11. Emerging diseases and the future

Pandemics and demographic collapse

Today our planet holds approximately 6 billion humans and 5 × 10³⁰ (5 million trillion trillion) bacteria. We are outnumbered by nearly 10²¹ (1 sextillion) to 1. At the moment, we are catching up. But will this trend last? The human population does not climb smoothly. Periods of growth are followed by population crashes. When will the next population implosion happen? How?

The earliest major population collapse for which we have reliable records occurred in the Roman Empire as a combined result of the unidentified pestilences of 165 A.D. and 251 A.D. The plague of Justinian, which began in 542, with secondary epidemics until 750, was another period of major population decline in Europe and the Middle East. Both population and prosperity increased from the mid-700s to the mid-1300s. In England, the population expanded roughly threefold from 1000 A.D. to 1348, to reach roughly four million. It then collapsed to less than half of this due to the Black Death and regained its 1348 level only in the early 1600s, some 250 years later. Europe, North Africa, the Middle East, and China suffered similar catastrophic die-offs during the same period. In the New World, these multiple die-offs combined into one spectacular population crash when the diseases of the Old World were imported into the Americas, beginning in 1492.

Since around 1600, despite the ravages of tuberculosis and other infections, the population of most parts of the world has steadily increased. Today the threat from infectious disease is growing. The industrial nations are shielded by wealth and technology from the infections that assault the poor nations. Yet despite the poverty, crowding, malnutrition, and lack of hygiene, the populations of the Third World nations continue to rise. Whether we are likely to succumb to some new plague in the near future and suffer another major population collapse is hotly debated.

The various types of emerging diseases

The widespread publicity given to AIDS, mad cow disease, and Ebolavirus has set a trend. Virtually every infection now clamors to be accredited as an emerging disease. Diphtheria is increasing in the former Soviet Union, and syphilis is increasing among American homosexuals. Are these emerging diseases? Not really. Localized lapses in social order or hygiene provide familiar diseases with the opportunity to briefly expand. However, the idea of emerging disease implies something truly novel that threatens a world grown smug in the belief that infectious disease has been conquered. Changes in one or more of four major areas can qualify a disease as novel.

Genuine emergence of a novel infection is rare. Many so-called emerging diseases have survived unnoticed for many years and only recently come to our attention as a result of changing conditions. Others are truly novel and have emerged by a combination of genetic changes and movements between host species, the most clear-cut case being AIDS.

Changes in knowledge

Many “novel” diseases have clearly been around for a while but were only identified recently. Previously unnoticed diseases include Legionnaire’s disease and Lyme disease. A hundred years ago, deaths from Legionnaire’s disease would have been attributed to tuberculosis. The decline in tuberculosis means that rare diseases affecting the lungs are more likely to be noticed. Similarly, the decline in yellow fever, due to vaccination, has revealed many less common tropical fevers that were once lumped together with yellow fever. Conditions such as diarrhea or hepatitis that have been known for a long time are caused by multiple infectious agents. Many of these have only recently been individually identified, including hepatitis viruses C to G.

Other diseases went unnoticed because they occurred only in out-of-the-way places or among low-status people. Frontiersmen and American Indians have undoubtedly suffered from sporadic cases of Lyme disease for centuries, but the disease was investigated only when it began to affect leisured landowners.

Changes in the agent of disease

Totally novel diseases such as AIDS and mad cow disease appear from time to time. These infectious agents are of recent origin, and there has never been a recorded outbreak before our own time. Mad cow disease, though bizarrely unique, causes few deaths. Its main effects have been economic.

As agents of a catastrophic die off, these two diseases share the same drawback: ineffective transmission. If AIDS were spread by insects or mad cow disease wafted through the air like measles, we would be in real trouble. Perhaps most diseases with efficient distribution mechanisms are already in circulation. Diseases still lurking in the shadows are probably obscure for a good reason—they can’t effectively transmit themselves to humans. Although novelty dominates the headlines, I believe that greater real danger comes from known diseases that transmit themselves efficiently. If measles or flu changed to become highly virulent, we might face a real possibility of a major die-off.

Old diseases can evolve to protect themselves against human counterattack. They might gain resistance to antibiotics or change their surface components to outwit the immune system. Influenza virus changes its surface properties for each new epidemic, and AIDS virus mutates so rapidly that multiple variants appear within a single patient.

