20 SMALL WORLD

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    IT’S PROBABLY NOT a good idea to take too personal an i in your microbes. LouisPasteur, the great French chemist and bacteriologist, became so preoccupied with them that hetook to peering critically at every dish placed before him with a magnifying glass, a habit thatpresumably did not win him ma invitations to dinner.

    In fact, there is no point in trying to hide from your bacteria, for they are on and around youalways, in numbers you ’t ceive. If you are in good health and averagely diligent abouthygiene, you will have a herd of about orillion bacteria grazing on your fleshy plains—about a huhousand of them on every square timeter 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 venience of warmth and stant 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 yut and nasal passages, ging to your hair and eyelashes, swimming over thesurface of your eyes, drilling through the enamel of your teeth. Yestive system alone ishost to more than a hurillion microbes, of at least four huypes. Some deal withsugars, some with starches, some attack other bacteria. A surprising number, like theubiquitous iinal spirochetes, have able fun at all. They just seem to like tobe with you. Every human body sists 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 produd utilize antibiotiddisiants, it is easy to vince ourselves that we have banished bacteria to the fringes ofexistence. Don’t you believe it. Bacteria may not build cities or have iing social lives,but they will be here when the Sun explodes. This is their pla, and we are on it onlybecause they allow us to be.

    Bacteria, never fet, 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 diligentmung nothing would rot. They purify our water and keep our soils productive. Bacteriasynthesize vitamins in ut, vert the things we eat into useful sugars andpolysaccharides, and go to war on alien microbes that slip down ullet.

    We depend totally on bacteria to pluitrogen from the air and vert it into usefulides and amino acids for us. It is a prodigious and gratifyi. As Margulis andSagan o do the same thing industrially (as when makiilizers) manufacturers mustheat the source materials to 500 degrees tigrade and squeeze them to three huimesnormal pressures. Bacteria do it all the time without fuss, and thank goodness, for neranism could survive without the nitrogen they pass on. Above all, microbes tioprovide us with the air we breathe and to keep the atmosphere stable. Microbes, including themodern versions of obacteria, supply the greater part of the pla’s breathable oxygen.

    Algae and other tiny anisms 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  yield a new geionihan ten minutes; Clostridium perfringens, the disagreeable little anism that causesgangrene,  reprodu nine minutes. At such a rate, a single bacterium could theoreticallyproduce more offspring in two days than there are protons in the universe. “Given aesupply of nutrbbr>.９９ｌiｂ.</abbr>ients, a single bacterial cell  gee 280,000 billion individuals in a singleday,” acc to the Belgian biochemist and Nobel laureate Christian de Duve. In the sameperiod, a human cell  just about manage a single division.

    About once every million divisions, they produce a mutant. Usually this is bad luck for themutant—ge is always risky for an anism—but just occasionally the n<mark></mark>ew bacterium isendowed with some actal 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  take pieces of geic g from any other.

    Essentially, as Margulis and Sagan put it, all bacteria swim in a single gene pool. Anyadaptive ge that occurs in one area of the bacterial universe  spread to any other. It’srather as if a human could go to an io get the necessary geic g to sprout wingsor walk on ceilings. It means that from a geic point of view bacteria have bee a singlesuperanism—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 ter—and they will bloom asif created from nothing. They will eat wood, the glue in aper, the metals in hardenedpaint. Stists in Australia found microbes known as Thiobacillus cretivorans that livedin—indeed, could not live without—trations of sulfuric acid strong enough to dissolvemetal. A species called Micrococcus radiophilus was found living happily in the waste tanksof nuclear react itself on plutonium and whatever else was there. Some bacteriabreak down chemical materials from which, as far as we  tell, they gain no be 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 O where pressures are more than athousand times greater than at the surface, or equivalent to being squashed beh fiftyjumbo jets. Some of them seem to be practically iructible. Deinococcus radiodurans is,acc to theEist , “almost immuo 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 enviros in which bacteria aren’t prepared to live. “They arefinding now that when they push probes into o vents so hot that the probes actually startto melt, there are bacteria even there,” Victoria Beold me.

