Soldier Died of Antibiotic Resistant Dysentary

Back in 1915, before the invention of antibiotics

Scientists who unlocked the genetic code of bacteria grown from a soldier who died of dysentery in World War I say it revealed a superbug already resistant to penicillin and other antibiotics decades before they were in common use.

The discovery sheds light on the history of antibiotic resistance - now a global health threat. It also offers fresh clues on how to tackle dysentery, a disease that kills hundreds of thousands of children every year in developing countries.

'Even before the description and widespread use of penicillin, this bacterium was resistant to it,' said Kate Baker of Britain's Wellcome Trust Sanger Institute, who worked on the research with colleagues at Public Health England (PHE).

Researchers focused on a bacterial sample retrieved from the British soldier - Private Ernest Cable of the East Surrey Regiment - who died in March of 1915.

Dysentery is a life-threatening disease that is becoming increasingly hard to treat due to its growing ability to evade antibiotic treatment.

It was rife in the trenches during World War I, and still spreads now in unsanitary conditions in poor countries and in conflict zones.

This is less surprising than it sounds. Most antibiotics are natural products produced by fungi or bacteria to inhibit the growth of bacteria that compete with them for substrates or actually infect them. Therefore, bacteria have been intermittently exposed to antibiotics since, well who knows; probably millions if not billions of years, and it's not shocking that many strains of antibiotic resistant bacteria are found in nature. The microorganisms have been conducting chemical war on each other down through evolutionary time.

This does not mean we don't have to worry about accelerating the evolution of antibiotic resistant bacteria with profligate use of man made antibiotics; quite the opposite, it means the seeds of antibiotic resistance are widely spread in nature, and ready to spring into the gap when antibiotics are used to kill their nonresistant kin.