Old diseases can evolve new means of attack. They might acquire novel virulence factors (such as with E. coli O157) or reshuffle their genes, creating virulent variants from time to time, as occurs with flu. Other diseases venture into new territory by changing the tissue invaded. A good example is the evolution of the spirochete that causes the skin disease yaws into syphilis, which specifically affects the genital regions.

Changes in the human population

Humans with defective immune systems provide easy opportunities for infection. The AIDS epidemic has created by far the largest number of immune-compromised victims. This, in turn, has allowed the spread of many novel opportunistic diseases. However, the use of drugs whose side effects harm the immune system and the increasing numbers of older people also contribute. Malnutrition also makes humans more susceptible to many infections. Denser human populations allow more virulent variants of a disease to spread, as discussed in Chapter 3, “Transmission, Overcrowding, and Virulence.” This is especially true of the growing cities of the Third World, where poor hygiene exacerbates the effect.

Genetic alteration of humans might protect against one problem but increase vulnerability to others. A single copy of the cystic fibrosis mutation protects against diseases such as typhoid and cholera, but if both copies of the gene are defective, the lungs become more susceptible to infection by a variety of bacteria.

Multiple genetic changes have occurred within historical times that make most Europeans relatively resistant to smallpox, measles, tuberculosis, and many other diseases. Because we do not know the identity of most of these mutations, we remain in the dark about any possible side effects.

Changes in contact between victims and germs

A variety of factors can greatly change the probability of an infectious microbe finding suitable victims. Natural disasters such as earthquakes, floods, hurricanes, and storms provide temporary opportunities for disease to spread. Generally, when the disaster is past, associated infections fade away, too. Changes in climate have more permanent long-term effects. In particular, higher temperatures allow insects to spread into new regions, carrying with them diseases such as malaria or yellow fever.

Old diseases can make a comeback due to a breakdown in public health caused by wars, revolutions, and political upheavals. Disruption of vaccination programs after the collapse of the Soviet Union resulted in an upsurge of diphtheria.

Opening up new land for settlement or clearing forest for agriculture brings people into contact with previously unknown diseases, such as Ebolavirus. More serious in practice are irrigation projects that create new bodies of standing water. These permit the spread of mosquitoes carrying malaria, yellow fever, and dengue fever. Deforestation also helps the spread of disease-carrying insects. Even technological advances can backfire. More efficient food technology relies on processing larger volumes. This allows localized bacterial contamination to spread more widely, resulting in the massive meat recalls of recent years. Air-conditioning opened new opportunities for Legionnaire’s disease.

The supposed re-emergence of tuberculosis

Tuberculosis is not an emerging disease. Indeed, it scarcely merits classification as re-emerging. We include it here because of the publicity it receives. Tuberculosis spread through the cities of Europe during the industrial revolution. By the mid-twentieth century, when the first effective antibiotics appeared, the tuberculosis epidemic was already largely burned out in Europe. A colossal death toll over the past few hundred years had killed off most people who were sensitive. Antibiotic therapy merely finished off the tail end of the epidemic in the industrial nations. Today only an estimated 10% of the white population is susceptible to tuberculosis.

Thus, tuberculosis is not re-emerging; the epidemic that started in seventeenth-century Europe did not end; it merely vanished from the advanced nations. Today it is moving inexorably across the world and is still expanding among populations who have not been previously exposed. Today tuberculosis accounts for around three million deaths annually, most in the Third World. Data from Chicago in the 1920s showed that tuberculosis was six times worse among blacks than whites. Remember that some 75% of American whites are descendents of Europeans who entered the United States between the American Civil War and World War I. The whites thus came from a pre-exposed population, whereas the blacks did not. After World War II, tuberculosis found fresh victims in the crowded slums of expanding Third World cities. Susceptibility is greatly increased by the protein-poor diets often found in poor countries where little meat is eaten.

Diseases are constantly emerging

Quite frequently, die-offs occur among wild animals. Most of these are not noticed. Most that are noticed, usually by local farmers or hunters, are not recorded, and most of those recorded are never explained. For example, in 1994, bald eagles in Arkansas came down with a mystery disease and many died. Some die-offs are probably the result of new diseases. Perhaps an existing infection mutates to a more lethal form, or perhaps a disease crosses over from another animal. This new disease is so virulent that it wipes out most of the population and then, with no more victims to infect, goes extinct itself. This undoubtedly happened many times to early human settlements in the days before the human population was dense enough to keep new diseases in circulation. For every disease that emerges successfully, many must make abortive attempts. Even if a disease ultimately emerges into new prominence or jumps into a new host, it might make many tries before it succeeds. Let’s look at some recent candidates for fame and glory.