    In the 1920s two stists at the Uy of Chicago, Edson Bastin and Frank Greer,annouhat they had isolated from oil wells strains of bacteria that had been living atdepths of two thousa. The notion was dismissed as fually preposterous—therewas nothing to live on at two thousa—and for fifty years it was assumed that theirsamples had been inated 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 theanic 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, , cobalt, even uranium. Suchprocesses may be instrumental in trating gold, copper, and other preetals, andpossibly deposits of oil and natural gas. It has even been suggested that their tireless nibblingscreated the Earth’s crust.

    Some stists now think that there could be as much as 100 trillion tons of bacteria livih our feet in what are known as subsurface lithoautotrophic microbial ecosystems—SLiME for short. Thomas Gold of ell has estimated that if you took all the bacteria out ofthe Earth’s interior and dumped it on the surface, it would cover the plao a depth of fivefeet. If the estimates are correct, there could be more life uhe Earth than on top of it.

    At depth microbes shrink in size and bee extremely sluggish. The liveliest of them maydivide no more than once a tury, some no more than perhaps on five hundred years.

    As the Eist 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 stists successfully activated some anthrax spores that had lain dormant fhty years in a museum display in Trondheim, Norway. Other micranisms have leaptback to life after being released from a 118-year-old eat and a 166-year-old bottle ofbeer. In 1996, stists at the Russian Academy of Sce 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 Uy in Pennsylvaniain 2000, when they annouhat they had resuscitated 250-million-year-old bacteria calledBacillus permians that had been trapped in salt deposits two thousa underground inCarlsbad, New Mexico. If so, this microbe is older than the tis.

    The report met with some uandable dubiousness. Many biochemists maintaihatover such a span the microbe’s pos would have bee uselessly degraded uhebacterium 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 stists suggested that the sample may have been inated, if not during itsretrieval then perhaps while still buried. In 2001, a team from Tel Aviv Uy argued thatB. permians were almost identical to a strain of modern bacteria, Bacillus marismortui, foundin the Dead Sea. Only two of its geic 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 geic differehat 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. Micranisms hardly featured.

    Amoebas and similar single-celled anisms were treated as proto-animals and algae asproto-plants. Bacteria were usually lumped in with plants, too, even though everyone khey didn’t belong there. As far back as the late eenth tury 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 catong biologists until the 1960s andthen only among some of them. (I hat my trusty Ameri Heritage desk diaryfrom 1969 doesn’t reize the term.)Many anisms 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 theyreprodud respire, how they build themselves—matches anything in the plant world.

    Structurally they have more in on 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 is 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. Ihey grow directly on their food source,which  be almost anything. Fungi will eat the sulfur off a crete wall or the degmatter between your toes—two things no plant will do. Almost the only plantlike quality theyhave is that they root.

    Even less fortably susceptible to categorization was the peculiar group anismsformally called myxomycetes but more only 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 earhese extraordinary entities amore immediate share of the attention they deserve, for slime molds are, make no mistake,among the most iing anisms in nature. When times are good, they exist as one-celled individuals, much like amoebas. But when ditions grow tough, they crawl to atral gathering plad bee, 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 tri 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 refigure, like the members of a tiny marg band, to make a stalk atopof whis a bulb known as a fruiting body. Ihe fruiting body are millions ofspores that, at the appropriate moment, are released to the wind to blow away and beesingle-celled anisms that  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. Wheic 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 o each other.

    In 1969, in an attempt t some order to the growing inadequacies of classification, anecologist from ell Uy named R. H. Whittaker unveiled in the journalSce 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 earlierterm, Protoctista, which had been suggested a tury earlier by a Scottish biologist namedJohn Hogg, and was meant to describe any anisms that were her plant nor animal.

    Though Whittaker’s new scheme was a great improvement, Protista remained ill defined.

    Some taxonomists reserved it for large unicellular anisms—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 sulted) slime molds, amoebas,and even seaweed, among much else. By one calculation it tained as many as 200,000different species anism 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 Uy of Illinois was groping his way toward adiscovery that would challenge everything. His name was Carl Woese (rhymes with rose), andsihe mid-1960s—or about as early as it ossible to do so—he had been quietlystudyiic sequences in bacteria. In the early days, this was an exceedingly painstakingprocess. Work on a single bacterium could easily e a year. At that time, acc 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 aedanisms whose biographies fill the annals of biology.

