20 SMALL WORLD
《万物简史英文版》章节: 20 SMALL WORLD,宠文网网友提供全文无弹窗免费在线阅读。!
In fact, there is no point in trying to hide from your bacteria, for they are on and around youalways, in numbers you can’t conceive. If you are in good health and averagely diligent abouthygiene, you will have a herd of about one trillion bacteria grazing on your fleshy plains—about a hundred thousand of them on every square centimeter of skin. They are there to dineoff the ten billion or so flakes of skin you shed every day, plus all the tasty oils and fortifyingminerals that seep out from every pore and fissure. You are for them the ultimate food court,with the convenience of warmth and constant mobility thrown in. By way of thanks, they giveyou B.O.
And those are just the bacteria that inhabit your skin. There are trillions more tucked awayin your gut and nasal passages, clinging to your hair and eyelashes, swimming over thesurface of your eyes, drilling through the enamel of your teeth. Your digestive system alone ishost to more than a hundred trillion microbes, of at least four hundred types. Some deal withsugars, some with starches, some attack other bacteria. A surprising number, like theubiquitous intestinal spirochetes, have no detectable function at all. They just seem to like tobe with you. Every human body consists of about 10 quadrillion cells, but about 100quadrillion bacterial cells. They are, in short, a big part of us. From the bacteria’s point ofview, of course, we are a rather small part of them.
Because we humans are big and clever enough to produce and utilize antibiotics anddisinfectants, it is easy to convince ourselves that we have banished bacteria to the fringes ofexistence. Don’t you believe it. Bacteria may not build cities or have interesting social lives,but they will be here when the Sun explodes. This is their planet, and we are on it onlybecause they allow us to be.
Bacteria, never forget, got along for billions of years without us. We couldn’t survive a daywithout them. They process our wastes and make them usable again; without their diligentmunching nothing would rot. They purify our water and keep our soils productive. Bacteriasynthesize vitamins in our gut, convert the things we eat into useful sugars andpolysaccharides, and go to war on alien microbes that slip down our gullet.
We depend totally on bacteria to pluck nitrogen from the air and convert it into usefulnucleotides and amino acids for us. It is a prodigious and gratifying feat. As Margulis andSagan note, to do the same thing industrially (as when making fertilizers) manufacturers mustheat the source materials to 500 degrees centigrade and squeeze them to three hundred timesnormal pressures. Bacteria do it all the time without fuss, and thank goodness, for no larger organism could survive without the nitrogen they pass on. Above all, microbes continue toprovide us with the air we breathe and to keep the atmosphere stable. Microbes, including themodern versions of cyanobacteria, supply the greater part of the planet’s breathable oxygen.
Algae and other tiny organisms bubbling away in the sea blow out about 150 billion kilos ofthe stuff every year.
And they are amazingly prolific. The more frantic among them can yield a new generationin less than ten minutes; Clostridium perfringens, the disagreeable little organism that causesgangrene, can reproduce in nine minutes. At such a rate, a single bacterium could theoreticallyproduce more offspring in two days than there are protons in the universe. “Given an adequatesupply of nutrients, a single bacterial cell can generate 280,000 billion individuals in a singleday,” according to the Belgian biochemist and Nobel laureate Christian de Duve. In the sameperiod, a human cell can just about manage a single division.
About once every million divisions, they produce a mutant. Usually this is bad luck for themutant—change is always risky for an organism—but just occasionally the new bacterium isendowed with some accidental advantage, such as the ability to elude or shrug off an attack ofantibiotics. With this ability to evolve rapidly goes another, even scarier advantage. Bacteriashare information. Any bacterium can take pieces of genetic coding from any other.
Essentially, as Margulis and Sagan put it, all bacteria swim in a single gene pool. Anyadaptive change that occurs in one area of the bacterial universe can spread to any other. It’srather as if a human could go to an insect to get the necessary genetic coding to sprout wingsor walk on ceilings. It means that from a genetic point of view bacteria have become a singlesuperorganism—tiny, dispersed, but invincible.
