Multi-drug resistant tuberculosis in Russia. Lessons from a cholera epidemic. Feline immunodeficiency virus. Leaf-cutter ants and symbiosis. Allergies and the importance of interactions among species.
"The Cold War is history," the narrator begins, "but Russia is in the grip of an arms race--an evolutionary arms race, with an enemy the naked eye cannot see." After some scenes of predators catching their prey, and bacteria multiplying under a microscope, we find ourselves in a room crowded with prison inmates--some of them coughing. "A deadly microbe is evolving in Russia's prisons," the narrator continues ominously, "consuming the bodies of men. As it escapes prison walls, it attacks new prey, without preference, without warning." Suddenly we are transported to New York City. "Now the killer is spreading beyond Russia, and no one is immune. Unseen, the microbe is evolving into mutants that may soon elude our best defenses. Will we lose this arms race, or can we reach an evolutionary truce with a mortal enemy?"
The scene switches to western Oregon, "home to one of evolution's most extreme and deadly creations"--a species of newt that defends itself from predatory snakes with tetrodotoxin, a potent nerve poison. Each newt produces enough toxin to kill scores of other animals, but why so much? Research shows that the garter snakes that prey on them have a certain amount of resistance to the toxin. A newt that produces slightly more toxin than its neighbors might overcome the snakes' resistance and survive. If its offspring inherit the ability to produce more toxin, subsequent generations might evolve higher toxin levels. The snakes, in like manner, might evolve higher levels of resistance, and the result would be an "evolutionary arms race" between the two species.
Evolution, we are told, is driven not just by physical forces such as climatic change, but even more by biological forces--the ways species interact with each other. As we watch some more wildlife photography, the narrator asks: "What made the lion fast, and the zebra fierce? What drove the development of tooth and claw? The deadly dance of predator and prey has shaped the evolution of countless species. There may have been a time on an ancient savanna when hungry beasts hunted our ancestors, and drove the evolution of our own species."
We find ourselves once again on crowded city streets, as the narrator continues: "But since the dawn of civilization, only one kind of predator has truly threatened us. The microorganisms that cause disease consume us from the inside out." They also reproduce much faster than we do--a fact dramatized by time-lapse microphotography. "By evolving much faster than we do, microbes have eluded the body's defenses, and left their mark on our history."
The bacteria that cause tuberculosis have been detected in Egyptian mummies, and have preyed on people for thousands of years. A different microbe caused the "Black Death" in the fourteenth century, which killed a third of all Europeans. And still another caused the 1918 flu epidemic, which claimed 20 million lives. "We were virtually defenseless against these microscopic killers until recently," the narrator says. An old newsreel shows a hospital--"a battlefield in man's total war against disease"--and calls antibiotics "the miracle drugs of our time." Antibiotics initially seemed to be so successful that by 1969 the U. S. Surgeon General thought the war on infectious disease had been won. But he spoke too soon.
We return to Russia, to the room crowded with prison inmates. Since the fall of the Soviet Union, the narrator says, Russia's prison population has soared. "But overcrowding, poor nutrition, and scant sanitation are not the worst of the prisoners' worries. Now tuberculosis stalks these men." Microbes that might lie dormant in otherwise healthy people erupt into active disease in these men, because their immune systems have been weakened by unhealthy lifestyles and prison over-crowding.
Many of these victims were previously treated for tuberculosis (TB), but their treatment was not continued long enough to cure them completely. Describing one such victim, the narrator says: "Evolution has occurred inside his body." When he was first diagnosed with TB, he was given drugs that killed some bacteria but spared "the ones with mutations that made them resistant to the drugs. As these survivors multiplied, they passed along their protective mutations to all their descendants. In this way, the bacteria evolved into a new drug-resistant strain."
In fact, he and more than 30,000 other Russian prison inmates have TB that is resistant to more than one drug. Although there are now new antibiotics to treat strains with multi-drug resistance, they are expensive and hard to get. When the prisoners are released, they can spread these resistant strains to the general population--and thus to the rest of the world, including the U.S.
