Cry ‘Havoc,’ and let slip the dogs of war — Julius Caesar, Act III, Scene I
A wastewater treatment plant’s job description is pretty straightforward: Remove contaminants from sewage so it can be returned to the environment without harming people or wildlife.
But a new study suggests that the treatment process can have an unintended consequence of promoting the spread of extra-hardy bacteria.
Some bugs are resistant to antibiotics, so they dodge the medical bullets that wipe out others. The more drugs that are used, the more robust they become. Since bacteria reproduce quickly – one organism might turn into a billion overnight – and they share DNA with others, antibiotic-resistant genes spread like Darwinian wildfire when conditions are right. — Scientific American, 16.4.09
The World Health Organisation has said that the E coli bacterium responsible for an outbreak that has left 17 dead and infected hundreds in Europe is a new strain that has never been seen before.
Preliminary genetic sequencing suggests that the strain is a mutant form of two different E coli bacteria, with lethal genes that could explain why the Europe-wide outbreak appears to be so big and dangerous, the agency said.
Hilde Kruse, a food safety expert at the WHO told The Associated Press that “this is a unique strain that has never been isolated from patients before”.
She added that the new strain has “various characteristics that make it more virulent and toxin-producing”. — The Grauniad, today
Two hundred thousand bacteria could easily lurk under the top half
of this semicolon; but for the sake of focussing on a subject that’s too
often out of sight and out of mind, let’s pretend otherwise. Let’s pretend
that a bacterium is about the size of a railway tank car.
Now that our fellow creature the bacterium is no longer three
microns long, but big enough to crush us, we can get a firmer mental grip
on the problem at hand. The first thing we notice is that the bacterium is
wielding long, powerful whips that are corkscrewing at a blistering
12,000 RPM. When it’s got room and a reason to move, the bacterium can
swim ten body-lengths every second. The human equivalent would be
sprinting at forty miles an hour.
The butt-ends of these spinning whips are firmly socketed inside
rotating, proton-powered, motor-hubs. It seems very unnatural for a
living creature to use rotating wheels as organs, but bacteria are serenely
untroubled by our parochial ideas of what is natural.
The bacterium, constantly chugging away with powerful interior
metabolic factories, is surrounded by a cloud of its own greasy spew. The
rotating spines, known as flagella, are firmly embedded in the bacterium’s
outer hide, a slimy, lumpy, armored bark. Studying it closely (we evade
the whips and the cloud of mucus), we find the outer cell wall to be a
double-sided network of interlocking polymers, two regular, almost
crystalline layers of macromolecular chainmail, something like a tough
The netted armor, wrinkled into warps and bumps, is studded with
hundreds of busily sucking and spewing orifices. These are the
bacterium’s “porins,” pores made from wrapped-up protein membrane,
something like damp rolled-up newspapers that protrude through the
armor into the world outside.
On our scale of existence, it would be very hard to drink through a
waterlogged rolled-up newspaper, but in the tiny world of a bacterium,
osmosis is a powerful force. The osmotic pressure inside our bacterium
can reach 70 pounds per square inch, five times atmospheric pressure.
Under those circumstances, it makes a lot of sense to be shaped like a
Our bacterium boasts strong, highly sophisticated electrochemical
pumps working through specialized fauceted porins that can slurp up and
spew out just the proper mix of materials. When it’s running its osmotic
pumps in some nutritious broth of tasty filth, our tank car can pump
enough juice to double in size in a mere twenty minutes. And there’s
more: because in that same twenty minutes, our bacterial tank car can
build in entire duplicate tank car from scratch.
Inside the outer wall of protective bark is a greasy space full of
chemically reactive goo. It’s the periplasm. Periplasm is a treacherous
mess of bonding proteins and digestive enzymes, which can yank tasty
fragments of gunk right through the exterior hide, and break them up for
further assimilation, rather like chemical teeth. The periplasm also
features chemoreceptors, the bacterial equivalent of nostrils or taste-
Beneath the periplasmic goo is the interior cell membrane, a tender
and very lively place full of elaborate chemical scaffolding, where pump
and assembly-work goes on.
Inside the interior membrane is the cytoplasm, a rich ointment of
salts, sugars, vitamins, proteins, and fats, the tank car’s refinery
If our bacterium is lucky, it has some handy plasmids in its custody.
A plasmid is an alien DNA ring, a kind of fly-by-night genetic franchise
which sets up work in the midst of somebody else’s sheltering cytoplasm.
If the bacterium is unlucky, it’s afflicted with a bacteriophage, a virus
with the modus operandi of a plasmid but its own predatory agenda.
And the bacterium has its own native genetic material. Eukaryotic
cells — we humans are made from eukaryotic cells — possess a neatly
defined nucleus of DNA, firmly coated in a membrane shell. But bacteria
are prokaryotic cells, the oldest known form of life, and they have an
attitude toward their DNA that is, by our standards, shockingly
promiscuous. Bacterial DNA simply sprawls out amid the cytoplasmic
goo like a circular double-helix of snarled and knotted Slinkies.