Lassa fever, Hantavirus, and Ebolavirus are three of the emerging viruses to hit the headlines recently. All three are harbored by small animals with large populations. Lassa and Hanta are carried by rodents, and Ebola most likely by bats. As with the Asian marmots that harbor the Black Death, the natural hosts for Lassa, Hanta, and Ebola suffer relatively mild disease. Man is very susceptible, and the death rates during the reported outbreaks are in the same range as for bubonic plague.

These three, together with Junin, Machupo, Marburg, O’nyong Nyong, and several other novel viruses, were mostly identified more than 25 years ago. However, it wasn’t so much the viruses that emerged—it was the emergence of cell culture techniques for viruses in the 1950s that allowed the identification of exotic viruses in remote parts of the world. Before this, viruses had to be grown in fertilized chicken eggs, an extremely laborious and clumsy procedure that was not always successful. Few novel viruses of major significance have appeared in the last 25 years, although there have been new outbreaks of those listed earlier in new places (for example, Hantavirus in the United States in 1993). Most recently, Lujo virus, a relative of Lassa fever, emerged in Southern Africa in late 2008.

Despite the hype, these novel viruses have had little global impact. About 50 million people die each year on Earth. Of these, about 16 million succumb to infections, with AIDS, malaria, and TB accounting for roughly 3 million each. Deaths per year from the newly emerging viruses are numbered in the hundreds. For example, between its emergence in 1976 and the outbreak in 1996, there were approximately 1,000 official cases of Ebolavirus infection, with an overall death rate of 80%. Undoubtedly several thousand more victims died unreported in isolated villages; nevertheless, in global terms, these numbers are negligible.

How dangerous are novel viruses?

Should we be alarmed about these novel viruses? Worried, yes—panicked, no. Consider Lassa fever, discovered in 1969 in Lassa, Nigeria. Like Ebolavirus, Lassa fever virus has undoubtedly been around for much longer. Sporadic outbreaks in isolated areas must have occurred from time to time without drawing attention. Earlier outbreaks were probably misdiagnosed as severe cases of malaria or yellow fever. In its natural hosts, small rodents, Lassa fever often causes mild long-term infections. The virus emerges in the urine and can be breathed in by humans under dry, dusty conditions. In humans, Lassa fever is virulent and short-lived—as is the patient, in the majority of cases. Human survivors also excrete virus particles in their urine for up to a month after infection.

The story is similar for Ebolavirus, named after the Ebola River in Zaire. Bats can be infected with Ebolavirus, whereas many other animals, including rodents, cannot. As expected for the natural host, bats allow the virus to replicate but do not fall severely ill. Outbreaks of Ebolavirus in the Sudan were traced to a cotton factory whose rafters were home to thousands of bats. An outbreak in Uganda was traced to the bat-infested Kitum Cave. Despite this, no bats trapped near these human outbreaks actually carried Ebolavirus. So although bats are the chief suspects, the case remains unproven.

However, despite being highly lethal, Ebolavirus is not especially infective until the final stages, when the blood is full of virus and the patient bleeds from all the bodily orifices. Obviously, at this stage, the patient is immobile. Lassa fever and Hantavirus are much the same. Exposure to blood or tissue samples has infected health workers, but casual contact rarely transfers the virus. During the 1995 Ebolavirus outbreak in Zaire, of 28 relatives who stayed in the hospital to help nurse the sick (often sharing the same room or even the same beds), 17 got Ebola. Of 78 who just visited, none fell ill. Similarly, in 1990, an American returning to Chicago from Nigeria was hospitalized and died of Lassa fever. No one else was infected, although no special precautions were taken because the infection was identified only after he died.

Lassa, Ebola, and Hantavirus are not as evil as originally believed. Mild versions of all three viruses are surprisingly widespread. Investigations during the 1980s in the rain forests of Cameroon found that 15% of the pygmies had antibodies to Ebolavirus in their blood, implying that they had been infected. No massive death toll was noted. Similarly, screening of large numbers of Africans from Nigeria and nearby nations found many who had signs of having been infected with Lassa fever but remembered only mild illnesses.