Doctors and nurses scurry around an emergency room to dramatize the possible consequences of a TB epidemic in a U.S. city. The scene is frightening. "And TB is just the tip of the iceberg," says the narrator. "The microbes that cause malaria, pneumonia, gonorrhea, and scores of other infectious diseases are evolving drug resistance."
"We've created this problem," a researcher tells us. "Multi-drug resistance is a man-made problem." This is because antibiotics are being used too much. "By developing as many antibiotics as we have over the last fifty years, we've essentially accelerated an evolutionary process. The outcome is that we're going to have more drug-resistant microbes--to the point where some of the most dangerous bacteria will not be treatable. We're racing against the microbe every day, and unfortunately we're losing."See . Multi-drug-resistant TB is an important public health problem. For more information, go to:
There may be a solution, however. "In an arms race without end, the more drugs we launch at microbes the more resistance they evolve," the narrator says. "It may be time to change our strategy, and make evolution work for us."
Amherst College evolutionary biologist Paul Ewald explains: "When people are looking at the antibiotic resistance problem, they see evolution as sort of the bad guy. It's the evolutionary process that's led to antibiotic resistance--and that's true. But just as easily, we can have evolution being the solution. In other words, we can have evolutionary processes leading to organisms becoming more mild."
According to Ewald, microbes that are transmitted through direct person-to-person contact--such as cold viruses--tend to be mild, because they require basically healthy people for their transmission. But microbes that are transmitted through insects, food, or water--such as cholera--tend to make people very sick. "Once we understand the factors that favor increased harmfulness and decreased harmfulness," Ewald reasons, "then we can look at all of the things we do in society. We can ask the question, `Are we doing certain things, or can we do certain things, that would favor organisms evolving towards mildness.'"
Ewald studied a 1991 cholera outbreak in South America that sickened over a million people and killed almost 11,000, in order to "document evolution in action." Ewald explains: "If you have contaminated water allowing transmission, we expect the cholera organism to evolve to a particularly high level of harmfulness. And that's exactly what we see. We find that bacteria that had invaded countries with poor water supplies evolved increased harmfulness over time."
"If, instead, we clean up the water supplies," Ewald continues, "then we force the bacteria to be transmitted only by routes that require healthy people. And what we find is that when cholera invaded countries with clean water supplies, the organism dropped in its harmfulness. Those bacteria evolved [a] lower level of toxin production--they actually became more mild through time.
"People would still be getting infected, but the infections would be so mild that most people wouldn't even be sick. So the cholera outbreak in Latin America suggests that we may need only a few years to change the cholera organism from one that would often kill people to one that hardly ever causes the disease. What we're suggesting here is that we can domesticate these disease organisms."
But there are serious problems with Ewald's story. First, he claims that microbes spread through person-to-person contact tend to be less harmful than those spread by insects, food and water. But TB--the harmfulness of which was just impressed on us--spreads through person-to-person contact. So did the 1918 flu, which killed more people in less time than the infamous Black Death. Since cholera is transmitted through water or food--not through person-to-person contact--regardless of whether it is mild or harmful, Ewald's hypothesis is wrong from the start.
Second, the solution Ewald proposes--to clean up water supplies--owes nothing to Darwinian evolution. Clean water prevents cholera epidemics primarily because it prevents the bacteria from spreading, not because it spreads bacteria that have evolved to become "more mild." And before Darwin even published his theory, deaths from infectious diseases in England had already declined dramatically because of the general improvement in sanitation and nutrition during the eighteenth and nineteenth centuries.See . For more information on Ewald's hypothesis, see Paul W. Ewald, Evolution of Infectious Diseases (Oxford: Oxford University Press, 1996). For more information about cholera, go to:
The lesson to be learned from this is that our first lines of defense against infectious diseases are to keep our food and water clean, and to maintain our general health by eating nutritious foods. Although no one who has ever needed antibiotics will dispute their usefulness, their contribution to public health is minor compared to improved sanitation and nutrition.
Like all other infectious diseases, TB declined dramatically in England before the advent of modern medicine, and for the same reasons. As we were told a few minutes ago, Russian prison inmates develop active TB because their immune systems have been weakened by unhealthy lifestyles and poor nutrition. Add overcrowding and poor sanitation, and illness is to be expected. Of course, the problem of multi-drug resistance cannot be ignored; but once again, general sanitation and nutrition turn out to be far more important than evolutionary considerations.
