TO THE usual list of terrible things that appeared in the 1980s – bad hairdos, pleated acid-washed jeans, Miami Vice – we must now add flesh-eating bacteria. It was in the early 80s that an innocuous bacterium gained the weapons it needed to cause flesh-eating disease, or necrotising fasciitis.

Group A Streptococcus are some of the most common bacteria, causing diseases from strep throat to rheumatic fever. But few are ickier than M1 Streptococcus A, which makes toxins that dissolve muscle and skin. Such flesh-eating bacteria attack their host rapidly, and can kill if the infection is not cut out. But it wasn’t always so.

James Musser at the Methodist Hospital Research Institute in Houston, Texas, and his colleagues sequenced 3615 strains of M1 Streptococcus A from the US, Canada and northern Europe, to reconstruct its genetic history. This revealed four events that transformed a fairly benign bug into a pathogen with global reach.

In the first two events, the bacterium acquired two genes from a virus, allowing it to make two toxins. Next, one of those genes mutated, producing a more powerful toxin. But the clincher was when the bacterium gained another chunk of DNA, coding for a further two toxins (PNAS, DOI: 10.1073/pnas.1403138111).


This final upgrade happened around 1982, in one cell. “Once that occurred, it spread rapidly,” says Musser. “Disease frequency and severity increased.”

The study shows that genetics can define when a potential killer becomes a real one, and could help predict epidemics.

This article appeared in print under the headline “Flesh-eating bacterium is a child of the 80s”