Another factor contributing to the panic of the early Lassa and Ebola outbreaks was their artificial spread by hospitals. Thus, many victims of the 1976 Ebola outbreak in Zaire were infected while in the hospital. Viruses from patients infected with Ebola were transferred to others by reusing hypodermic needles that were improperly sterilized. Less than 10% of those who got Ebola injected directly into their bloodstream survived. Of those who caught Ebola from another person, between 40% and 50% survived. Similar scenarios are seen with Lassa fever. Thus, these diseases are less dangerous when spread by natural means.

Transmission of emerging viruses

It is sometimes suggested that highly virulent diseases cannot spread very far unless they are carried by vectors such as fleas or mosquitoes. Granted, milder variants of a disease tend to spread further. Nonetheless, if Ebolavirus or Lassa fever had started out capable of infecting humans efficiently, the diseases could have spread much further. We know this from what happened when smallpox and measles first reached the American continent.

So why have the outbreaks of Ebolavirus and Lassa fever burned out so rapidly? For a person-to-person disease, two factors affect transmission. First, how many other people does the infected victim contact? This depends on how long he survives and how far he can move. Clearly, this factor reduces the spread of more virulent diseases. Second, how well does the virus jump from one person to another upon contact? This is a property of the virus itself and varies greatly. As noted earlier, although both are highly virulent, neither Ebolavirus nor Lassa fever is especially infectious to humans.

Moreover, for every person exposed to deadly viruses such as Ebola or Lassa, a thousand are exposed to other unknown viruses from rats, bats, monkeys, zebra, elephants, and other animals. Most of these unknown viruses will never make the headlines because the body’s immune system zaps them as soon as they set foot inside. In summary, humans could be highly susceptible to viruses they have never been exposed to, but most viruses that have not adapted to humans will be extremely susceptible to immune system destruction. Occasional strange viruses do escape the immune system and cause a great deal of damage. But because they are not adapted to humans, these chance invaders rarely have an effective way to move from person to person.

Efficient transmission and genuine threats

For a genuinely new human plague to emerge, the agent of disease must evolve (or already possess) some way to spread efficiently. Probably the best way is to spread through the air, directly from person to person, as with flu or measles. Despite killing only a tiny fraction of their victims, measles and flu both kill far more people than all the novel emerging viruses combined. This is because they infect vast numbers of victims.

Influenza virus changes both by rapid mutation and by exchanging genes between flu strains from people, pigs, and poultry. Most new flu strains have only minor alterations, but now and then, major changes occur that produce variants with increased virulence. In the twentieth century, this occurred in 1918 and, less impressively, in 1933, 1957, 1968, and 1977. The virulent flu of 1918 had an overall mortality of only 2% to 3%, but because it infected most of the human population, the total death toll was huge: 30 million to 100 million, according to different estimates.

In 1920, the world population was a little less than 1.5 billion, and in the year 2000, it was a trifle more than 6 billion. Thus, today’s population is about four times as dense as during the Spanish flu of 1918. As we know, the denser the host population, the more this favors the spread of virulent infections. Influenza and assorted respiratory infections, ranging in mildness down to the common cold, are caused by hundreds of different viruses that constantly mutate. These viruses are well adapted to transmission among humans. Sooner or later, one of these, not necessarily flu itself, will likely throw up a virulent variant. As Pasteur might have put it, chance favors the prepared microbe.

The history and future of influenza

The first definite flu epidemics were recorded in Europe in 1510, 1557, and 1580. The mortality rates of up to 20% were vastly more lethal than any recent epidemic except the 1918 Spanish flu. Over the centuries, either flu has been getting milder or humans have been getting more resistant. The flu epidemics of the 1500s killed a substantial proportion of the population and must have weeded out many sensitive members of the population.

Flu is shared among people, pigs, and poultry. Most new variants of flu originate in China, where large numbers of ducks and pigs live close to humans. The Asian flu of 1957 and the Hong Kong flu of 1968 are typical examples. Direct chicken-to-human transfer of influenza is very rare. Generally, flu goes via ducks and pigs. However, in Hong Kong in 1997, a handful of people died from avian flu that was apparently transferred directly from chickens. Luckily, this flu virus did not transfer between humans. It’s unlikely that future outbreaks of flu will result from direct fowl-to-human transfer of a virus that is both lethal and capable of spreading from person to person, but this is still a nasty possibility.