    It isn’t simple indifferehat keeps the total low. Bacteria  be exasperatingly difficultto isolate and study. Only about 1 pert will grow in culture. sidering 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, deing every i to bloom. Any bacterium that thrives in a lab is bydefinition exceptional, ahese were, almost exclusively, the anisms studied bymicrobiologists. It was, said Woese, “like learning about animals from visiting zoos.”

    Genes, however, allowed Woese to approach micranisms from anle. As heworked, Woese realized that there were more fual divisions in the microbial worldthan anyone suspected. A lot of little anisms 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 anisms archaebacteria, later shorteoarchaea.

    It has be said that the attributes that distinguish archaea from bacteria are not the sort thatwould qui the pulse of any but a biologist. They are mostly differences in their lipids andan absence of something called peptidogly. 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 fualthat 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 aying attention—byredrawing the tree of life to incorporate not five main divisions, but twenty-three. These hegrouped uhree 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 ighem. Woese, accto Frances Ashcroft, “felt bitterly disappointed.” But slowly his new scheme began to catong 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 oermost 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 differeh their owhey didn’t like it. And so they persisted with the traditional five-kingdom division—an arrahat 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 i and theiriions often ot be perceived through direct observation.”

    In 1998 the great and a Harvard zoologist Ernst Mayr (who then was in his y-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 Sces,Mayr said that Woese’s findings were iing but ultimately misguided, noting that“Woese was not trained as a biologist and quite naturally does not have aensivefamiliarity with the principles of classification,” which is perhaps as close as oinguished stist  e to saying of ahat he doesn’t know what he is talkingabout.

    The specifiayr’s criticisms are too teical to need extensive airiheyinvolve issues of meiotic sexuality, Hennigian cladification, and troversial interpretationsof the genome of Methanobacterium thermoautrophicum, among rather a lot else—butessentially he argues that Woese’s arra unbalahe tree of life. The bacterialrealm, Mayr notes, sists of no more than a few thousand species while the archaean has amere 175 named spes, with perhaps a few thousand more to be found—“but hardlymore than that.” By trast, the eukaryotic realm—that is, the plicated anisms withed cells, like us—numbers already in the millions. For the sake of “the principle ofbalance,” Mayr argues for bining the simple bacterial anisms in a siegory,Prokaryota, while plag the more plex 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 divisioween simple cells and plex cells “iswhere the great break is in the living world.”

    The distin between halophilic archaeans ahanosara 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 arraeaches 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  of improvements, of a never-ending advaoward largeness andplexity—in a word, toward us. We flatter ourselves. Most of the real diversity inevolution has been small-scale. We lar<u></u>ge things are just flukes—an iing 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 tain species that are microscopic.

    Indeed, acc to Woese, if you totaled up all the biomass of the pla—every livingthing, plants included—microbes would at for at least 80 pert 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? ossible satisfa 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 micranisms are ral or evenbeneficial to human well-being. The most rampantly iious anism oh, abacterium called Wolbachia, doesn’t hurt humans at all—or, e to that, any othervertebrates—but if you are a shrimp or worm or fruit fly, it  make you wish you had neverbeen born. Altogether, only about one microbe in a thousand is a pathogen for humans,acc to National Geographic —though, knowing what some of them  do, we couldbe fiven for thinking that that is quite enough. Even if mostly benign, microbes are still thehree killer in the Western world, and even many less lethal ones of course make usdeeply rue their existence.

    Making a host unwell has certain bes for the microbe. The symptoms of an illnessofteo spread the disease. Vomiting, sneezing, and diarrhea are excellehods ofgetting out of one host and into position for ahe most effective strategy of all is toenlist the help of a mobile third party. Iious anisms love mosquitoes because themosquito’s sting delivers them directly to a bloodstream where they  get straight to workbefore the victim’s defense meisms  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 rapaaladies—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 owabolism. Whenthe day es that the virus mutates its way around this, we may be irouble.

