Why We Get Sick (11 page)

An unsanitary water supply is only one example of what Ewald calls
cultural vectors
. The history of medicine shows repeatedly that the best place to acquire a fatal disease is not a brothel or a crowded sweatshop but a hospital. In hospitals, large numbers of patients may be admitted with infectious diseases normally transmitted by personal contact. People who are acutely ill do not move around much, but hospital personnel and equipment move rapidly from such people to others not yet infected. Inadequately cleaned hands, thermometers, or eating utensils can be quite effective cultural vectors, and the transmitted diseases may rapidly become more virulent.

Take, for instance, the streptococci that can cause uterine infection in women after childbirth. Most nineteenth-century women knew that they risked their lives by having their babies in the hospital, but some still did so. Viennese physician Ignaz Semmelweis noted in 1847 that women in a clinic staffed by medical personnel contracted childbed fever three times as frequently as those in a clinic staffed by mid wives. On investigating, he found that doctors came directly from doing autopsies on women who had died from childbed fever to do pelvic examinations on women in labor. Semmelweis proposed that they were transmitting the causative agent and showed that infections were less frequent when examiners washed their hands in a bleach solution. Was he thanked for his wonderful discovery? No. He was dismissed from his post for suggesting that doctors were causing the deaths of patients. He became more and more frantic in his efforts to save the thousands of women who were dying unnecessarily, but he was ignored, and finally, at age forty-seven, he died in an insane asylum. Nowadays, we all accept the need for hygiene in hospitals, but whenever it becomes lax, conditions are perfect for selecting for increased virulence, as in the virulent hospital-acquired (versus community-acquired) infantile diarrhea studied by Paul Ewald.

It is widely believed that HIV is a new pathogen, perhaps originating from a monkey infected with simian immunodeficiency virus (SIV). However, evidence now suggests that monkeys might have acquired SIV from people with HIV. While HIV may have been present in some humans for many generations, AIDS is apparently a new disease, resulting from the evolutionary origin in recent decades of highly virulent HIV strains. AIDS may have arisen because of changed sexual behavior resulting from the socioeconomic disruption of some traditional societies. Large numbers of prostitutes serving hundreds of men per year were so effective at spreading infection that host survival became much less important to virus survival. Those strains that most rapidly exploited their hosts came to prevail within the hosts, and even the highly virulent strains had plenty of opportunity to disperse to new hosts before the old ones died.

In Western countries, AIDS appeared initially as a disease mainly of male homosexuals because their large numbers of sex partners greatly accelerated sexual transmission, and of intravenous drug users because the drug users’ needles were effective vectors. As in Africa, the most virulent HIV strains prevailed over the less virulent because between-host selection for lower virulence was greatly weakened. Even highly virulent viruses had abundant opportunities to reach new hosts before the original host died. Conversely, the use of clean needles and condoms can not only curtail the transmission of the virus,
it can also cause the evolution of lower virulence
.

A
s described in the previous chapter, natural selection has given us a fiendishly effective system of chemical warfare. For every invading pathogen there will be a worst-case scenario as to what kind of molecules it might encounter. Our immune systems have been shaped over a hundred million years to make the pathogen’s worst nightmares come true. Unfortunately, every effective weapon can sometimes be dangerous to the one who wields it.

The immune system can make two kinds of mistakes: failing to attack when it should and attacking something when it shouldn’t. The first kind of mistake results from inadequate response, so that a disease that should have been nipped in the bud becomes serious. The second kind of mistake results from mounting too aggressive a response to minute chemical differences. Autoimmune diseases such as lupus erythematosus and rheumatoid arthritis could be the result. The average person’s degree of sensitivity and responsiveness is presumably close to what has historically been the optimum: enough to counter pathogens but not so great as to attack the body’s own structure.

Given that we have this chemical superweapon—immunity—how can we possibly remain vulnerable to infectious diseases? Once again, it is because the infectious agents can evolve rapidly and become better adapted by natural selection. Those variants that are least vulnerable to immunological attack will be those whose genes are best represented in future generations. So the pathogens may evolve one or another kind of defensive superweapon. Molecular mimicry, mentioned in the last chapter, is one such weapon.

S
cientists first developed the concept of mimicry to describe the patterns on butterflies’ wings. For instance, the viceroy butterfly looks almost exactly like the monarch butterfly, which birds do not attack because they want to avoid the toxins the monarch caterpillar gets from eating milkweed leaves. The viceroy has no such toxins, but birds mistake it for its bitter look-alike and likewise shun it. Examples are now also known in many other animal groups. Any edible species that by chance resembles a toxic species will have an advantage, and selection will make this
mimic
species look increasingly like the toxic
model
. This is bad for the model because predators that eat the edible mimic learn to go after the model as well. This sets up an arms race between the mimic, which evolves an ever closer resemblance to the model, and the model, which evolves to be as different as possible from its edible neighbors. Some environmental circumstances favor the mimic to such an extent that really detailed resemblances between unrelated species may evolve. We notice such mimicry easily because we perceive
so much of the world visually. Detection of chemical mimicry requires more subtle techniques, but there is no reason to think it less common than visual examples.

The molecular mimicry shown by pathogens turns out to be at least as subtle, complicated, and full of surprises as the visual mimicry shown by butterflies and other animals. Deceptive resemblances to human proteins are shown by the surfaces of various parasitic worms, protozoa, and bacteria. If there is any deficiency in the mimicry of human tissues by a bacterium, we can expect it to evolve an improvement rapidly. Pathogen surfaces may have a complex sculpturing of convexities and concavities, and the molecular forms most readily recognized by antibodies are hidden in crevices. As noted in the last chapter, some pathogens alter their exposed molecular structures so rapidly that the host has difficulty producing newly needed antibodies fast enough. This is rapid change without evolution, because the same pathogen genotype codes for a variety of molecular structures.

