Penicillin, the high-performing mould.

Imagine you come back to your workplace from holiday in early September 1928. On the table: a stack of Petri dishes you did not clear away before leaving. You are a bacteriologist, you culture staphylococci, and you are — let us put it kindly — not a particularly tidy person. One of the dishes has gone mouldy.

You are about to tip it into the sink.

Then you look more closely.

The man with the dish is called Alexander Fleming, a Scottish doctor and bacteriologist at St Mary’s Hospital in London. His laboratory is legendary — for its untidiness. Half-dried cultures, open windows, dishes standing about for weeks. It is precisely this sloppiness that is about to become world history.

On the mouldy dish grows a blue-green fungus. Nothing unusual in a draughty London laboratory. What is unusual is what happens around the fungus: a clean, germ-free ring. Where the mould sits, the staphylococci have not merely grown more weakly — they have simply vanished. Something this fungus secretes has dissolved the bacteria.

Fleming notes soberly what he sees. The fungus belongs to the genus Penicillium. The substance it exudes he christens with the name that is spoken today in every pharmacy in the world: penicillin.

And then — almost nothing happens.

For here begins the real, and often glossed-over, drama of the story. Fleming has discovered the active substance, but he cannot get it out of the broth. Penicillin is temperamental, unstable, hard to purify. Fleming is a bacteriologist, not a chemist. In 1929 he publishes a paper that is politely overlooked, gives a few talks at which nobody catches on — and more or less files the matter away. For over a decade the greatest medical find of the century is above all one thing: an interesting laboratory curiosity.

Only shortly before the Second World War does a team in Oxford take the idea out of the drawer. The pathologist Howard Florey, the biochemist Ernst Chain, who had fled Hitler’s Germany, and the tireless tinkerer Norman Heatley purify penicillin far enough to try it at last on living creatures. In 1940 they inject infected mice. The treated animals survive, the untreated ones die. The three know immediately: this changes everything.

In 1941 it is the turn of the first human being. Albert Alexander, a London policeman, has scratched himself on a rose bush — and is now dying of blood poisoning, half his face eaten away. He is given penicillin. Within days the fever recedes, the abscesses heal, the man wakes up. It is a miracle at the bedside.

Then the penicillin runs out.

The Oxford team even filters the substance out of the patient’s urine in order to keep treating him. It is not enough. Albert Alexander dies. Not because the medicine fails — but simply because there is too little of it.

That is precisely what the war solves. Since England, amid the bombs, has no spare factories for moulds, Florey travels to the USA. There they tinker with tanks, deep-frozen cultures and — no joke — a particularly productive mouldy melon from the market in Peoria, until penicillin flows on an industrial scale. Just in time for the Normandy landings in 1944, antibiotics save soldiers by the row who would previously have died of an infected wound.

In 1945 Fleming, Florey and Chain share the Nobel Prize. In his speech Fleming already warns of what we today call resistance: anyone who takes too little breeds the resistant germs themselves. A sentence that has lost none of its relevance at the pharmacy counter.

Which leaves the punchline that pharmacists may particularly appreciate: the medicine that since its introduction has saved an estimated 200 million human lives — more than almost any other — was not researched with determination, not invented in a large laboratory, not planned on a drawing board.

It grew by accident on a dish that somebody had forgotten to clear away.

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