The Anthropocene Reviewed(22)
Ogston was so obsessed with Lister’s carbolic acid spray that his students wrote a poem about it, which reads in part:
And we learned the thing of the future
Was using unlimited spray.
The spray, the spray, the antiseptic spray
A.O. would shower it morning, night and day
For every sort of scratch
Where others would attach
A sticking plaster patch
He gave the spray.
Ogston’s first wife, Mary Jane, died after childbirth a few years before these revelations, at the age of twenty-five. There’s no record of her cause of death, but most maternal deaths at the time were caused by postpartum infection, often due to Staphylococcus aureus. And Ogston had seen hundreds of his patients die of postsurgical infection.
No wonder, then, that he was obsessed with antiseptic protocols. Still, he wanted to understand not just how to prevent infection, but also what precisely was causing it. By the late 1870s, many discoveries were being made by surgeons and researchers about various bacteria and their role in infection, but Staphylococcus was not identified until Ogston lanced a pus-filled, abscessed leg wound belonging to one James Davidson.
Under the microscope, Davidson’s abscess was brimming with life. Ogston wrote, “My delight may be conceived when there were revealed to me beautiful tangles, tufts and chains of round organisms in great numbers.”
Ogston named these tufts and chains Staphylococcus, from the Greek word for bunches of grapes. And they do often look like grape bunches—plump spheres gathered together in tight clusters. But Ogston wasn’t content with just seeing bacteria. “Obviously,” he wrote, “the first step to be taken was to make sure the organisms found in Mr. Davidson’s pus were not there by chance.” So Ogston set up a laboratory in the shed behind his home and began trying to grow colonies of staph, eventually succeeding by using a chicken egg as the medium. He then injected the bacteria into guinea pigs and mice, which became violently ill. Ogston also noted that Staphylococcus seemed to be “harmless on the surface” despite being “so deleterious when injected.” I have also observed this—insofar as I am not much bothered by having my skin colonized by Staphylococcus aureus but find it deleterious indeed when it starts replicating inside my eye socket.
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.