They will live and thrive on almost anything you spill, dribble, or shake loose. Just givethem a little moisture—as when you run a damp cloth over a counter—and they will bloom asif created from nothing. They will eat wood, the glue in wallpaper, the metals in hardenedpaint. Scientists in Australia found microbes known as Thiobacillus concretivorans that livedin—indeed, could not live without—concentrations of sulfuric acid strong enough to dissolvemetal. A species called Micrococcus radiophilus was found living happily in the waste tanksof nuclear reactors, gorging itself on plutonium and whatever else was there. Some bacteriabreak down chemical materials from which, as far as we can tell, they gain no benefit at all.
They have been found living in boiling mud pots and lakes of caustic soda, deep insiderocks, at the bottom of the sea, in hidden pools of icy water in the McMurdo Dry Valleys ofAntarctica, and seven miles down in the Pacific Ocean where pressures are more than athousand times greater than at the surface, or equivalent to being squashed beneath fiftyjumbo jets. Some of them seem to be practically indestructible. Deinococcus radiodurans is,according to theEconomist , “almost immune to radioactivity.” Blast its DNA with radiation,and the pieces immediately reform “like the scuttling limbs of an undead creature from ahorror movie.”
Perhaps the most extraordinary survival yet found was that of a Streptococcus bacteriumthat was recovered from the sealed lens of a camera that had stood on the Moon for two years.
In short, there are few environments in which bacteria aren’t prepared to live. “They arefinding now that when they push probes into ocean vents so hot that the probes actually startto melt, there are bacteria even there,” Victoria Bennett told me.
In the 1920s two scientists at the University of Chicago, Edson Bastin and Frank Greer,announced that they had isolated from oil wells strains of bacteria that had been living at depths of two thousand feet. The notion was dismissed as fundamentally preposterous—therewas nothing to live on at two thousand feet—and for fifty years it was assumed that theirsamples had been contaminated with surface microbes. We now know that there are a lot ofmicrobes living deep within the Earth, many of which have nothing at all to do with theorganic world. They eat rocks or, rather, the stuff that’s in rocks—iron, sulfur, manganese,and so on. And they breathe odd things too—iron, chromium, cobalt, even uranium. Suchprocesses may be instrumental in concentrating gold, copper, and other precious metals, andpossibly deposits of oil and natural gas. It has even been suggested that their tireless nibblingscreated the Earth’s crust.
Some scientists now think that there could be as much as 100 trillion tons of bacteria livingbeneath our feet in what are known as subsurface lithoautotrophic microbial ecosystems—SLiME for short. Thomas Gold of Cornell has estimated that if you took all the bacteria out ofthe Earth’s interior and dumped it on the surface, it would cover the planet to a depth of fivefeet. If the estimates are correct, there could be more life under the Earth than on top of it.
At depth microbes shrink in size and become extremely sluggish. The liveliest of them maydivide no more than once a century, some no more than perhaps once in five hundred years.
As the Economist has put it: “The key to long life, it seems, is not to do too much.” Whenthings are really tough, bacteria are prepared to shut down all systems and wait for bettertimes. In 1997 scientists successfully activated some anthrax spores that had lain dormant foreighty years in a museum display in Trondheim, Norway. Other microorganisms have leaptback to life after being released from a 118-year-old can of meat and a 166-year-old bottle ofbeer. In 1996, scientists at the Russian Academy of Science claimed to have revived bacteriafrozen in Siberian permafrost for three million years. But the record claim for durability so faris one made by Russell Vreeland and colleagues at West Chester University in Pennsylvaniain 2000, when they announced that they had resuscitated 250-million-year-old bacteria calledBacillus permians that had been trapped in salt deposits two thousand feet underground inCarlsbad, New Mexico. If so, this microbe is older than the continents.
