A house finch (Haemorhous mexicanus) infected with the bacterium Mycoplasma gallisepticum.ANDY DAVIS, UNIVERSITY OF GEOROne of the most remarkable events in the history of infectious diseases began at the end of 1950. A smallpox-like virus that was being trialed as a biological control agent for the invasive rabbit populations in Australia escaped from test sites and caused an outbreak of unprecedented scale, speed, and carnage. Within just six months, it had spread up the river systems in four states and was decimating rabbit populations across a million square miles. “In places it was possible to drive for a day or more through country that had previously been swarming with rabbits and see only isolated survivors,” one research team reported.1 Tens, perhaps hundreds, of millions of rabbits were eliminated in that initial wave. For farmers whose livelihoods were being devoured by hordes of rabbits, it was something of a miracle.
To everyone’s delight, the carnage continued, helped by subsequent deliberate releases in other parts of Australia. Over the ensuing decade, rabbit populations in wide swaths of the country were reduced to a tenth of what they had been.2 Since that time, rabbit populations have rebounded somewhat, but are nowhere near what they once were. The culpable agent, myxoma virus (MYXV), has generated billions of dollars of savings for Australian agricultural industries to date,3 surely one of the most cost-effective interventions in the history of agriculture.
The episode also presented a unique opportunity to study the evolutionary arms race between a pathogen and its host animal. Australian microbiologist Frank Fenner took advantage, setting up just the right experiments at just the right time—and he and colleagues ...