The great influenza epidemic of 1918–1919

The outbreak started in the United States and spread to France in April 1918 with arriving American troops. From there, it spread to Spain, where it first caused public alarm (hence the name Spanish flu). It behaved strangely, in that half the victims killed were in the 20–40 age group. The greatest death toll, perhaps 20 million, occurred in India. In a few small communities where everyone fell ill simultaneously, leaving no one to attend the sick, nearly 50% died. Among people of European descent, about 5 per 1,000 died. The typical death toll among nonwhites was five to ten times higher. In South Africa, many baboons died alongside their human cousins; we cannot be sure, but they probably caught Spanish flu.

It is often suggested that the Spanish flu was somehow caused by the crowded trenches and troopships and was spread by the troop movements of World War I. However, Europe was far more disrupted by World War II, in which both troop and refugee movements occurred on a larger scale than in the earlier war. The crowded air-raid shelters of World War II were ideal breeding grounds for a respiratory disease such as flu. Yet from the beginning of World War II, no major influenza outbreak happened until 1949. A related question is why no lethal flu virus has yet emerged from the massively overcrowded postwar cities of the Third World. These questions suggest that Spanish flu was just a chance mutation to a rare virulent form that coincided with the end of World War I. Troop movements probably spread it faster than normal, but if the world had been at peace, the new variant would surely have spread by trade and civilian travel.

As I was writing this chapter, in April 2009, a novel version of swine flu has emerged from Mexico. Despite massive publicity, it has had little real effect, except on the Mexican tourist industry. Although it is aberrant in some ways, so far it is relatively mild. The World Health Organization has declared an official pandemic, based on the worldwide spread of the virus. However, most infected people have recovered without any need for medical care. Mutation to a more virulent form is always possible with flu, but as of now, it seems unlikely that this outbreak will bring about a major disaster.

Disease and the changing climate

The temperature of our planet has fluctuated considerably in the past. We have already mentioned the period of cooling in early medieval times that might have ultimately triggered the Black Death. Ice cores drilled in Greenland indicate that temperatures reached the most recent minimum (“mini Ice Age”) about a hundred years ago, when the Thames River that runs through London froze over in winter. Since then, the temperature has been slowly rising. Global warming will have a major impact on infectious disease—mostly for the worse, because disease tends to thrive in hotter moister climates.

One major effect will be to extend the range of mosquitoes and the diseases they carry, especially malaria, yellow fever, and dengue fever. Temperate zones that have been largely malaria-free will likely suffer major intrusions. Deforestation and the creation of large areas of stagnant water by irrigation projects have added to the effects of global warming. Other insect pests and tropical diseases will follow suit.

Global warming coupled with changing rainfall patterns also affects diseases spread by water, including cholera. Outbreaks of disease due to contaminated water in the United States mostly come when rainfall is unusually high. Cholera outbreaks are favored by warmer ocean temperatures and higher rainfall. Extra rainfall increases nutrient run-off from the land into the seas. This drives blooms of marine algae and plankton. This, in turn, allows the cholera bacteria that live inside plankton in coastal waters to proliferate. Cholera in coastal waters is presently moving northward from Peru, where the last major outbreaks occurred.

Floods, which are likely to increase in frequency due to a warmer, wetter climate, tend to aid the spread of disease, especially in poor countries, where hygiene is already dubious. Rodents driven from their homes during floods are apt to spread disease. One example is the outbreak of bubonic plague in Surat, India, in 1994. An earthquake followed by a flood left thousands homeless. Emergency supplies were provided for the human victims. However, hordes of rats were also flooded out and spread plague as they scavenged for food and shelter among the refugees.

Technology-borne diseases

Advances in technology both shut and open doorways for disease. Sewers remove human waste and decrease typhoid and dysentery. Sewers provide highways, or rather subways, for rats to scurry through carrying plague. Virtually every major change in technology has altered the risks of catching some infection. Today is no different. Irrigation projects can cause increased spread of malaria and bilharzia in Africa and Asia.

Changes in food processing have increased food poisoning in the United States. Processing food in ever-larger batches is economically efficient but provides better opportunities for bacteria to spread. Hamburger contaminated with E. coli and peanut butter with Salmonella have become staple news items in the last few years. Although not novel themselves, many bacteria responsible for food poisoning do carry newly acquired virulence factors. Mad cow disease is one of the few truly new emerging diseases. Its spread was also triggered by changes in animal husbandry.