The report met with some understandable dubiousness. Many biochemists maintained thatover such a span the microbe’s components would have become uselessly degraded unless thebacterium roused itself from time to time. However, if the bacterium did stir occasionallythere was no plausible internal source of energy that could have lasted so long. The moredoubtful scientists suggested that the sample may have been contaminated, if not during itsretrieval then perhaps while still buried. In 2001, a team from Tel Aviv University argued thatB. permians were almost identical to a strain of modern bacteria, Bacillus marismortui, foundin the Dead Sea. Only two of its genetic sequences differed, and then only slightly.
“Are we to believe,” the Israeli researchers wrote, “that in 250 million years B. permianshas accumulated the same amount of genetic differences that could be achieved in just 3–7days in the laboratory?” In reply, Vreeland suggested that “bacteria evolve faster in the labthan they do in the wild.”
Maybe.
It is a remarkable fact that well into the space age, most school textbooks divided the worldof the living into just two categories—plant and animal. Microorganisms hardly featured.
Amoebas and similar single-celled organisms were treated as proto-animals and algae as proto-plants. Bacteria were usually lumped in with plants, too, even though everyone knewthey didn’t belong there. As far back as the late nineteenth century the German naturalistErnst Haeckel had suggested that bacteria deserved to be placed in a separate kingdom, whichhe called Monera, but the idea didn’t begin to catch on among biologists until the 1960s andthen only among some of them. (I note that my trusty American Heritage desk dictionaryfrom 1969 doesn’t recognize the term.)Many organisms in the visible world were also poorly served by the traditional division.
Fungi, the group that includes mushrooms, molds, mildews, yeasts, and puffballs, were nearlyalways treated as botanical objects, though in fact almost nothing about them—how theyreproduce and respire, how they build themselves—matches anything in the plant world.
Structurally they have more in common with animals in that they build their cells from chitin,a material that gives them their distinctive texture. The same substance is used to make theshells of insects and the claws of mammals, though it isn’t nearly so tasty in a stag beetle as ina Portobello mushroom. Above all, unlike all plants, fungi don’t photosynthesize, so theyhave no chlorophyll and thus are not green. Instead they grow directly on their food source,which can be almost anything. Fungi will eat the sulfur off a concrete wall or the decayingmatter between your toes—two things no plant will do. Almost the only plantlike quality theyhave is that they root.
Even less comfortably susceptible to categorization was the peculiar group of organismsformally called myxomycetes but more commonly known as slime molds. The name no doubthas much to do with their obscurity. An appellation that sounded a little more dynamic—“ambulant self-activating protoplasm,” say—and less like the stuff you find when you reachdeep into a clogged drain would almost certainly have earned these extraordinary entities amore immediate share of the attention they deserve, for slime molds are, make no mistake,among the most interesting organisms in nature. When times are good, they exist as one-celled individuals, much like amoebas. But when conditions grow tough, they crawl to acentral gathering place and become, almost miraculously, a slug. The slug is not a thing ofbeauty and it doesn’t go terribly far—usually just from the bottom of a pile of leaf litter to thetop, where it is in a slightly more exposed position—but for millions of years this may wellhave been the niftiest trick in the universe.
And it doesn’t stop there. Having hauled itself up to a more favorable locale, the slimemold transforms itself yet again, taking on the form of a plant. By some curious orderlyprocess the cells reconfigure, like the members of a tiny marching band, to make a stalk atopof which forms a bulb known as a fruiting body. Inside the fruiting body are millions ofspores that, at the appropriate moment, are released to the wind to blow away and becomesingle-celled organisms that can start the process again.
For years slime molds were claimed as protozoa by zoologists and as fungi by mycologists,though most people could see they didn’t really belong anywhere. When genetic testingarrived, people in lab coats were surprised to find that slime molds were so distinctive andpeculiar that they weren’t directly related to anything else in nature, and sometimes not evento each other.
In 1969, in an attempt to bring some order to the growing inadequacies of classification, anecologist from Cornell University named R. H. Whittaker unveiled in the journalScience aproposal to divide life into five principal branches—kingdoms, as they are known—calledAnimalia, Plantae, Fungi, Protista, and Monera. Protista, was a modification of an earlier term, Protoctista, which had been suggested a century earlier by a Scottish biologist namedJohn Hogg, and was meant to describe any organisms that were neither plant nor animal.
