A Short History of Nearly Everything: Special Illustrated Edition

by Bill Bryson

  Staphylothermus marinus, a heat-loving micro-organism of a type known as an extremophile, shown here enlarged 100,000 times. S. marinus can tolerate temperatures of up to 135°C. It is found on hydrothermal vents deep in the ocean. (credit 20.7)

  Genes, however, allowed Woese to approach micro-organisms from another angle. As he worked, Woese realized that there were more fundamental divisions in the microbial world than anyone suspected. A lot of little organisms that looked like bacteria and behaved like bacteria were actually something else altogether—something that had branched off from bacteria a long time ago. Woese called these organisms archaebacteria, later shortened to archaea.

  It has to be said that the attributes that distinguish archaea from bacteria are not the sort that would quicken the pulse of any but a biologist. They are mostly differences in their lipids and an absence of something called peptidoglycan. But in practice they make a world of difference. Archaea are more different from bacteria than you and I are from a crab or spider. Singlehandedly, Woese had discovered an unsuspected division of life, so fundamental that it stood above the level of kingdom at the apogee of the Universal Tree of Life, as it is rather reverentially known.

  In 1976 he startled the world—or at least the little bit of it that was paying attention—by redrawing the Tree of Life to incorporate not five main divisions, but twenty-three. These he grouped under three new principal categories—Bacteria, Archaea and Eukarya (sometimes spelled Eucarya)—which he called domains. The new arrangement (which has been subject to various modifications since) was as follows:

  Bacteria: cyanobacteria, purple bacteria, gram-positive bacteria, green non-sulphur bacteria, flavobacteria and thermotogales

  Archaea: halophilic archaeans, methanosarcina, methanobacterium, methanoncoccus, thermoceler, thermoproteus and pyrodictium

  Eukarya: diplomads, microsporidia, trichomonads, flagellates, entameba, slime moulds, ciliates, plants, fungi and animals

  A modified version of the tree of life derived from the findings of Carl Woese, giving predominance to unicellular organisms. (credit 20.8)

  Woese’s new divisions did not take the biological world by storm. Some dismissed his system as much too heavily weighted towards the microbial. Many just ignored it. Woese, according to Frances Ashcroft, “felt bitterly disappointed.” But slowly his new scheme began to catch on among microbiologists. Botanists and zoologists were much slower to appreciate its virtues. It’s not hard to see why. In Woese’s model, the worlds of botany and zoology are relegated to a few twigs on the outermost branch of the Eukaryan limb. Everything else belongs to unicellular beings.

  “These folks were brought up to classify in terms of gross morphological similarities and differences,” Woese told an interviewer in 1996. “The idea of doing so in terms of molecular sequence is a bit hard for many of them to swallow.” In short, if they couldn’t see a difference with their own eyes, they didn’t like it. And so they persisted with the more conventional five-kingdom division—an arrangement that Woese called “not very useful” in his milder moments and “positively misleading” much of the rest of the time. “Biology, like physics before it,” Woese wrote, “has moved to a level where the objects of interest and their interactions often cannot be perceived through direct observation.”

  In 1998 the great and ancient Harvard zoologist Ernst Mayr (who then was in his ninety-fourth year) stirred the pot further by declaring that there should be just two prime divisions of life—“empires” he called them. In a paper published in the Proceedings of the National Academy of Sciences, Mayr said that Woese’s findings were interesting but ultimately misguided, noting that “Woese was not trained as a biologist and quite naturally does not have an extensive familiarity with the principles of classification,” which is perhaps as close as one distinguished scientist can come to saying of another that he doesn’t know what he is talking about.

