Scientists pinpoint when harmless bacteria became flesh-eating monsters

Bacterial diseases cause millions of deaths every year. Most of these bacteria were benign at some point in their evolutionary past, and we don’t always understand what turned them into disease-causing pathogens. In a new study, researchers have tracked down when this switch happened in a flesh-eating bacteria. They think the knowledge might help predict future epidemics.
These bacteria appeared to have affected humans since the 1980s. Scientists think that GAS must have evolved from a less harmful streptococcus strain. The new study, published in the Proceedings of the National Academy of Sciences, reconstructs that evolutionary history.

Genetic gymnastics
Musser’s work required analysis of the bacterial genetic data from across the world – a total of about 3,600 streptococcus strains were collected and their genomes recorded. It revealed that a series of distinct genetic events turned this bacteria rogue.

First, foreign DNA moved into the original harmless streptococcus by horizontal gene transfer – a phenomenon that is common among bacteria. Such DNA is often provided by bacteriophages, viruses that specifically target bacteria. Picking up foreign genes can be useful because it can improve the bacteria’s survival.
In this case, the foreign DNA that was incorporated in the host’s genome allowed the streptococcus cell to produce two harmful toxins. A further mutation to one of these toxin genes made it even more virulent.

Continental drift
That timing makes a lot of sense. “The date we deduced coincided with numerous mentions of streptococcus epidemics in the literature,” Musser said. Since 1983, there have been several outbreaks of streptococcus infections across the world. For example, in the UK, streptococcus infections increased in number and severity between 1983 and 1985.

It is the same story for many other countries, with Sweden, Norway, Canada and Australia falling victim to what is now an inter-continental epidemic. The symptoms ranged from pharyngitis to the flesh-eating disease, necrotizing fasciitis.

“In the short term, this discovery will help us determine the pattern of genetic change within a bacteria, and may help us work out how often bacterial vaccines need to be updated,” Musser said. “In the long term, this technique may have an important predictive application – we may be able to nip epidemics in the bud before they even start.”

What Musser is suggesting is that if enough bacterial genomes are regularly recorded and monitored, there is a chance that mutations or gene transfers, such as those GAS experienced, could be found ahead of time.

But Oggioni is sceptical. “While making such predictions may not be possible, this research will have other applications,” he said. “Knowing which genetic changes happen when can help tailor drug discovery research in a certain direction.”

Oggioni added that Musser’s work with GAS is only a model. Using Musser’s methods to record the evolutionary histories of other pathogens could be quite useful to tackle the diseases they cause now and, perhaps, even those that they may cause in the future.