    It is a mistake, however, to sider the matter too carefully from the position of logicbecause micranisms clearly are not calculatiies. 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 tinuing well-being is ofsequeo a pathogen is when it kills you too well. If they eliminate you before they move on, then they may well die out themselves. This in faetimes happens. History,Jared Diamond notes, is full of diseases that “once caused terrifying epidemid thendisappeared as mysteriously as they had e.” He cites the robust but mercifully traEnglish sweating siess, which raged from 1485 to 1552, killing tens of thousands as itwent, before burning itself out. Too much efficy is not a good thing for any iianism.

    A great deal of siess arises not because of what the anism has doo you but whatyour body is trying to do to the anism. 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 respoo iion. Sick people retire to their beds and thus areless of a threat to the wider unity. Resting also frees more of the body’s resources toattend to the iion.

    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, eachdesigo identify aroy a particular sort of invader. It would be impossibly ineffitto maintain ten million separate standing armies, so each variety of white cell keeps only afew scouts on active duty. When an iious agent—what’s known as an antigen—invades,relevant scouts identify the attacker and put out a call for reinforts of the right type.

    While your body is manufacturing these forces, you are likely to feel wretched. The o ofrecovery begins wheroops finally swing into a.

    White cells are merciless and will hunt down and kill every last pathogen they  find. Toavoid extin, attackers have evolved two elemental strategies. Either they strike quicklyand move on to a new host, as with on iious illnesses like flu, or they disguisethemselves so that the white cells fail to spot them, as with HIV, the virus responsible forAIDS, which  sit harmlessly and unnoticed in the nuclei of cells for years before springinginto a.

    One of the odder aspects of iion 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 iious diseases specialist at Dartmouth–Hitedical ter inLebanon, Nehire. “It happens all the time with car acts when people sufferinternal injuries. Microbes that are normally benign i get into other parts of thebody—the bloodstream, for instand cause terrible havoc.”

    The scariest, most out-of-trol bacterial disorder of the moment is a disease calledizing fasciitis in which bacteria essentially eat the victim from the i, devinternal tissue and leaving behind a pulpy, noxious residue. Patients often e in withparatively mild plaints—a skin rash and fever typically—but then dramaticallydeteriorate. When they are opened up it is often found that they are simply being ed.

    The only treatment is what is known as “radical excisional surgery”—cutting out every bit ofied area. Seventy pert of victims die; many of the rest are left terribly disfigured. Thesource of the iion is a mundane family of bacteria called Group A Streptococcus, whially 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 pletely resistant to antibiotics. About athousand cases a year occur in the Uates, and no one  say that it won’t get worse.

    Precisely the same thing happens with meningitis. At least 10 pert of young adults, andperhaps 30 pert of teenagers, carry the deadly meningococcal bacterium, but it lives quiteharmlessly ihroat. Just occasionally—in about one young person in a huhousand—it gets into the bloodstream and makes them very ill indeed. In the worst cases,death  e in twelve hours. That’s shogly quick. “You  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 beston against them: antibiotics. Remarkably, by oimate some 70 pert 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 iion. Such applications givebacteria every opportunity to evolve a resistao them. It is an opportunity that they haveenthusiastically seized.

    In 1952, penicillin was fully effective against all strains of staphylococcus bacteria, to su extent that by the early 1960s the U.S. surgeon general, William Stewart, felt fidentenough to declare: “The time has e to close the book on iious diseases. We havebasically wiped out iion in the Uates.” Even as he spoke, however, some 90pert of those strains were in the process of developing immunity to penicillin. Soohese rains, called Methicilliant Staphylococcus Aureus, began to show up inhospitals. Only oype of antibiotic, vany, 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 fromiions 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 panies not surprisingly opt for the latter.

    Although a few antibiotics have been toughened up a bit, the pharmaceutical industry hasn’tgiven us airely new antibiotice the 1970s.

    Our carelessness is all the more alarming sihe discovery that many other ailments maybe bacterial in in. The process of discovery began in 1983 when Barry Marshall, a doctorih, Western Australia, found that many stomach cers 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.

    Sihen further research has shown that there is or may well be a bacterial po inall kinds of other disorders—heart disease, asthma, arthritis, multiple sclerosis, several typesof mental disorders, many cers, even, it has been suggested (inSo less), obesity.

    The day may not be far off when we desperately require an effective antibiotid haven’tgot oo call on.