In contrast, Legionnaire’s disease is not new, but its emergence from obscurity did rely on new technology. The bacteria can accumulate in water tanks or cooling towers and spread when humans breathe in the aerosols generated by showers, ventilators, and air-conditioners. Legionnaire’s disease was first identified following an outbreak at the American Legion convention in Philadelphia in 1976. Consequently, the bacterium causing it was named Legionella, in honor of the American Legion. Since then, sporadic outbreaks of Legionella have occurred at hotels and other institutions. Despite the journalistic hype that greeted its emergence on the world stage, Legionella is only a minor irritation in global terms. A few hundred cases a year, with a fatality rate of about 10%, occur in the industrial nations. This will probably continue for the foreseeable future.

Emergence of antibiotic resistance

In addition to the threat from truly novel infectious agents, well-established infections can gain new abilities. Since antibiotics were introduced in the 1930s, many bacteria have evolved resistance. Similar problems have been seen with antiviral drugs and with the insecticides used to control insects that carry disease. Before getting too panicky, we should remind ourselves that the great decline in infectious disease happened before antibiotics were discovered. Sanitation and vaccination eliminated most of the dangerous infections from industrial nations.

Antibiotic resistance can appear as a result of a novel mutation or can be transferred from one bacterium to another. Even in the early days of antibiotic use, sporadic cases of resistance arose. Most of these were due to mutations in the bacteria that were being treated, and relatively few of these resistant strains spread. In the absence of the antibiotic, most resistance mutations are harmful to the bacteria. For example, spontaneous mutants of bacteria resistant to streptomycin have defects in protein synthesis. Mutants resistant to kanamycin or neomycin cannot respire properly. The situation is reminiscent of human mutations that give resistance to malaria but cause sickle-cell anemia or give resistance to typhoid but cause cystic fibrosis. In the absence of the threat (antibiotics for bacteria, malaria for people), the resistant mutants fade away.

The bigger threat comes from transmissible antibiotic resistance. Plasmids are circular segments of extra genetic information that many bacteria carry. Some plasmids move from one bacterial strain to another and carry genes that are “optional extras”—handy under some conditions, but useless or a burden under others. Plasmids can confer the ability to grow on rare and unusual nutrients. They can also carry genes that protect bacteria against antibiotics or toxic metals, both due to human activity. The antibiotic resistance genes carried on plasmids rarely interfere with normal bacterial growth. Instead of risking alterations in vital bacterial genes, plasmids bring in extra genes from outside. These often destroy the antibiotic with no detrimental side effects on the bacteria. Consequently, even in the absence of antibiotics, the antibiotic-resistance plasmids are lost only very slowly. A single plasmid can carry resistance to several antibiotics. Alternatively, a single bacterium can contain several plasmids, each conferring resistance to a single antibiotic. Either way, the result is multiple-antibiotic resistance that can be passed from bacterium to bacterium.

The emergence of antibiotic resistance was inevitable. When living creatures are killed in large numbers, a few resistant individuals usually survive to breed. Nonetheless, the rapid spread of antibiotic resistance has been helped by human greed and stupidity. Farmers often include antibiotics in animal feed. This keeps infection down and supposedly results in more meat per dollar. It also encourages the spread of resistance plasmids that can later transfer to bacteria that infect humans. Many European nations were smart enough to realize that the costs of extra hospital care vastly outweighed the few pennies saved by cheaper bacon and have greatly restricted this practice.

Today agriculture consumes about two-thirds of antibiotics, and only about one-third is used medically. Third World nations are becoming major contributors to this problem, as the increasing demand for meat has led to widespread abuse of antibiotics. While the industrial nations start to clean up their act, many poorer nations are using more antibiotics to increase meat and chicken yields. The only factor in choosing which antibiotics to put in animal feed in poorer countries is the price. This undermines the growing tendency in advanced nations to reserve certain antibiotics for human use.

Another problem is overprescription. Although antibiotics kill only bacteria, doctors often prescribe them for virus infections, such as colds and flu. This abuse is vastly more common in the United States. Partly, Americans want to get something to “cure” them. Explaining that antibiotics don’t cure viruses to people with the lowest education standard of any industrial nation is just too much effort. Doctors, in turn, are frightened that if they are honest, they might lose their patients to another, more obliging physician. (In reality, a recent survey by the CDC showed that few patients actually wander from doctor to doctor.) Doctors are also frightened of being sued for failing to provide “appropriate treatment.” In England, children with ear or throat infections are given antibiotics only in rare cases when the infection continues. In the United States, “Shoot first, ask questions later” is the motto not just of yesterday’s cowboy, but also of today’s yuppie parent.