Though Whittaker’s new scheme was a great improvement, Protista remained ill defined.
Some taxonomists reserved it for large unicellular organisms—the eukaryotes—but otherstreated it as the kind of odd sock drawer of biology, putting into it anything that didn’t fitanywhere else. It included (depending on which text you consulted) slime molds, amoebas,and even seaweed, among much else. By one calculation it contained as many as 200,000different species of organism all told. That’s a lot of odd socks.
Ironically, just as Whittaker’s five-kingdom classification was beginning to find its wayinto textbooks, a retiring academic at the University of Illinois was groping his way toward adiscovery that would challenge everything. His name was Carl Woese (rhymes with rose), andsince the mid-1960s—or about as early as it was possible to do so—he had been quietlystudying genetic sequences in bacteria. In the early days, this was an exceedingly painstakingprocess. Work on a single bacterium could easily consume a year. At that time, according toWoese, only about 500 species of bacteria were known, which is fewer than the number ofspecies you have in your mouth. Today the number is about ten times that, though that is stillfar short of the 26,900 species of algae, 70,000 of fungi, and 30,800 of amoebas and relatedorganisms whose biographies fill the annals of biology.
It isn’t simple indifference that keeps the total low. Bacteria can be exasperatingly difficultto isolate and study. Only about 1 percent will grow in culture. Considering how wildlyadaptable they are in nature, it is an odd fact that the one place they seem not to wish to live isa petri dish. Plop them on a bed of agar and pamper them as you will, and most will just liethere, declining every inducement to bloom. Any bacterium that thrives in a lab is bydefinition exceptional, and yet these were, almost exclusively, the organisms studied bymicrobiologists. It was, said Woese, “like learning about animals from visiting zoos.”
Genes, however, allowed Woese to approach microorganisms from another angle. As heworked, Woese realized that there were more fundamental divisions in the microbial worldthan anyone suspected. A lot of little organisms that looked like bacteria and behaved likebacteria were actually something else altogether—something that had branched off frombacteria a long time ago. Woese called these organisms archaebacteria, later shortened toarchaea.
It has be said that the attributes that distinguish archaea from bacteria are not the sort thatwould quicken the pulse of any but a biologist. They are mostly differences in their lipids andan absence of something called peptidoglycan. But in practice they make a world ofdifference. Archaeans are more different from bacteria than you and I are from a crab orspider. Singlehandedly Woese had discovered an unsuspected division of life, so fundamentalthat it stood above the level of kingdom at the apogee of the Universal Tree of Life, as it israther reverentially known.
In 1976, he startled the world—or at least the little bit of it that was paying attention—byredrawing the tree of life to incorporate not five main divisions, but twenty-three. These hegrouped under three new principal categories—Bacteria, Archaea, and Eukarya (sometimesspelled Eucarya)—which he called domains.
Woese’s new divisions did not take the biological world by storm. Some dismissed them asmuch too heavily weighted toward the microbial. Many just ignored them. Woese, according to Frances Ashcroft, “felt bitterly disappointed.” But slowly his new scheme began to catchon among microbiologists. Botanists and zoologists were much slower to admire its virtues.
It’s not hard to see why. On Woese’s model, the worlds of botany and zoology are relegatedto a few twigs on the outermost branch of the Eukaryan limb. Everything else belongs tounicellular beings.
“These folks were brought up to classify in terms of gross morphological similarities anddifferences,” Woese told an interviewer in 1996. “The idea of doing so in terms of molecularsequence is a bit hard for many of them to swallow.” In short, if they couldn’t see a differencewith their own eyes, they didn’t like it. And so they persisted with the traditional five-kingdom division—an arrangement that Woese called “not very useful” in his mildermoments and “positively misleading” much of the rest of the time. “Biology, like physicsbefore it,” Woese wrote, “has moved to a level where the objects of interest and theirinteractions 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 and at the time of my writing is nearing one hundred and still going strong) stirredthe 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 extensivefamiliarity with the principles of classification,” which is perhaps as close as onedistinguished scientist can come to saying of another that he doesn’t know what he is talkingabout.
