Once a leading cause of death for children across the Western world, scarlet fever was nearly eradicated thanks to 20th-century medicine. But new outbreaks in the UK and Northeast Asia in recent years suggest we still have a long way to go.
Why we are experiencing a rebirth of the deadly pathogen is a mystery. A new study has uncovered clues in the genome of one of the responsible bacterial strains, showing just how complex the infectious disease family tree can be.
The species behind the disease is group A streptococcus, or Streptococcus pyogenes; a ball-shaped microbe that can churn out toxic compounds called superantigens, which can wreak havoc within the body. Especially in children.
The results can be as mild as a nagging case of pharyngitis or a bad rash, or as severe as a toxic shock that causes organ failure.
With the advent of antibiotics, epidemics could be easily managed before they got out of hand. In the 1
Everything seems to be changing.
“After 2011, the global reach of the pandemic became evident with reports of a second outbreak in the UK, starting in 2014, and we have now discovered isolates from the outbreak here in Australia,” says the University’s molecular biologist of Queensland Stephan Brouwer.
“This global re-emergence of scarlet fever has caused a more than fivefold increase in the disease rate and more than 600,000 cases worldwide.”
Leading an international team of researchers in a study of Group A streptococcal genes, Brouwer was able to characterize a variety of superantigens produced by a particular Northeast Asian strain.
Among them was a species of superantigen that appears to give bacterial invaders a clever new way to access the insides of host cells, never seen before among bacteria.
Its novelty implies that these outbreaks are not descended from the same strains of bacteria that have spread to communities in past centuries. Rather, they are closely related populations of Group A strep that have learned a new trick or two on their own.
One way similar organisms can evolve the same characteristics – such as advanced virulence – is for natural selection to independently fine-tune shared genes in the same way.
But other studies have already suggested that this strain of bacteria received a hand in the form of an infection of its own, from a type of virus called phage.
“The toxins would have been transferred to the bacterium when it was infected with viruses that carried the genes for the toxin,” says bioscientist Mark Walker, also of the University of Queensland.
“We have shown that these acquired toxins allow this Streptococcus pyogenes to better colonize its host, which probably allows it to compete with other strains. “
In a process known as horizontal gene transfer, a gene that has evolved into a microbe can be incorporated into the genome of a virus and modified into the DNA of a new host, creating a kind of clone of the original.
While hardly limited to bacteria, it is a quick and practical way for single-celled microbes to adapt. Such stolen genes can provide pathogens with new ways to access host tissues or withstand the chemical warfare that would otherwise keep them at bay.
In this case, he helped a less severe strain of bacteria develop a weapon that makes him as troubling as his defeated cousin.
To double-check the importance of the acquired superantigen, the researchers used gene editing to disable their coding. As a result, the strains lost the ability to colonize the animal models used to test the virulence of the bacteria.
For now, our handling of an even greater threat appears to contain the most recent scarlet fever outbreaks. Spread through aerosols much like SARS-CoV-2, group A strep is unlikely to become an epidemic under the current restrictions.
“But when social distancing is finally relaxed, scarlet fever is likely to return,” Walker says.
“Just like COVID-19, eventually a vaccine will be critical for the eradication of scarlet fever, one of the most pervasive and deadly childhood diseases in history.”
This research was published in Nature Communications.