Any plasmid or transposon wandering by with a pair of genetic
shears and a zipper is welcome to snip some data off or zip some data in,
and if the mutation doesn’t work, well, that’s just life. A bacterium
usually has 200,000 or so clone bacterial sisters around within the space
of a pencil dot, who are more than willing to take up the slack from any
failed experiment in genetic recombination. When you can clone yourself
every twenty minutes, shattering the expected laws of Darwinian heredity
merely adds spice to life.
Bacteria live anywhere damp. In water. In mud. In the air, as
spores and on dust specks. In melting snow, in boiling volcanic springs. In
the soil, in fantastic numbers. All over this planet’s ecosystem, any liquid
with organic matter, or any solid foodstuff with a trace of damp in it,
anything not salted, mummified, pickled, poisoned, scorching hot or frozen
solid, will swarm with bacteria if exposed to air. Unprotected food
always spoils if it’s left in the open. That’s such a truism of our lives
that it may seem like a law of physics, something like gravity or entropy;
but it’s no such thing, it’s the relentless entrepreneurism of invisible
organisms, who don’t have our best interests at heart.
Bacteria live on and inside human beings. They always have;
bacteria were already living on us long, long before our species became
human. They creep onto us in the first instants in which we are held to
our mother’s breast. They live on us, and especially inside us, for as long
as we live. And when we die, then other bacteria do their living best to
An adult human being carries about a solid pound of commensal
bacteria in his or her body; about a hundred trillion of them. Humans have
a whole garden of specialized human-dwelling bacteria — tank-car E. coli,
balloon-shaped staphylococcus, streptococcus, corynebacteria,
micrococcus, and so on. Normally, these lurkers do us little harm. On the
contrary, our normal human-dwelling bacteria run a kind of protection
racket, monopolizing the available nutrients and muscling out other rival
bacteria that might want to flourish at our expense in a ruder way.
But bacteria, even the bacteria that flourish inside us all our lives,
are not our friends. Bacteria are creatures of an order vastly different
from our own, a world far, far older than the world of multicellular
mammals. Bacteria are vast in numbers, and small, and fetid, and
So our tank car is whipping through its native ooze, shuddering from
the jerky molecular impacts of Brownian motion, hunting for a
chemotactic trail to some richer and filthier hunting ground, and
periodically peeling off copies of itself. It’s an enormously fast-paced
and frenetic existence. Bacteria spend most of their time starving,
because if they are well fed, then they double in number every twenty
minutes, and this practice usually ensures a return to starvation in pretty
short order. There are not a lot of frills in the existence of bacteria.
Bacteria are extremely focussed on the job at hand. Bacteria make ants
look like slackers.
And so it went in the peculiar world of our acquaintance the tank
car, a world both primitive and highly sophisticated, both frenetic and
utterly primeval. Until an astonishing miracle occurred. The miracle of
“miracle drugs,” antibiotics.
Sir Alexander Fleming discovered penicillin in 1928, and the power
of the sulfonamides was recognized by drug company researchers in 1935,
but antibiotics first came into general medical use in the 1940s and 50s.
The effects on the hidden world of bacteria were catastrophic. Bacteria
which had spent many contented millennia decimating the human race
were suddenly and swiftly decimated in return. The entire structure of
human mortality shifted radically, in a terrific attack on bacteria from
the world of organized intelligence.
At the beginning of this century, back in the pre-antibiotic year of
1900, four of the top ten leading causes of death in the United States
were bacterial. The most prominent were tuberculosis (“the white
plague,” Mycobacterium tuberculosis) and pneumonia (Streptococcus
pneumoniae, Pneumococcus). The death rate in 1900 from
gastroenteritis (Escherichia coli, various Campylobacter species,
etc.) was higher than that for heart disease. The nation’s number ten
cause of death was diphtheria (Corynebacterium diphtheriae). Bringing
up the bacterial van were gonorrhea, meningitis, septicemia, dysentery,
typhoid fever, whooping cough, and many more.
At the end of the century, all of these festering bacterial afflictions
(except pneumonia) had vanished from the top ten. They’d been replaced
by heart disease, cancer, stroke, and even relative luxuries of
post-industrial mortality, such as accidents, homicide and suicide. All
thanks to the miracle of antibiotics.
Penicillin in particular was a chemical superweapon of devastating
power. In the early heyday of penicillin, the merest trace of this
substance entering a cell would make the hapless bacterium literally
burst. This effect is known as “lysing.”
Penicillin makes bacteria lyse because of a chemical structure
called “beta-lactam.” Beta-lactam is a four-membered cyclic amide ring,
a molecular ring which bears a fatal resemblance to the chemical
mechanisms a bacterium uses to build its cell wall.