    It may e as a slight fort to know that bacteria  themselves get sick. They aresometimes ied 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 i and harmless. But introduce them into a suitablehost and they burst into busyness—into life. About five thousand types of virus are known,aweehey afflict us with many hundreds of diseases, ranging from the flu andon cold to those that are most invidious to human well-being: smallpox, rabies, yellowfever, ebola, polio, and the human immunodeficy virus, the source of AIDS.

    Viruses prosper by hijag the geic material of a living cell and using it to producemore virus. They reprodu a fanatical mahen burst out in searore cells toinvade. Not being living anisms themselves, they  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, muall to be seen with a ventional microscope.

    It wasn’t until 1943 and the iion of the eleicroscope that sce got its first lookat them. But they  do immense damage. Smallpox iweh tury alone killed aimated 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 e down with a strange sleeping siess, which becameknown as encephalitis lethargica. Victims would go to sleep and not wake up. They could beroused without great difficulty to take foo 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 batodeepest 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 sciousness but nottheir former liveliness. They existed in a state of profound apathy, “like extinct voloes,” inthe words of one doctor. In ten years the disease killed some five million people and thely went away. It didn’t get much lasting attention because in the meantime an <samp></samp>even worseepidemideed, the worst in history—swept across the world.

    It is sometimes called the Great Swine Flu epidemid sometimes the Great Spanish Fluepidemic, but iher 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 pert of Americasualties in the Firs<cite></cite>t World War came not from enemy fire, but from flu. In some units themortality rate was as high as 80 pert.

    Swine flu arose as a normal, hal 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 Uates, the first deaths were recorded among sailors in Boston in late August1918, but the epidemic quickly spread to all parts of the try. Schools closed, publitertais were shut down, people everywhere wore masks. It did little good. Betweeumn 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 Frand Germany.

    No one knows the global toll, as records ihird World were often poor, but it was han 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 vae, medical authorities ducted 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 wereied with ied lung tissue taken from the dead and then sprayed in the eyes, nose, andmouth with iious aerosols. If they still failed to succumb, they had their throats swabbedwith discharges taken from the sid 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 tracted the flu—not ohe 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 uood poorly or not at all. One mystery is how it eruptedsuddenly, all over, in places separated by os, mountain ranges, and other earthlyimpediments. A virus  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  all. Even in normal outbreaks, about 10 pert of people have the flubut are unaware of it because they experieno ill effects. And because they remain incirculatioend to be the great spreaders of the disease.

    That would at for the 1918 outbreak’s widespread distribution, but it still doesn’texplain how it mao lay low for several months before erupting so explosively at moreor less the same time all over. Even more mysterious is that it rimarily 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 iwenties and thirties. Olderpeople may have beed 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, a againin the 1970s. Where it went in the meantime each time is uain. One suggestion is thatviruses hide out unnoticed in populations of wild animals before trying their hand at a newgeion of humans. No one  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 teo flare up and die down again, but no one say that they aren’t quietly mutating away somewhere, or simply awaiting the rightopportunity to burst forth in a catastrophiner. It is noarent that AIDS has beenamong us much lohan anyone inally suspected. Researchers at the MaerRoyal Infirmary in England discovered that a sailor who had died of mysterious, uablecauses in 1959 in fact had AIDS. But for whatever reasons the disease remained generallyquiest for awenty years.

    The miracle is that other such diseases haven’t gone rampant. Lassa fever, which wasn’tfirst detected until 1969, i Africa, is extremely virulent and little uood. In 1969, adoctor at a Yale Uy lab in New Haven, ecticut, who was studying Lassa fevercame down with it. He survived, but, more alarmingly, a tei in a nearby lab, with nodirect exposure, also tracted the disease and died.

    Happily the outbreak stopped there, but we ’t t on such good fortune always. Ourlifestyles invite epidemics. Air travel makes it possible to spread iious agents across thepla 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 o 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 returo the Uates.

    He died in a Chicago hospital without diagnosis and without aaking any specialprecautions iing him, unaware that he had one of the most lethal and iious diseaseson the pla. Miraculously, no one else was ied. We may not be so luext time.

    And on that s ’s time to return to the world of the visibly living.

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