In any case, evolution in cholera virulence and TB antibiotic resistance involves only changes within existing species--just as we saw in the case of HIV. The TB we battle today is the same species as the TB found in Egyptian mummies.
We didn't need Darwin to teach us about minor changes within existing species; in the form of domestic breeding, such changes have been understood and used for centuries. True, Darwin realized that a similar selection process operates in the wild. But where is the evidence for his theory that this process explains the origin of new species--in fact, of every species?
If we were going to find evidence for Darwin's theory anywhere, we would expect to find it in bacteria. Many species of bacteria reproduce several times an hour, so scientists can study thousands of generations in a single year. Bacteria have been experimentally subjected to intense selection and potent mutation-causing agents for decades, yet no new species have emerged. As British bacteriologist Alan H. Linton wrote just recently: "Throughout 150 years of the science of bacteriology, there is no evidence that one species of bacteria has changed into another." But none of this information is shared with the viewers of the PBS Evolution series.See . Alan H. Linton is emeritus professor of bacteriology at the University of Bristol (U.K.). The quotation is from The Times Higher Education Supplement (April 20, 2001), 29.
We leave the Amherst College campus and go to the National Zoo in Washington, DC, as the narrator says: "Peaceful co-existence with disease organisms may seem like a revolutionary idea. But throughout evolution, other species have also reached a truce with these microscopic killers."
Geneticist Stephen J. O'Brien describes his study of feline immunodeficiency virus (FIV), which is associated with an immune-deficiency disease in domestic cats. He examined DNA from every species of cat--from cheetahs to ocelots, and lynxes to lions--and concluded that "virtually every species of cats on the planet had been exposed to and infected with a version of feline immunodeficiency virus." But no species of wild cats suffer from immune-deficiency disease. Apparently, they are immune to the effects of FIV.
Applying evolutionary thinking, O'Brien speculates that FIV first infected the cats' ancestors three to six million years ago. The narrator describes the supposed consequences: "It decimated the animals. But a lucky few were born with mutations that happened to make them immune to the virus. These survivors passed on their protective genes to most cat species alive today. Domestic cats are a young species, and a recent conquest for FIV. But wild cats have reached the end of a long phase of adapting to a once-deadly foe."
"Sadly," the narrator continues, "we have just begun such a phase with a close relative of FIV--the human immunodeficiency virus. But the example of the cats convinced O'Brien that some people must be endowed with genetic mutations that make them immune to HIV. He set out to find them." And O'Brien found a mutation that he concluded helps protect some people from HIV infection. Applying evolutionary thinking again, O'Brien speculates that this mutation may also have protected Europeans from the Black Death in the fourteenth century.
There are problems with the FIV story, however. First, if all modern members of the cat family inherited a mutation from their common ancestor that protects them from the effects of FIV infection, and domestic cats are the youngest members of the family, then why didn't they inherit the mutation, too? Perhaps the immunity of wild cats is not due to a mutation at all, and it is the environment of domestic cats that renders them susceptible to disease. But this possibility is not even mentioned.
Second, and more importantly, nothing in this story helps us to understand how FIV or HIV--much less cats or humans--evolved. As we have already seen, changes in an existing species are a far cry from the origin of a new species. Even if everything we have just been told about FIV and HIV were true, it would not provide evidence that "leopards and lichens, minnows and whales, flowering plants and flatworms, apes and human beings" evolved from a common ancestor through natural selection and random variation, as Darwin's theory implies.
Third, nothing in this story shows that an understanding of evolution is necessary to medical research. O'Brien's speculations about the evolutionary history of FIV have done nothing to cure domestic cats of their disease. And his finding that some people have a mutation that supposedly protects them from AIDS has done nothing for the victims of that disease. The producers of Evolution claim that evolution "touches our daily lives in extraordinary ways," especially when it comes to medicine. Yet this story shows nothing like that.
There is another force, we are told, that is just as important as competition in building up "the magnificent super-structure" of the world of living things, and that is "cooperation--what we call symbiosis, and particularly mutualistic symbiosis. That is intimate living-together of different kinds of organisms, in which there is a partnership which benefits both of the partners."