The specifics of Mayr’s criticisms are too technical to need extensive airing here—theyinvolve issues of meiotic sexuality, Hennigian cladification, and controversial interpretationsof the genome of Methanobacterium thermoautrophicum, among rather a lot else—butessentially he argues that Woese’s arrangement unbalances the tree of life. The bacterialrealm, Mayr notes, consists of no more than a few thousand species while the archaean has amere 175 named specimens, with perhaps a few thousand more to be found—“but hardlymore than that.” By contrast, the eukaryotic realm—that is, the complicated organisms withnucleated cells, like us—numbers already in the millions. For the sake of “the principle ofbalance,” Mayr argues for combining the simple bacterial organisms in a single category,Prokaryota, while placing the more complex and “highly evolved” remainder in the empireEukaryota, which would stand alongside as an equal. Put another way, he argues for keepingthings much as they were before. This division between simple cells and complex cells “iswhere the great break is in the living world.”
The distinction between halophilic archaeans and methanosarcina or between flavobacteriaand gram-positive bacteria clearly will never be a matter of moment for most of us, but it isworth remembering that each is as different from its neighbors as animals are from plants. IfWoese’s new arrangement teaches us anything it is that life really is various and that most ofthat variety is small, unicellular, and unfamiliar. It is a natural human impulse to think ofevolution as a long chain of improvements, of a never-ending advance toward largeness andcomplexity—in a word, toward us. We flatter ourselves. Most of the real diversity inevolution has been small-scale. We large things are just flukes—an interesting side branch. Ofthe twenty-three main divisions of life, only three—plants, animals, and fungi—are largeenough to be seen by the human eye, and even they contain species that are microscopic.
Indeed, according to Woese, if you totaled up all the biomass of the planet—every living thing, plants included—microbes would account for at least 80 percent of all there is, perhapsmore. The world belongs to the very small—and it has for a very long time.
So why, you are bound to ask at some point in your life, do microbes so often want to hurtus? What possible satisfaction could there be to a microbe in having us grow feverish orchilled, or disfigured with sores, or above all expire? A dead host, after all, is hardly going toprovide long-term hospitality.
To begin with, it is worth remembering that most microorganisms are neutral or evenbeneficial to human well-being. The most rampantly infectious organism on Earth, abacterium called Wolbachia, doesn’t hurt humans at all—or, come to that, any othervertebrates—but if you are a shrimp or worm or fruit fly, it can make you wish you had neverbeen born. Altogether, only about one microbe in a thousand is a pathogen for humans,according to National Geographic —though, knowing what some of them can do, we couldbe forgiven for thinking that that is quite enough. Even if mostly benign, microbes are still thenumber-three killer in the Western world, and even many less lethal ones of course make usdeeply rue their existence.
Making a host unwell has certain benefits for the microbe. The symptoms of an illnessoften help to spread the disease. Vomiting, sneezing, and diarrhea are excellent methods ofgetting out of one host and into position for another. The most effective strategy of all is toenlist the help of a mobile third party. Infectious organisms love mosquitoes because themosquito’s sting delivers them directly to a bloodstream where they can get straight to workbefore the victim’s defense mechanisms can figure out what’s hit them. This is why so manygrade-A diseases—malaria, yellow fever, dengue fever, encephalitis, and a hundred or soother less celebrated but often rapacious maladies—begin with a mosquito bite. It is afortunate fluke for us that HIV, the AIDS agent, isn’t among them—at least not yet. Any HIVthe mosquito sucks up on its travels is dissolved by the mosquito’s own metabolism. Whenthe day comes that the 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 logicbecause microorganisms clearly are not calculating entities. They don’t care what they do toyou any more than you care what distress you cause when you slaughter them by the millionswith a soapy shower or a swipe of deodorant. The only time your continuing well-being is ofconsequence to a pathogen is when it kills you too well. If they eliminate you before they canmove on, then they may well die out themselves. This in fact sometimes happens. History,Jared Diamond notes, is full of diseases that “once caused terrifying epidemics and thendisappeared as mysteriously as they had come.” He cites the robust but mercifully transientEnglish sweating sickness, which raged from 1485 to 1552, killing tens of thousands as itwent, before burning itself out. Too much efficiency is not a good thing for any infectiousorganism.
