transferred between bacteria, and closer analysis of this plasmid indicated mechanisms by which it could be transferred.

This is the first time that the plasmids carrying the type E toxin gene have been characterised in detail.

“We have uncovered evolutionary evidence suggesting that the type E toxin gene may be shuttling between the chromosome and plasmid, and also for its potential transfer to other bacterial species as must have occurred with strains of C. butyricum that form type E neurotoxin,” commented Dr Carter.

Reference:

Evolution of chromosomal Clostridium botulinum type E neurotoxin gene clusters: evidence provided by their rare plasmid borne counterparts. Andrew T. Carter, John W. Austin, Kelly A. Weedmark, and Michael W. Peck. Genome Biology and Evolution doi: 10.1093/gbe/evw017