The doctors could relax slightly. The dairy farmers could lament their losses. But the scientists knew that Coxiella burnetii wasn’t gone. It had waited for ideal conditions before, and it could wait again.
47
Back in Australia, around the time of his work on Q fever and psittacosis, smart and curmudgeonly Macfarlane Burnet began thinking more broadly about infectious diseases, not so much from the medical perspective as from the viewpoint of a biologist. During the late 1930s he drafted a book on the subject, in the opening pages of which he paid tribute to the great nineteenth-century founders of bacteriology, especially Pasteur and Koch, who had finally provided a rational basis for concerns over clean drinking water, decent sewage disposal, food untainted with rot, and antiseptic surgical techniques. It was a qualified tribute, concluding on page two, after which Burnet got to his real point.
Those men and their colleagues, he wrote, “were on the whole too busy to think of anything but the diseases for which bacteria were responsible, and how these might be prevented.” They gave little consideration to the microbes as beings in their own right, or to “how their nature and activities fitted into the scheme of living things.” Most bacteriologists were trained as medical men—Burnet himself had been, before going into bacteriological research—and “their interest in general biological problems was very limited.” They cared about curing and preventing diseases, which was well and good; less so about pondering infection as a biological phenomenon, a relationship between creatures, equal in fundamental importance to such other relationships as predation, competition, and decomposition. Burnet’s purpose in the book was to rectify that slight. He published Biological Aspects of Infectious Disease in 1940, a landmark along the route to modern understandings of zoonoses on a crowded, changing planet.
Burnet didn’t claim that the broader perspective was uniquely his own. He recognized it as a salubrious trend. Biochemists had begun applying their methods to disease-related questions, with considerable success, and there was also new interest at the level of organisms (even single-celled organisms) as highly adapted creatures with their own life histories in the wild. He wrote:
Other workers with an appreciation of modern developments in biology are finding that infectious disease can be thought of with profit along ecological lines as a struggle for existence between man and micro-organisms of the same general quality as many other types of competition between species in nature.
The italics are mine. Thinking “along ecological lines,” and about the “struggle for existence” (a phrase that came straight from Darwin), was what Burnet specially offered: a book on the ecology and evolution of pathogens.
He preferred the term “parasites,” used in its looser sense. “The parasitic mode of life is essentially similar to that of the predatory carnivores. It is just another method of obtaining food from the tissues of living animals,” though with parasites the consumption tends to be slower and more internalized within the prey. Small creatures eat bigger ones, generally from the inside out. This is just what I was getting at, back at the start, when I mentioned lions and wildebeests, owls and mice. The main problem facing a parasite over the long term, Burnet noted, is the issue of transmission: how to spread its offspring from one individual host to another. Various methods and traits have developed toward that simple end, ranging from massive replication, airborne dispersal, environmentally resistant life-history stages (like the small form of C. burnetii), direct transfer in blood and other bodily fluids, behavioral influence on the host (as exerted by the rabies virus, for instance, causing infected animals to bite), passage through intermediate or amplifier hosts, and the use of insect and arachnid vectors as means of transportation and injection. “It will be clear, however,” Burnet wrote, “that no matter by what method a parasite passes from host to host, an increased density of the susceptible population will facilitate its spread from infected to uninfected individuals.” Increased density: Crowded hosts allow pathogens to thrive. Macfarlane Burnet may or may not have been influenced by those early mathematical works on infectious disease—the differential equations of Ronald Ross, the 1927 paper by Kermack and McKendrick—but he was putting some of the same points into plain English prose in a book that was both authoritative and accessible.
Biological Aspects of Infectious Disease was later revised and reissued, in 1972, as Natural History of Infectious Disease. Though even its revised version seems antiquated today (new diseases have emerged, as well as new insights and new methods),