James Davidson, by the way, went on to live for many decades after his staph infection, thanks to a thorough debriding and Ogston’s liberal use of the spray, the spray, the antiseptic spray. But Staphylococcus aureus remained an exceptionally dangerous infection until another Scottish scientist, Alexander Fleming, discovered penicillin by accident. One Monday morning in 1928, Fleming noticed that one of his cultures of Staphylococcus aureus had been contaminated by a fungus, penicillium, which seemed to have killed all the staph bacteria. He remarked aloud, “That’s funny.”

Fleming used what he called his “mold juice” to treat a couple of patients, including curing his assistant’s sinus infection, but mass production of the antibiotic substance secreted by penicillium proved quite challenging.

It wasn’t until the late 1930s that a group of scientists at Oxford began testing their penicillin stocks, first on mice, and then, in 1941, on a human subject, a policeman named Albert Alexander. After being cut by shrapnel during a German bombing raid, Alexander was dying of bacterial infections—in his case, both Staphylococcus aureus and Streptococcus. The penicillin caused a dramatic improvement in Alexander’s condition, but the researchers didn’t have enough of the drug to save him. The infections returned, and Alexander died in April of 1941. His seven-year-old daughter Sheila ended up in a local orphanage.

Scientists sought out more productive strains of the mold, and eventually the bacteriologist Mary Hunt found one on a cantaloupe in a Peoria, Illinois, grocery store. That strain became even more productive after being exposed to X-rays and ultraviolet radiation. Essentially all penicillin in the world descends from the mold on that one cantaloupe in Peoria.*

Even as penicillin stocks increased—from 21 billion units in 1943 to 6.8 trillion units in 1945—there was growing awareness that the bacteria killed by penicillin were evolving resistance to it, especially Staphylococcus aureus. A 1946 Saturday Evening Post article worried that antibiotic use would “unwittingly aid and speed up the subtle evolution forces which arrange for the survival of the fittest microbes.” So it was to be. By 1950, 40 percent of Staphylococcus aureus samples in hospitals were resistant to penicillin; by 1960, 80 percent. Today, only around 2 percent of Staphylococcus aureus infections are sensitive to penicillin.

This all happened so, so quickly. Sixty-four years elapsed between Alexander Ogston’s discovery of Staphylococcus and the mass production of penicillin, and sixty-four years elapsed between the mass production of penicillin and my 2007 bout with orbital cellulitis. In the end, my infection did not respond to penicillin, or to the next two lines of antibiotics, but did fortunately respond to the fourth. Antibiotic resistance is not a problem for the future—this year, some fifty thousand people in the U.S. will die of Staphylococcus aureus infections.

How recent is penicillin? That police officer’s daughter, who ended up in the orphanage, is still alive as of this writing. Sheila Alexander married an American soldier and moved to California. She’s a painter. One of her recent paintings depicts a block of homes in an English village. Ivy grows up along the wall of one home, creeping over rough stone.