  The specifics of Mayr’s criticisms are highly technical—they involve issues of meiotic sexuality, Hennigian cladification and controversial interpretations of the genome of Methanobacterium thermoautrophicum, among rather a lot else—but essentially he argued that Woese’s arrangement unbalanced the Tree of Life. The bacterial realm, Mayr noted, consists of no more than a few thousand species while the archaean has a mere 175 named specimens, with perhaps a few thousand more to be found—“but hardly more than that.” By contrast, the eukaryotic realm—that is, the complicated organisms with nucleated cells, like us—numbers already in the millions of species. For the sake of “the principle of balance,” Mayr argued for combining the simple bacterial organisms in a single category, Prokaryota, while placing the more complex and “highly evolved” remainder in the empire Eukaryota, which would stand alongside as an equal. Put another way, he argued for keeping things much as they were before. This division between simple cells and complex cells “is where the great break is in the living world.”

  The late Ernst Mayr of Harvard. Mayr was extremely critical of Woese’s rearrangement of the tree of life, claiming that it lacked balance. (credit 20.9)

  If Woese’s new arrangement teaches us anything it is that life really is various and that most of that variety is small, unicellular and unfamiliar. It is a natural human impulse to think of evolution as a long chain of improvements, of a never-ending advance towards largeness and complexity—in a word, towards us. We flatter ourselves. Most of the real diversity in evolution has been small-scale. We large things are just flukes—an interesting side branch. Of the twenty-three main divisions of life, only three—plants, animals and fungi—are large enough to be seen by the human eye, and even they contain species that are microscopic. Indeed, according to Woese, if you totalled up all the biomass of the planet—every living thing, plants included—microbes would account for at least 80 per cent of all there is, perhaps more. The world belongs to the very small—and it has done for a very long time.

  A 1928 public health information poster issued by the city council in Brisbane, Australia, following a dengue fever outbreak the previous year. The poster urged citizens to clear away sources of standing water where dangerous mosquitoes bred. (credit 20.10)

  So why, you are bound to ask at some point in your life, do microbes so often want to hurt us? What possible satisfaction could there be to a microbe in having us grow feverish or chilled, or disfigured with sores, or above all deceased? A dead host, after all, is hardly going to provide long-term hospitality.

  To begin with, it is worth remembering that most micro-organisms are neutral or even beneficial to human well-being. The most rampantly infectious organism on Earth, a bacterium called Wolbachia, doesn’t hurt humans at all—or, come to that, any other vertebrates—but if you are a shrimp or worm or fruit fly, it can make you wish you had never been born. Altogether, only about one microbe in a thousand is a pathogen for humans, according to the National Geographic—though, knowing what some of them can do, we could be forgiven for thinking that that is quite enough. Even if most of them are benign, microbes are still the number three killer in the Western world—and even many that don’t kill us make us deeply rue their existence.

  Making a host unwell has certain benefits for the microbe. The symptoms of an illness often help to spread the disease. Vomiting, sneezing and diarrhoea are excellent methods of getting out of one host and into position for boarding another. The most effective strategy of all is to enlist the help of a mobile third party. Infectious organisms love mosquitoes because the mosquito’s sting delivers them directly into a bloodstream where they can get straight to work before the victim’s defence mechanisms can figure out what’s hit them. This is why so many grade A diseases—malaria, yellow fever, dengue fever, encephalitis and a hundred or so other less celebrated but often rapacious maladies—begin with a mosquito bite. It is a fortunate fluke for us that HIV, the AIDS agent, isn’t among them—at least not yet. Any HIV the mosquito sucks up on its travels is dissolved by the mosquito’s own metabolism. When the day comes that t
he virus mutates its way around this, we may be in real trouble.

  It is a mistake, however, to consider the matter too carefully from the position of logic because micro-organisms clearly are not calculating entities. They don’t care what they do to you any more than you care what distress you cause when you slaughter them by the millions with a soapy shower or a swipe of deodorant. The only time your continuing well-being is of consequence to a pathogen is when it kills you too well. If they eliminate you before they can move on, then they may well die out themselves. History, Jared Diamond notes, is full of diseases that “once caused terrifying epidemics and then disappeared as mysteriously as they had come.” He cites the robust but mercifully transient English sweating sickness, which raged from 1485 to 1552, killing tens of thousands as it went, before burning itself out. Too much efficiency is not a good thing for any infectious organism.

