person who was eaten. It was transmitted by cannibalism, when highland babies made the fatal mistake of licking their fingers after playing with raw brains that their mothers had just cut out of dead kuru victims awaiting cooking. Some microbes don't wait for the old host to die and get eaten, but LETHALGIFT OF LIVESTOCK • 199 instead hitchhike in the saliva of an insect that bites the old host and flies off to find a new host. The free ride may be provided by mosquitoes, fleas, lice, or tsetse flies that spread malaria, plague, typhus, or sleeping sickness, respectively. The dirtiest of all tricks for passive carriage is perpetrated by microbes that pass from a woman to her fetus and thereby infect babies already at birth. By playing that trick, the microbes responsible for syphilis rubella, and now AIDS pose ethical dilemmas with which believers in a fundamentally just universe have had to struggle desperately. Other germs take matters into their own hands, figuratively speaking. They modify the anatomy or habits of their host in such a way as to accelerate their transmission. From our perspective, the open genital sores caused by venereal diseases like syphilis are a vile indignity. From the microbes' point of view, however, they're just a useful device to enlist a host's help in inoculating microbes into a body cavity of a new host. The skin lesions caused by smallpox similarly spread microbes by direct or indirect body contact (occasionally very indirect, as when U.S. whites bent on wiping out 'belligerent' Native Americans sent them gifts of blankets previously used by smallpox patients). More vigorous yet is the strategy practiced by the influenza, common cold, and pertussis (whooping cough) microbes, which induce the victim to cough or sneeze, thereby launching a cloud of microbes toward prospective new hosts. Similarly, the cholera bacterium induces in its victim a massive diarrhea that delivers bacteria into the water supplies of potential new victims, while the virus responsible for Korean hemorrhagic fever broadcasts itself in the urine of mice. For modification of a host's behavior, nothing matches rabies virus, which not only gets into the saliva of an infected dog but drives the dog into a frenzy of biting and thus infecting many new victims. But for physical effort on the bug's own part, the prize still goes to worms such as hookworms and schistosomes, which actively burrow through a host's skin from the water or soil into which their larvae had been excreted in a previous victim's feces. Thus, from our point of view, genital sores, diarrhea, and coughing are symptoms of disease.' From a germ's point of view, they're clever evolutionary strategies to broadcast the germ. That's why it's in the germ's interests to 'make us sick.' But why should a germ evolve the apparently self-defeating strategy of killing its host? From the germ's perspective, that's just an unintended by- product (fat consolation to us!) of host symptoms promoting efficient transmission of Z O O •GUNS,GERMS, AND STEEL microbes. Yes, an untreated cholera patient may eventually die from producing diarrheal fluid at a rate of several gallons per day. At least for a while, though, as long as the patient is still alive, the cholera bacterium profits from being massively broadcast into the water supplies of its next victims. Provided that each victim thereby infects on the average more than one new victim, the bacterium will spread, even though the first host happens to die. '* So much FOR our dispassionate examination of the germ's interests. Now let's get back to considering our own selfish interests: to stay alive and healthy, best done by killing the damned germs. One common response of ours to infection is to develop a fever. Again, we're used to considering fever as a 'symptom of disease,' as if it developed inevitably without serving any function. But regulation of body temperature is under our genetic control and doesn't just happen by accident. A few microbes are more sensitive to heat than our own bodies are. By raising our body temperature, we in effect try to bake the germs to death before we get baked ourselves. Another common response of ours is to mobilize our immune system. White blood cells and other cells of ours actively seek out and kill foreign microbes. The specific antibodies that we gradually build up against a particular microbe infecting us make us less likely to get reinfected once we become cured. As we all know from experience, there are some illnesses, such as flu and the common cold, to which our resistance is only temporary; we can eventually contract the illness again. Against other illnesses, though—including measles, mumps, rubella, pertussis, and the now defeated smallpox—our antibodies stimulated by one infection confer lifelong immunity. That's the principle of vaccination: to stimulate our antibody production without our having to go through the actual experience of the disease, by inoculating us with a dead or weakened strain of microbe. Alas, some clever microbes don't just cave in to our immune defenses. Some have learned to trick us by changing those molecular pieces of the microbe (its so-called antigens) that our antibodies recognize. The constant evolution or recycling of new strains of flu, with differing antigens, explains why your having gotten flu two years ago didn't protect you LETHALGIFT OF LIVESTOCK • 2.OI eainst the different strain that arrived this year. Malaria and sleeping sickness are even more slippery customers in their ability rapidly to change their antigens– Among the slipperiest of all is AIDS, which evolves new antigens even as it sits within an individual patient, thereby eventually overwhelming his or her immune system. Our slowest defensive response is through natural selection, which changes our gene frequencies from generation to generation. For almost any disease, some people prove to be genetically more resistant than are others. In an epidemic those people with genes for resistance to that particular microbe are more likely to survive than are people lacking such genes. As a result, over the course of history, human populations repeatedly exposed to a particular pathogen have come to consist of a higher proportion of individuals with those genes for resistance—just because unfortunate Individuals without the genes were less likely to survive to pass their genes on to babies. Fat consolation, you may be thinking again. This evolutionary response is not one that does the genetically susceptible dying individual any good. It does mean, though, that a human population as a whole becomes better protected against the pathogen. Examples of those genetic defenses include the protections (at a price) that the sickle-cell gene, Tay-Sachs gene, and cystic fibrosis gene may confer on African blacks, Ashkenazi Jews, and northern Europeans against malaria, tuberculosis, and bacterial diarrheas, respectively. In short, our interaction with most species, as exemplified by hummingbirds, doesn't make us or the hummingbird 'sick.' Neither we nor hummingbirds have had to evolve defenses against each other. That peaceful relationship was able to persist because hummingbirds don't count on us to spread their babies or to offer our bodies for food. Hummingbirds evolved instead to feed on nectar and insects, which they find by using their own wings. But microbes evolved to feed on the nutrients within our own bodies, and they don't have wings to let them reach a new victim's body once the original victim is dead or resistant. Hence many germs have had to evolve tricks to let them spread between potential victims, and many of those tricks are what we experience as 'symptoms of disease.' We've evolved countertricks of our own, to which the germs have responded by evolving counter-couritertricks. We and our pathogens are now locked in an escalat- 1 O 2 •GUNS,GERMS, AND STEEL