A great deal of sickness arises not because of what the organism has done to you but whatyour body is trying to do to the organism. In its quest to rid the body of pathogens, theimmune system sometimes destroys cells or damages critical tissues, so often when you areunwell 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 areless of a threat to the wider community. Resting also frees more of the body’s resources toattend to the infection.
Because there are so many things out there with the potential to hurt you, your body holdslots of different varieties of defensive white cells—some ten million types in all, eachdesigned to identify and destroy a particular sort of invader. It would be impossibly inefficientto maintain ten million separate standing armies, so each variety of white cell keeps only afew 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 ofrecovery begins when the troops finally swing into action.
White cells are merciless and will hunt down and kill every last pathogen they can find. Toavoid extinction, attackers have evolved two elemental strategies. Either they strike quicklyand move on to a new host, as with common infectious illnesses like flu, or they disguisethemselves so that the white cells fail to spot them, as with HIV, the virus responsible forAIDS, which can sit harmlessly and unnoticed in the nuclei of cells for years before springinginto action.
One of the odder aspects of infection is that microbes that normally do no harm at allsometimes 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 inLebanon, New Hamphire. “It happens all the time with car accidents when people sufferinternal injuries. Microbes that are normally benign in the gut get into other parts of thebody—the bloodstream, for instance—and cause terrible havoc.”
The scariest, most out-of-control bacterial disorder of the moment is a disease callednecrotizing fasciitis in which bacteria essentially eat the victim from the inside out, devouringinternal tissue and leaving behind a pulpy, noxious residue. Patients often come in withcomparatively mild complaints—a skin rash and fever typically—but then dramaticallydeteriorate. 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 ofinfected area. Seventy percent of victims die; many of the rest are left terribly disfigured. Thesource of the infection is a mundane family of bacteria called Group A Streptococcus, whichnormally do no more than cause strep throat. Very occasionally, for reasons unknown, someof these bacteria get through the lining of the throat and into the body proper, where theywreak the most devastating havoc. They are completely resistant to antibiotics. About athousand 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 percent of young adults, andperhaps 30 percent of teenagers, carry the deadly meningococcal bacterium, but it lives quiteharmlessly in the throat. Just occasionally—in about one young person in a hundredthousand—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 inperfect 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 bestweapon against them: antibiotics. Remarkably, by one estimate some 70 percent of theantibiotics used in the developed world are given to farm animals, often routinely in stockfeed, simply to promote growth or as a precaution against infection. Such applications givebacteria every opportunity to evolve a resistance to them. It is an opportunity that they haveenthusiastically seized.
In 1952, penicillin was fully effective against all strains of staphylococcus bacteria, to suchan extent that by the early 1960s the U.S. surgeon general, William Stewart, felt confidentenough to declare: “The time has come to close the book on infectious diseases. We havebasically wiped out infection in the United States.” Even as he spoke, however, some 90percent of those strains were in the process of developing immunity to penicillin. Soon one ofthese new strains, called Methicillin-Resistant Staphylococcus Aureus, began to show up inhospitals. Only one type of antibiotic, vancomycin, remained effective against it, but in 1997a hospital in Tokyo reported the appearance of a strain that could resist even that. Withinmonths it had spread to six other Japanese hospitals. All over, the microbes are beginning towin the war again: in U.S. hospitals alone, some fourteen thousand people a year die frominfections they pick up there. As James Surowiecki has noted, given a choice betweendeveloping antibiotics that people will take every day for two weeks or antidepressants thatpeople will take every day forever, drug companies not surprisingly opt for the latter.