  A sixteenth-century German medical text outlining the symptoms and treatment of the mysterious but mercifully shortlived English sweating sickness. (credit 20.11)

  A great deal of sickness arises not because of what the organism has done to you but because of what your body is trying to do to the organism. In its quest to rid the body of pathogens, the immune system sometimes destroys cells or damages critical tissues, so often when you are unwell what you are feeling is not the pathogens but your own immune responses. Anyway, getting sick is a sensible response to infection. Sick people retire to their beds and thus are less of a threat to the wider community.

  Because there are so many things out there with the potential to hurt you, your body holds lots of different varieties of defensive white blood cells—some ten million types in all, each designed to identify and destroy a particular sort of invader. It would be impossibly inefficient to maintain ten million separate standing armies, so each variety of white blood cell keeps only a few scouts on active duty. When an infectious agent—what’s known as an antigen—invades, relevant scouts identify the attacker and put out a call for reinforcements of the right type. While your body is manufacturing these forces, you are likely to feel wretched. The onset of recovery begins when the troops finally swing into action.

  White cells are merciless and will hunt down and kill every last pathogen they can find. To avoid extinction, attackers have evolved two elemental strategies. Either they strike quickly and move on to a new host, as with common infectious illnesses like flu, or they disguise themselves so that the white cells fail to spot them, as with HIV, the virus responsible for AIDS, which can sit harmlessly and unnoticed in the nuclei of cells for years before springing into action.

  One of the odder aspects of infection is that microbes that normally do no harm at all sometimes get into the wrong parts of the body and “go kind of crazy,” in the words of Dr. Bryan Marsh, an infectious diseases specialist at Dartmouth-Hitchcock Medical Center in Lebanon, New Hampshire. “It happens all the time with car accidents when people suffer internal injuries. Microbes that are normally benign in the gut get into other parts of the body—the bloodstream, for instance—and cause terrible havoc.”

  The scariest, most out-of-control bacterial disorder of the moment is a disease called necrotizing fasciitis in which bacteria essentially eat the victim from the inside out, devouring internal tissue and leaving behind a pulpy, noxious residue. Patients often come in with comparatively mild complaints—a skin rash and fever, typically—but then dramatically deteriorate. When they are opened up it is often found that they are simply being consumed. The only treatment is what is known as “radical excisional surgery”—cutting out every bit of infected area. Seventy per cent of victims die; many of the rest are left terribly disfigured. The source of the infection is a mundane family of bacteria called Group A Streptococcus, which normally do no more than cause strep throat. Very occasionally, for reasons unknown, some of these bacteria get through the lining of the throat and into the body proper, where they wreak the most devastating havoc. They are completely resistant to antibiotics. About a thousand cases a year occur in the United States and no-one can say that it won’t get worse.

  Precisely the same thing happens with meningitis. At least 10 per cent of young adults, and perhaps 30 per cent of teenagers, carry the deadly meningococcal bacterium, but it lives quite harmlessly in the throat. Just occasionally—in about one young person in a hundred thousand—it gets into the bloodstream and makes them very ill indeed. In the worst cases, death can come in twelve hours. That’s shockingly quick. “You can have a person who’s in perfect health at breakfast and dead by evening,” says Marsh.

  We would have much more success with bacteria if we weren’t so profligate with our best weapon against them: antibiotics. Remarkably, by one estimate some 70 per cent of the antibiotics used in the developed world are given to farm animals, often routinely in stock feed, simply to promote growth or as a precaution against infection. Such applications give bacteria every opportunity to evolve a resistance to them. It is an opportunity that they have enthusiastically seized.