Mimicry may not only permit pathogens to escape from immunological attack but also make active use of hosts’ cellular processes. For instance, streptococcal bacteria make molecules similar to host hormones that have receptor sites on cell membranes. In effect, the bacterium has a key to the lock on the door that normally admits a hormone. Once inside the cell, the bacterium is shielded from immunological and other host defenses. The host has an endosomelysosome complex that can attack pathogens within its cells, but molecular mimicry and other countermeasures protect the pathogen there too.

B
efore leaving infectious disease, we will anticipate a theme of
Chapter 10
by noting the large proportion of epidemics that have resulted from novel environmental circumstances. We have already mentioned how changed social conditions may have initiated the AIDS epidemic, but the same is true for many other plagues. Richard Krause, of the National Institutes of Health, reports that early measles and smallpox epidemics spread along caravan routes in the second and third centuries and
killed a third of the people in some communities. Bubonic plague, the black death, had long festered in Asia, but became epidemic only when Mongol invaders brought it to unexposed populations in Europe who lived with large populations of flea-infested rats. While we like to imagine that such events are in the past, AIDS continues to spread alarmingly, and the causes of other sudden outbreaks of infection are unknown. The Ebola virus ravaged parts of Africa in the 1980s, killing half of those who became ill, including most of the doctors and nurses who cared for the patients. It stopped as suddenly as it started, for reasons that remain unclear.

Some infectious diseases stem directly from modern technology. Legionnaires’ disease arose from an organism that was able to grow and be dispersed from the water in a hotel air-conditioning system. Toxic shock syndrome arose when a new superabsorbent tampon material allowed enough surface area and oxygen for the growth of unusually large concentrations of toxic staphylococcal bacteria. Lyme disease became a problem only when deer populations multiplied adjacent to new suburbs. Influenza has become a major threat since mass worldwide transportation began spreading new strains that contain new genes. It is often called the
Asian flu
because new strains so often originate on Asian farms, where people, ducks, and pigs (some strains are called
swine flu
) live in such close proximity that genes from one influenza strain can easily be passed from one to another.

Tuberculosis became epidemic in Europe with the rise of large, crowded cities. Unsanitary practices and poverty are always cited as causes, but we wonder if the disease didn’t become epidemic simply because large numbers of people began spending large amounts of time together indoors. Air exhausted from a TB ward reliably produces infection in guinea pigs but no longer causes infection if it is briefly exposed to ultraviolet light. A single sneeze can produce a million droplets, which settle to the ground at a rate of only about one centimeter per minute in still air. In the open air they would be dispersed or killed by sunlight, but indoors they might last for weeks, as they no doubt did in 1651, when tuberculosis caused 20 percent of all deaths in London.

Finally, we note that epidemics can result from the best of intentions. Polio was not an epidemic disease that caused paralysis until the early twentieth century. Before that time, most children got the disease in the first years of life, when it usually produces only mild effects. By midcentury, improving sanitation delayed the infection
until late childhood, when it can be much more severe. Mononucleosis is also less severe at earlier ages. In each of these examples, a disease became a serious problem only when its mode of transmission was changed by novel environments. We will return in
Chapter 10
to other novel environmental factors and their role in disease.

W
hen Huck Finn’s drunken “Pap” fell over a tub of salt pork and barked both shins, he

Pap acted as if the tub wanted to hurt him, as if kicking and cursing it could deter future harm to his shins. But the kicking and cussing were wasted effort. The tub was not a rival trying to steal Pap’s mate, a predator trying to catch him, or even a microorganism stealthily trying to devour his tissues. It was merely inanimate wood.

In discussing such things as tubs of salt pork as sources of injury, we leave behind the conflicting interests, strategies, and arms races that complicate contests between living opponents. The problems associated with injuries are conceptually simpler than those of infectious diseases, but there is complexity aplenty. Some dangers, like being struck by a meteorite, have always been so rare and unpredictable that we have no evolved defenses and can repair the damage
only by using general-purpose mechanisms. Others, like exposure to high levels of gamma rays, are so new that we have not had time to evolve adequate defenses. But some dangers, like drowning or attack by predators, have happened often enough in evolutionary history that we have evolved ways to avoid them. This chapter is about the ways we avoid, escape, and repair damage from sources of injury such as mechanical trauma, radiation, burning, and freezing. It is also about why these adaptations do not always work as well as we might wish.

C
ooled by milk, the coffee needed to be warmed up just a bit. The microwave oven sounded its three pleasant beeps, and, as one of the authors opened the door, the air filled with the aroma of steaming café au lait. As he grabbed the handle of the ceramic mug, searing pain struck in a fraction of a second, too soon, too intense even to get the hot-handled mug to the counter. It crashed to the floor, splattering hot coffee for yards. After he got his painful hand under cold water, the victim realized that this mug must be different from others, which stay cool to the touch after microwaving. In fact, its handle must have had a metal core. The pain prevented the worse damage that would have resulted from more prolonged contact. The fearful memory of the pain, months later, still makes him shy away from using that particular mug.

Pain and fear are useful, and people who lack them are seriously handicapped. As noted already, the rare individuals who are born without the sense of pain are almost all dead by age thirty. If there are people born without the capacity for fear, you might well look for them in the emergency room or the morgue. We need our pains and our fears. They are normal defenses that warn us of danger. Pain is the signal that tissue is being damaged. It has to be aversive to motivate us to set aside other activities to do whatever is necessary to stop the damage. Fear is a signal that a situation may be dangerous, that some kind of loss or damage is likely, that escape is desirable.