back in Melbourne, he got interested in psittacosis.
Keying off the American study, Burnet ordered himself a crate of parrots and cockatoos from Adelaide. He found that a third of them were infected. He ordered another dozen from Melbourne. At least nine of those were probable carriers. Another two dozen from Melbourne yielded still more positives. So much for the myth of Australia as a prelapsarian psittacosis-free Eden.
But if the country’s wild bird populations were riddled with this bacterium, how could the country’s people—so many of whom doted upon their pet budgerigars and talking cockatoos—be entirely as unaffected as they seemed? The likely answer, Burnet guessed, was not some magical form of immunity but ignorance and underdiagnosis. Australian doctors didn’t know psittacosis when it wheezed in their faces. To test that guess, Burnet started chasing down cases of human illness that looked like psittacosis but might have been diagnosed as influenza or typhoid. He and a co-investigator found seventeen people, sick with fever, cough, headache, pneumonia, et cetera, all of whom had been exposed to pet birds—either captive-bred budgerigars or parrots and cockatoos lately caught from the wild. His most interesting cluster was a group of twelve people infected from one batch of sulphur-crested cockatoos.
Those birds, all forty-nine of them, had been sold by the bird catcher to a Melbourne man, a laborer, who dabbled in bird dealing for a bit of seasonal income. Burnet called the man Mr. X, giving him the usual medical anonymity. Mr. X kept his avian merchandise in a small, dark, backyard shed. The first signal of disease in the birds, several weeks after their transfer to his “aviary,” was that eight or nine of them died. But by then Mr. X, wasting no time, had sold seven others to people in the neighborhood and sent his twelve-year-old son off to the local market with twenty more. Mr. X’s son got sick, and his daughter, and his wife, and his mother-in-law. Five neighbors and three other people, each of whom lived in a house with a cockatoo bought from Mr. X or his son, also fell ill, some of them severely. Nobody died. Mr. X himself didn’t sicken, not on this occasion—possibly because there is no justice in the world, though more likely because exposure to Rickettsia psittaci during his earlier bird dealings had given him some acquired immunity.
Macfarlane Burnet, as a biologist as well as a physician, was interested in the birds and the bacterium, not just in the people. He knew that the sulphur-crested cockatoo nests in tree holes, producing two or three eggs in a clutch, and that bird catchers typically raided the nest holes just before fledging. He suspected that almost all the young became infected with the bacterium as hatchlings, before leaving (or being taken from) the nest. “If the young cockatoo, after capture, is kept under good conditions,” he and his coauthor wrote, “it remains healthy and presents no danger to human beings.” Likewise, the wild bird populations might carry a high prevalence of infection but suffer little impact in terms of damaged health or mortality. “When, on the other hand, birds are crowded into small spaces, with inadequate food and sunlight, their latent infection is lit up.” The bacterium multiplies and “is excreted in large amounts.” It floats out of the cages along with downy feathers, powdered dung, and dust. It rides the air like a Mosaic plague. People inhale it and become ill. Burnet acknowledged that no government in Australia was likely to prohibit the sale of cockatoos, not in those days, nor even to insist they be kept under decent conditions. But that’s what is needed, he added gruffly. Then he turned to another disease.
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The other disease was Q fever. Remember those abattoir workers in Brisbane, during the early 1930s, who suffered mysterious, feverish ailments resembling typhus? The job of investigating that cluster of cases fell first to a man named Edward H. Derrick, newly appointed as director of the microbiology laboratory at the Queensland Health Department. Using guinea pigs inoculated with patients’ blood to start a sequence of infections and then infecting one guinea pig from another, Derrick established the presence of “a distinct clinical entity,” a new sort of pathogen, not recognizable by any of the standard lab tests for typhus, undulant fever, or other familiar possibilities. But he couldn’t see the new thing through a microscope, nor could he get it to grow in a dish. That led him to suspect it was a