Although a few antibiotics have been toughened up a bit, the pharmaceutical industry hasn’tgiven us an entirely new antibiotic since the 1970s.
Our carelessness is all the more alarming since the discovery that many other ailments maybe bacterial in origin. The process of discovery began in 1983 when Barry Marshall, a doctorin Perth, Western Australia, found that many stomach cancers and most stomach ulcers arecaused 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 generallyaccepted. America’s National Institutes of Health, for instance, didn’t officially endorse theidea until 1994. “Hundreds, even thousands of people must have died from ulcers whowouldn’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 inall kinds of other disorders—heart disease, asthma, arthritis, multiple sclerosis, several typesof mental disorders, many cancers, even, it has been suggested (inScience no less), obesity.
The day may not be far off when we desperately require an effective antibiotic and haven’tgot one to call on.
It may come as a slight comfort to know that bacteria can themselves get sick. They aresometimes infected by bacteriophages (or simply phages), a type of virus. A virus is a strangeand unlovely entity—“a piece of nucleic acid surrounded by bad news” in the memorablephrase of the Nobel laureate Peter Medawar. Smaller and simpler than bacteria, viruses aren’tthemselves alive. In isolation they are inert and harmless. But introduce them into a suitablehost 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 andcommon cold to those that are most invidious to human well-being: smallpox, rabies, yellowfever, ebola, polio, and the human immunodeficiency virus, the source of AIDS.
Viruses prosper by hijacking the genetic material of a living cell and using it to producemore virus. They reproduce in a fanatical manner, then burst out in search of more cells toinvade. 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 severalthousand. 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 lookat them. But they can do immense damage. Smallpox in the twentieth century alone killed anestimated 300 million people.
They also have an unnerving capacity to burst upon the world in some new and startlingform and then to vanish again as quickly as they came. In 1916, in one such case, people inEurope and America began to come down with a strange sleeping sickness, which becameknown as encephalitis lethargica. Victims would go to sleep and not wake up. They could beroused without great difficulty to take food or go to the lavatory, and would answer questionssensibly—they knew who and where they were—though their manner was always apathetic.
However, the moment they were permitted to rest, they would sink at once back intodeepest slumber and remain in that state for as long as they were left. Some went on in thismanner for months before dying. A very few survived and regained consciousness but nottheir former liveliness. They existed in a state of profound apathy, “like extinct volcanoes,” inthe words of one doctor. In ten years the disease killed some five million people and thenquietly went away. It didn’t get much lasting attention because in the meantime an even worseepidemic—indeed, the worst in history—swept across the world.
It is sometimes called the Great Swine Flu epidemic and sometimes the Great Spanish Fluepidemic, but in either case it was ferocious. World War I killed twenty-one million people infour years; swine flu did the same in its first four months. Almost 80 percent of Americancasualties in the First World War came not from enemy fire, but from flu. In some units themortality rate was as high as 80 percent.
Swine flu arose as a normal, nonlethal flu in the spring of 1918, but somehow over thefollowing months—no one knows how or where—it mutated into something more severe. Afifth of victims suffered only mild symptoms, but the rest became gravely ill and often died.
Some succumbed within hours; others held on for a few days.
In the United States, the first deaths were recorded among sailors in Boston in late August1918, but the epidemic quickly spread to all parts of the country. Schools closed, publicentertainments were shut down, people everywhere wore masks. It did little good. Betweenthe autumn of 1918 and spring of the following year, 548,452 people died of the flu inAmerica. The toll in Britain was 220,000, with similar numbers dead in France and Germany.
No one knows the global toll, as records in the Third World were often poor, but it was notless than 20 million and probably more like 50 million. Some estimates have put the globaltotal as high as 100 million.