After being shown several examples of this, we are introduced to leaf-cutter ants in the Amazonian jungle. These ants are like gardeners--they harvest leaves that they chew into a pulp, then they use the pulp to grow a fungus that supplies them with sugar. This is mutualistic symbiosis: The fungus depends on the pulp provided by the ants, and the ants depend on the sugar produced by the fungus.
Remarkably, the ant's "gardens" are pest-free, unlike human gardens. It turns out that the many of the ant-gardeners are covered with a white, waxy coating of Streptomyces bacteria. Streptomyces--the source of medically useful antibiotics such as streptomycin--keeps in check an aggressive mold that would otherwise devastate the cultivated fungus.
"The ants have been using antibiotics to kill the mold in their gardens for some fifty million years," says the narrator, "so why hasn't the mold evolved antibiotic resistance?" The answer, we are told, is that the Streptomyces bacteria covering the ants is probably evolving along with the aggressive mold that it keeps in check. The result is supposedly "an evolutionary arms race that has continued for fifty million years"--though we are not shown any evidence for this at all.
So leaf-cutter ants provide us with an excellent example of mutualistic symbiosis, and may also provide us with another example of an evolutionary arms race. This is a fascinating story. But what does it have to do with Darwinian evolution? We have seen that several species can co-exist in a symbiotic relationship. But we have not seen evidence for how that relationship developed, much less for how the species originated in the first place.
We visit a German pediatrician who treats allergies and asthma--"disorders in which the immune system overreacts to harmless substances," explains the narrator. Research conducted by the pediatrician suggests that children who live in villages suffer more from such disorders than children who live on nearby farms. She finds that children who come into regular contact with livestock are less likely to develop allergies and asthma.
The pediatrician suspects that high levels of microorganisms in the stables help children to form healthier immune systems. "Microbes have been around us always," she concludes, "and probably we need to find the balance between eradicating the harmful effect of bacteria, and maybe also taking the beneficial components of this."
As the episode closes, we are told that it's a big mistake to separate ourselves too much from the rest of living things. After all, most species are our friends rather than our enemies. In fact they are essential to our existence, and we would do well to learn more about them. Surely, these are wise words. But do we really need to understand Darwinian evolution in order to appreciate them?
In fact, most of what we've heard in this episode would have made just as much sense if the word "evolution" hadn't been used at all. True, we can use the word to explain why newts make an excessive amount of poison; but we haven't thereby explained how newts acquired the ability to make the poison, much less how newts originated in the first place. Minor changes within species have been known for centuries. What we need to see is evidence that the same process can produce the big changes required by Darwin's theory, but that evidence has not been forthcoming.
Nor does this episode show that we need to understand evolution in order to practice good medicine. True, we can use the word to describe how TB becomes resistant to antibiotics; but it's still the same TB we find in Egyptian mummies, and a healthy lifestyle may still be the best defense against it. Cholera epidemics can be prevented without knowing anything at all about evolution, and studying FIV evolution has done nothing to help AIDS sufferers.
Clearly, the "evolutionary arms race" metaphor is not the only way--and may not even be the best way--to understand our relationship to bacteria. Although this episode started with ominous warnings of a microbial holocaust, it ends with the comforting assurance that most microbes are our friends. Darwinism seems to explain everything and its opposite equally well. But if competition and cooperation are equally compatible with evolution, what difference does Darwinism really make?
The decline in infectious diseases (including TB) from the seventeenth century to the nineteenth largely preceded the advent of modern medicine, and was due to general improvements in sanitation and nutrition. See Thomas McKeown, The Role of Medicine (Princeton: Princeton University Press, 1979).
The person who has probably come closer than anyone to producing new species of bacteria is Michigan State University biologist Richard E. Lenski. But Lenski has only been able to produce "an incipient genetic barrier between formerly identical lines"--a barrier which he admits is "much smaller than the barrier between such clearly distinct species as E. coli and Salmonella enterica." See Martin Vulic, Richard E. Lenski, and Miroslav Radman, "Mutation, recombination, and incipient speciation of bacteria in the laboratory," Proceedings of the National Academy of Sciences USA 96 (1999), 7348-7351.