One way to combat resistance is to replace old antibiotics with newly invented ones. Soon after they were first discovered, there was a big rush to discover new antibiotics or modify old ones chemically, yielding new variants. When most known bacterial diseases had cures, complacency set in. Recently, drug resistance has hit the headlines and research has picked up again. Although some new antibiotics are now in the pipeline, it takes several years to get a new drug from laboratory to hospital. As new antibiotics are deployed, resistance will inevitably appear. We can look forward to a permanent cold war between bacteria and pharmaceutical companies.

Where do the resistance genes on plasmids come from? They are gifts from Mother Nature, like most antibiotics. Long before humans isolated penicillin from the mold Penicillium, or streptomycin from the bacterium Streptomyces, these antibiotics were deployed to wage biological warfare in the soil. Bacteria and molds have been slugging it out for eons before humans joined in the fray. Not only did microorganisms develop antibiotics to kill each other, but they developed resistance mechanisms to counter each other’s attacks. Some bacterial cultures stored before penicillin was discovered already had resistance genes. Thus, resistance to most antibiotics probably predates their use by humans. Increased use has led to the spread of these resistance genes.

Disease and the food supply

We have focused on human disease, but remember that livestock and crop plants suffer from infections, too. Modern farmers tend to rely heavily on a few main crops, with little crop rotation. Large areas of a single crop provide the same opportunities for plant diseases that overcrowded cities provide for human infections. The warmer, wetter weather that is becoming more prevalent favors fungal infections that attack plants. For example, wheat scab outbreaks in the United States and Canada caused massive losses in the 1990s.

Decreased surpluses in the major grain exporters undermine the safety net for overpopulated third world nations. If major drought in tropical areas such as Africa or India coincides with major crop losses in the grain exporters, the result could be widespread famine. In 2006–2007, world grain reserves fell to 57 days of consumption, the lowest since 1972.

Perhaps the most serious current threat to our food supply is the wheat rust fungus (Puccinia graminis). A new and highly virulent strain emerged from Uganda in 1999 and was, therefore, named Ug99. It is presently in Africa and parts of Asia. Because the spores are airborne, this fungus will inevitably spread worldwide. Breeding resistant wheat varieties is in progress but takes several years.

Overpopulation and microbial evolution

Overpopulation does not merely threaten starvation; it sets the scene for the evolution of new infectious diseases. The more people there are—and the more crowded, unhygienic, and malnourished they are—the greater the opportunity for some new and virulent plague to emerge. So far, we have kept ahead.

A related issue is the growing number of humans with deficient immune systems. Some people are immunocompromised due to drugs used to suppress rejection of organ transplants or drugs used in cancer therapy, but the vast majority are AIDS victims who are infested with a growing variety of opportunistic diseases. Some of these diseases rarely infect healthy people, but others, such as tuberculosis, sometimes infect the healthy. AIDS patients have become evolutionary staging areas where previously harmless microorganisms can adapt to growth in humans without being promptly eradicated by the immune system. As drugs keep AIDS patients alive longer, opportunistic infections get more time to grow and evolve. Long-term antibiotic treatment provides ideal conditions for antibiotic resistance to arise and perhaps spread to other bacteria that are dangerous to people with healthy immune systems.

Predicting the future

“Clearly, the future is still to come.”
—Peter Brooke, member of U.K. Parliament, 1986

Clever prophets take care to make their pronouncements ambiguous. That way, they can claim to be right about whatever happens. Moreover, it doesn’t take much insight to realize that wars, earthquakes, famine, and pestilence will make continuing appearances on the world stage.

In his futuristic work The Shape of Things to Come, published in 1933, H. G. Wells relies on a novel plague to eliminate half the population of Earth in 1955–1956 and usher in a new era. Although this epidemic was largely modeled on the Black Death, Wells had his “maculated fever” waft around the world on the wind instead of spread by fleas. His fictitious disease emerged from captive baboons in the London Zoological Gardens. The Shape of Things to Come was written as a prediction of the future in an age when most scientists foresaw only the eventual eradication of infectious disease, not its resurgence.

So what should we predict? First, let’s consider the global situation. The British Empire was the last great civilization. Improved hygiene, originating from the industrialized West, led to worldwide decreased infant mortality. That, in turn, created a population boom that undermined the profitability of the European colonial empires. Despite poor hygiene and rampant disease relative to the industrial nations, the birth rate still outstrips infant mortality in Third World countries. The ongoing population explosion is the single most important biological trend in today’s world.