In an attempt to devise a vaccine, medical authorities conducted tests on volunteers at amilitary prison on Deer Island in Boston Harbor. The prisoners were promised pardons if theysurvived a battery of tests. These tests were rigorous to say the least. First the subjects wereinjected with infected lung tissue taken from the dead and then sprayed in the eyes, nose, andmouth with infectious aerosols. If they still failed to succumb, they had their throats swabbedwith discharges taken from the sick and dying. If all else failed, they were required to sitopen-mouthed while a gravely ill victim was helped to cough into their faces.
Out of—somewhat amazingly—three hundred men who volunteered, the doctors chosesixty-two for the tests. None contracted the flu—not one. The only person who did grow illwas the ward doctor, who swiftly died. The probable explanation for this is that the epidemichad passed through the prison a few weeks earlier and the volunteers, all of whom hadsurvived that visitation, had a natural immunity.
Much about the 1918 flu is understood poorly or not at all. One mystery is how it eruptedsuddenly, all over, in places separated by oceans, mountain ranges, and other earthly impediments. A virus can survive for no more than a few hours outside a host body, so howcould it appear in Madrid, Bombay, and Philadelphia all in the same week?
The probable answer is that it was incubated and spread by people who had only slightsymptoms or none at all. Even in normal outbreaks, about 10 percent of people have the flubut are unaware of it because they experience no ill effects. And because they remain incirculation they tend to be the great spreaders of the disease.
That would account for the 1918 outbreak’s widespread distribution, but it still doesn’texplain how it managed to lay low for several months before erupting so explosively at moreor less the same time all over. Even more mysterious is that it was primarily devastating topeople in the prime of life. Flu normally is hardest on infants and the elderly, but in the 1918outbreak deaths were overwhelmingly among people in their twenties and thirties. Olderpeople may have benefited from resistance gained from an earlier exposure to the same strain,but why the very young were similarly spared is unknown. The greatest mystery of all is whythe 1918 flu was so ferociously deadly when most flus are not. We still have no idea.
From time to time certain strains of virus return. A disagreeable Russian virus known asH1N1 caused severe outbreaks over wide areas in 1933, then again in the 1950s, and yet againin the 1970s. Where it went in the meantime each time is uncertain. One suggestion is thatviruses hide out unnoticed in populations of wild animals before trying their hand at a newgeneration of humans. No one can rule out the possibility that the Great Swine Flu epidemicmight once again rear its head.
And if it doesn’t, others well might. New and frightening viruses crop up all the time.
Ebola, Lassa, and Marburg fevers all have tended to flare up and die down again, but no onecan say that they aren’t quietly mutating away somewhere, or simply awaiting the rightopportunity to burst forth in a catastrophic manner. It is now apparent that AIDS has beenamong us much longer than anyone originally suspected. Researchers at the ManchesterRoyal Infirmary in England discovered that a sailor who had died of mysterious, untreatablecauses in 1959 in fact had AIDS. But for whatever reasons the disease remained generallyquiescent for another twenty years.
The miracle is that other such diseases haven’t gone rampant. Lassa fever, which wasn’tfirst detected until 1969, in West Africa, is extremely virulent and little understood. In 1969, adoctor at a Yale University lab in New Haven, Connecticut, who was studying Lassa fevercame down with it. He survived, but, more alarmingly, a technician in a nearby lab, with nodirect exposure, also contracted the disease and died.
Happily the outbreak stopped there, but we can’t count on such good fortune always. Ourlifestyles invite epidemics. Air travel makes it possible to spread infectious agents across theplanet with amazing ease. An ebola virus could begin the day in, say, Benin, and finish it inNew York or Hamburg or Nairobi, or all three. It means also that medical authoritiesincreasingly need to be acquainted with pretty much every malady that exists everywhere, butof course they are not. In 1990, a Nigerian living in Chicago was exposed to Lassa fever on avisit to his homeland, but didn’t develop symptoms until he had returned to the United States.
He died in a Chicago hospital without diagnosis and without anyone taking any specialprecautions in treating him, unaware that he had one of the most lethal and infectious diseaseson the planet. Miraculously, no one else was infec