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ards of teleological reasoning. It is possible to rationalize virtually any
change in virulence for the worse or for the better as a response to
natural selection. Having accepted the logic of evolution, biologists are
sometimes too facile in its application.
Virulence is not the only determinant of microbial transmission.
The stability and resilience of microbes also have a say in the matter.
The more delicate a microbe, the more likely it is to be transmitted
by direct means, such as personal contact, inhalation, or insect vec-
tors. The treponematoses exemplify such fragile microbes. In contrast,
more robust microbes like poliovirus can survive prolonged periods
outside a living organism. The syphilis bacterium is both delicate and
fastidious, requiring the warmth and moisture of the genitourinary
tract to survive. In contrast, poliovirus is remarkably stable, having
been found in archaeological specimens that are many centuries old
it is transmitted in human feces and readily survives prolonged resi-
dence in soil, sewage, and even chlorinated swimming pools.
Watching a Virus Evolve
Human meddling with ecology has provided a dramatic and carefully
analyzed example of how microbes can evolve. Until 1859 Australia
had no rabbits. In that year, Thomas Austin released one dozen wild
European rabbits on his property near Geelong in Victoria. The rab-
bits thrived and spread like the plague, since they encountered no nat-
ural predator in Australia. By the turn of the century, the immigrant
rabbit had become the number one pest of Australian farmers. In des-
peration, the government of New South Wales solicited proposals for
how this problem might be solved. One submission came from none
other than Louis Pasteur. It was deemed unacceptable (one of Pasteur s
few failures in search of resources).
Nothing better came along until 1950. Then the Australian Com-
monwealth Quarantine Department turned to biological warfare, in-
troducing myxomatosis virus into the wild rabbit population. Myxo-
matosis virus lives in quiet concert with the Brazilian rabbit, causing
People and Pestilence 107
no disease and persisting effectively in the wild rabbit population. To
the European rabbit, however, myxomatosis virus is a deadly patho-
gen. The strain introduced into Australia in 1950 was known to kill 99
percent of all infected European rabbits in a matter of a few days after
infection.
Transmitted by mosquitoes, the virus spread over an area greater
than that of Western Europe within three months. The rabbit popula-
tion was ravaged. Australian farmers rejoiced in the prospect of extin-
guishing their worst pest, while Australian scientists followed with
morbid fascination this epidemic of a foreign pathogen in a previously
unexposed host population.
Then the epidemic reached Mildura on the Murray River, in the
northwest corner of Victoria, and uproar followed. At almost the same
time as the rabbits of Mildura began to show symptoms and die, a
dozen cases of severe encephalitis appeared in local children. There
had been no such disease in that region for a quarter of a century. The
encephalitis spread among the population, and suspicion grew that a
virus liberated by the public authorities to kill rabbits was now killing
children.
Into this nasty breech stepped two of Australia s most prestigious
scientists, Frank Fenner and MacFarlane Burnett. They and other of
the country s microbiologists had been chasing the cause of the epi-
demic encephalitis since its inception. They knew from their data that
the human disease could not be caused by myxomatosis virus.
To dramatize their point, Fenner and Burnett called a press confer-
ence and there injected themselves with enough myxomatosis virus to
kill one hundred rabbits. They suffered no adverse consequences, to
the relief of numerous bureaucrats, and continued their study of the
encephalitis, eventually demonstrating that it was caused by a virus
now known as Murray Valley encephalitis virus, transmitted by mos-
quitoes, but in no way related to myxomatosis virus. The concurrence
of the encephalitis with the spread of myxomatosis virus had been
mere coincidence, an object lesson to alarmists. Both scientists gained
considerable celebrity from this episode. But Burnett did even better
when he later received the Nobel Prize in Physiology or Medicine for
his work on the immune system.
108 People and Pestilence
What of the rabbits? By 1957, it was clear that Peter Rabbit had
again bested Mr. McGregor. Rabbits were still dying of myxomatosis,
but not nearly at the predicted rate, and not nearly fast enough to
cause more than a modest reduction in their numbers. The number of
wild rabbits in Australia soon rose to 300 million, at least ten on every
acre of the continent, each one consuming as much grass as a sheep, all
of them descended from those dozen released by Thomas Austin in
1859. And myxomatosis virus thrived with them. What caused this
dramatic adjustment in the interaction between host and parasite?
All good Darwinians would expect that a relatively resistant strain
of rabbit would emerge from this experiment in biological warfare,
and that clearly happened. Something more subtle also occurred, how-
ever. By 1957, the myxomatosis virus isolated from wild rabbits in
Australia had become less virulent. Mortality rates for infected rabbits
dropped from 99 percent to 70 percent, a seemingly modest decline,
but enough to assure that the virus would not eradicate itself by eradi-
cating its host. Moreover, when tested in the newly emerged resistant
strain of Australian rabbit, the virus caused mortality rates as low as 25
percent. In less than seven years, the virus and the host had evolved a
dramatically different relationship.
In summary, two selections were operating in this interaction be-
tween host and parasite: selection for the more resistant host (as in
survival of the fittest), and selection of the less virulent virus (so that
the host might survive to perpetuate the virus). The host-parasite in-
teractions we normally examine in humans have had much longer to
reach equilibrium, but the features of each must reflect the pressures
and accommodations that operated so rapidly in the early years of
Australia s first encounter with myxomatosis.45
Meanwhile, Australians are again trying biological warfare against
those long-suffering rabbits. This time they are using a distant cousin
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