Denser populations, coupled with poverty, are promoting the spread of disease. Although tuberculosis is in the lead right now, most of those infected do not fall ill. As the remaining sensitive humans are weeded out, the incidence of TB in the Third World will begin to decline naturally, just as it did in Europe a century ago.

In the advanced nations, AIDS will affect homosexuals and intravenous drug users but have marginal impact on the mainstream. Its major effect, especially in the United States, will be to increase the cost of health care in the inner cities. This will help enlarge the growing gap between rich and poor. In Africa and, to a lesser extent, other third world regions, AIDS will thin out the promiscuous and malnourished, and favor the spread of religious puritanism, particularly, Islamic sects.

Still more serious, in my opinion, are malaria and other insect-borne infections that are spreading in the tropics. Rising world temperatures promote the spread of insects that transmit many tropical or subtropical diseases. Human construction and irrigation projects are helping, as is the steady increase in insecticide resistance among the insect carriers. An ugly long-term threat is the possible adaptation of tropical viruses to be carried by insects that survive in colder climates.

Future emerging diseases

The growing Third World cities are the true danger zones for emerging disease. The threat is not so much that Ebola or Lassa might break loose in a crowded slum. More dangerous is the prospect that some disease that already has the capacity to spread effectively might increase in virulence while circulating among the tightly packed masses. A rogue variant of flu or measles that killed a higher proportion of its victims could easily sweep through a crowded Third World city. The denser such populations grow, the greater is the likelihood of such a mutant emerging and spreading.

Such a virus could spread across the world by air travel. As urban decay continues, the cities of industrial nations are gradually becoming more susceptible to such infection. One paradoxical effect of advancing technology is on air pollution. Fumes from automobiles and oil refineries kill most airborne microbes. Clean, pure air allows them to live. Reducing air pollution makes the transmission of airborne infections much easier. Centralized air-conditioning recirculates air, along with any germs it carries, among all the rooms within a building—or an airport complex.

Gloom and doom or a happy ending?

“This is the way the world ends
Not with a bang but a whimper.”
—T. S. Eliot

Until recently, most essays on infectious disease ended on a triumphant note. Human technology has taken care of the problem. Eat, drink, and be merry (at least, until you die of cancer or heart disease)! More recently, the emergence of novel infections, coupled with the problem of increasing antibiotic resistance, has heralded a move to gloom and doom. Perhaps not the next outbreak, nor even the one after that, but soon a plague will emerge that we cannot control. Civilization will collapse, and even if we survive, we will revert to savagery.

Gloom-and-doomers generally opt for a single highly virulent plague that creates unmitigated disaster. However, previous plagues rarely destroyed society as a whole. Instead, they transformed it. Even the medieval Black Death is a case in point. It fits rather well with Nietzsche’s maxim: “If it doesn’t kill [all of] you, it will make you [society] stronger.” Western society emerged improved and less restrictive.

Nonetheless, the Black Death was a terrible disaster, and we certainly do not wish to suffer a parallel experience in the mere hope of future improvement. Thankfully, although providing sufficient resources rapidly is a major problem, the advanced nations have the capacity to keep most foreseeable individual epidemics under reasonable control.

However, as global crowding and travel continue to increase, there will be steadily more novel infections. One can envisage an increasing cumulative disease burden, as opposed to a single devastating plague. In particular, we are swimming in a sea of viruses that constantly mutate. As our populations grow ever denser, we are favoring the emergence of variants of infectious agents with increased virulence.

At the same time, modern technology is spreading from the West to the rest of the world, especially Asia, and is also constantly improving. Essentially, we have become embroiled in a high-tech arms race with the rapidly mutating viruses and, to a lesser extent, with the bacteria, which change more slowly. Although we have suffered some recent setbacks, we are still winning. In most regions of the world, life expectancy and standards of living are increasing, albeit more slowly than in the twentieth century.

The two most populous nations, China and India, both have rapidly developing biotech industries. Indeed, artemisinin, the drug now most favored for treating malaria in the Third World, came from China. Although drug discovery, especially of novel antibiotics, has slowed in the West, I suspect that the emerging high-tech nations will pick up the slack rather soon.

Novel infections will continue to emerge and test our medical technology and health care systems. If we can plot a common-sense course between getting too smug and over-reacting to every minor outbreak, I think our chances are pretty good.