  In 1952, penicillin was fully effective against all strains of staphylococcus bacteria, to such an extent that by the early 1960s the US surgeon-general, William Stewart, felt confident enough to declare: “The time has come to close the book on infectious diseases. We have basically wiped out infection in the United States.” Even as he spoke, however, some 90 per cent of those strains were in the process of developing immunity to penicillin. Soon one of these new strains, called methicillin-resistant staphylococcus aureus, began to show up in hospitals. Only one type of antibiotic, vancomycin, remained effective against it, but in 1997 a hospital in Tokyo reported the appearance of a strain that could resist even that. Within months it had spread to six other Japanese hospitals. All over, the microbes are beginning to win the war again: in US hospitals alone, some fourteen thousand people a year die from infections they pick up there. As James Surowiecki noted in a New Yorker article, given a choice between developing antibiotics that people will take every day for two weeks and antidepressants that people will take every day for ever, drug companies not surprisingly opt for the latter. Although a few antibiotics have been toughened up a bit, the pharmaceutical industry hasn’t given us an entirely new antibiotic since the 1970s.

  The effects of evolving bacterial resistance are starkly demonstrated in two Petri dishes. In the top dish, a strain of bacteria that has not developed resistance is unable to grow close to a white penicillin tablet in the centre of the dish. In the bottom sample, a resistant strain of the same organism grows almost to the penicillin’s edge. (credit 20.12)

  Our carelessness is all the more alarming since the discovery that many other ailments may be bacterial in origin. The process of discovery began in 1983 when Barry Marshall, a doctor in Perth, Western Australia, found that many stomach cancers and most stomach ulcers are caused by a bacterium called Helicobacter pylori. Even though his findings were easily tested, the notion was so radical that more than a decade would pass before they were generally accepted. America’s National Institutes of Health, for instance, didn’t officially endorse the idea until 1994. “Hundreds, even thousands of people must have died from ulcers who wouldn’t have,” Marshall told a reporter from Forbes in 1999.

  Since then, further research has shown that there is or may well be a bacterial component in all kinds of other disorders—heart disease, asthma, arthritis, multiple sclerosis, several types of mental disorders, many cancers, even, it has been suggested (in Science no less), obesity. The day may not be far off when we desperately require an effective antibiotic and haven’t got one to call on.

  It may come as a slight comfort to know that bacteria can themselves get sick. They are sometimes infected by bacteriophages (or simply phages), a type of virus. A virus is a strange and unlovely entity—“a piece of nucleic acid surrounded by bad news” in the memorable phrase of the Nobel laureate Peter Medawar. Smaller and simpler than bacteria, viruses aren’t themselves alive. In isolation they are inert and harmless. But introduc
e them into a suitable host and they burst into busyness—into life. About five thousand types of virus are known, and between them they afflict us with many hundreds of diseases, ranging from the flu and common cold to those that are most invidious to human well-being: smallpox, rabies, yellow fever, Ebola, polio and AIDS.

  American soldiers march with face masks during the height of the global flu epidemic, which killed tens of millions of people in 1918–19. The soldiers’ masks were completely ineffectual as the fabric was not fine enough to trap something as tiny as a virus. (credit 20.13)

  Viruses prosper by hijacking the genetic material of a living cell, and using it to produce more virus. They reproduce in a fanatical manner, then burst out in search of more cells to invade. Not being living organisms themselves, they can afford to be very simple. Many, including HIV, have ten genes or fewer, whereas even the simplest bacteria require several thousand. They are also very tiny, much too small to be seen with a conventional microscope. It wasn’t until 1943 and the invention of the electron microscope that science got its first look at them. But they can do immense damage. Smallpox in the twentieth century alone killed an estimated 300 million people.

  They also have an unnerving capacity to burst upon the world in some new and startling form and then to vanish again as quickly as they came. In 1916, in one such case, people in Europe and America began to come down with a strange sleeping sickness, which became known as encephalitis lethargica. Victims would go to sleep and not wake up. They could be roused without great difficulty to take food or go to the lavatory, and would answer questions sensibly—they knew who and where they were—though their manner was always apathetic. However, the moment they were permitted to rest, they would at once sink back into deepest slumber and remain in that state for as long as they were left. Some went on in this manner for months before dying. A very few survived and regained consciousness but not their former liveliness. They existed in a state of profound apathy, “like extinct volcanoes,” in the words of one doctor. In ten years the disease killed some five million people and then quietly went away. It didn’t get much lasting attention because in the meantime an even worse epidemic—indeed, the worst in history—swept across the world.