Bacterial cell walls are mostly made from peptidoglycan, a plastic-
like molecule chained together to form a tough, resilient network. A
bacterium is almost always growing, repairing damage, or reproducing,
so there are almost always raw spots in its cell wall that require
It’s a sophisticated process. First, fragments of not-yet-peptided
glycan are assembled inside the cytoplasm. Then the glycan chunks are
hauled out to the cell wall by a chemical scaffolding of lipid carrier
molecules, and they are fitted in place. Lastly, the peptidoglycan is
busily knitted together by catalyzing enzymes and set to cure.
But beta-lactam is a spanner in the knitting-works, which attacks
the enzyme which links chunks of peptidoglycan together. The result is
like building a wall of bricks without mortar; the unlinked chunks of
glycan break open under osmotic pressure, and the cell spews out its
innards catastrophically, and dies.
Gram-negative bacteria, of the tank-car sort we have been
describing, have a double cell wall, with an outer armor plus the inner cell
membrane, rather like a rubber tire with an inner tube. They can
sometimes survive a beta-lactam attack, if they don’t leak to death. But
gram-positive bacteria are more lightly built and rely on a single wall
only, and for them a beta-lactam puncture is a swift kiss of death.
Beta-lactam can not only mimic, subvert and destroy the assembly
enzymes, but it can even eat away peptide-chain mortar already in place.
And since mammalian cells never use any peptidoglycans, they are never
ruptured by penicillin (although penicillin does sometimes provoke serious
allergic reactions in certain susceptible patients).
Pharmaceutical chemists rejoiced at this world-transforming
discovery, and they began busily tinkering with beta-lactam products,
discovering or producing all kinds of patentable, marketable, beta-lactam
variants. Today there are more than fifty different penicillins and
seventy-five cephalosporins, all of which use beta-lactam rings in one
form or another.
The enthusiastic search for new medical miracles turned up
substances that attack bacteria through even more clever methods.
Antibiotics were discovered that could break-up or jam-up a cell’s protein
synthesis; drugs such as tetracycline, streptomycin, gentamicin, and
chloramphenicol. These drugs creep through the porins deep inside the
cytoplasm and lock onto the various vulnerable sites in the RNA protein
factories. This RNA sabotage brings the cell’s basic metabolism to a
seething halt, and the bacterium chokes and dies.
The final major method of antibiotic attack was an assault on
bacterial DNA. These compounds, such as the sulphonamides, the
quinolones, and the diaminopyrimidines, would gum up bacterial DNA
itself, or break its strands, or destroy the template mechanism that reads
from the DNA and helps to replicate it. Or, they could ruin the DNA’s
nucleotide raw materials before those nucleotides could be plugged into
the genetic code. Attacking bacterial DNA itself was the most
sophisticated attack yet on bacteria, but unfortunately these DNA
attackers often tended to be toxic to mammalian cells as well. So they
saw less use. Besides, they were expensive.
In the war between species, humanity had found a full and varied
arsenal. Antibiotics could break open cell walls, choke off the life-giving
flow of proteins, and even smash or poison bacterial DNA, the central
command and control center. Victory was swift, its permanence seemed
assured, and the command of human intellect over the realm of brainless
germs was taken for granted. The world of bacteria had become a
commercial empire for exploitation by the clever mammals.
Antibiotic production, marketing and consumption soared steadily.
Nowadays, about a hundred thousand tons of antibiotics are
manufactured globally every year. It’s a five billion dollar market.
Antibiotics are cheap, far cheaper than time-consuming, labor-intensive
hygienic cleanliness. In many countries, these miracle drugs are routinely
retailed in job-lots as over-the-counter megadosage nostrums.
Nor have humans been the only mammals to benefit. For decades,
antibiotics have been routinely fed to American livestock. Antibiotics
are routinely added to the chow in vast cattle feedlots, and antibiotics are
fed to pigs, even chickens. This practice goes on because a meat animal
on antibiotics will put on poundage faster, and stay healthier, and supply
the market with cheaper meat. Repeated protests at this practice by
American health authorities have been successfully evaded in courts and
in Congress by drug manufacturers and agro-business interests.
The runoff of tainted feedlot manure, containing millions of pounds
of diluted antibiotics, enters rivers and watersheds where the world’s
free bacteria dwell.
In cities, municipal sewage systems are giant petri-dishes of
diluted antibiotics and human-dwelling bacteria.
Bacteria are restless. They will try again, every twenty minutes.
And they never sleep.
Experts were aware in the 1940s and 1950s that bacteria could, and
would, mutate in response to selection pressure, just like other
organisms. And they knew that bacteria went through many generations
very rapidly, and that bacteria were very fecund. But it seemed that any
bacteria would be very lucky to mutate to successfully resist even one
antibiotic. Compounding that luck by evolving to resist two antibiotics at
once seemed well-nigh impossible. Bacteria were at our mercy. They
didn’t seem any more likely to resist penicillin and tetracycline than a
rainforest can resist bulldozers and chainsaws.
However, thanks to convenience and the profit motive, once-
miraculous antibiotics had become a daily commonplace. A general
chemical haze of antibiotic pollution spread across the planet. Titanic
numbers of bacteria, in all niches of bacterial life, were being given an
enormous number of chances to survive antibiotics.
Worse yet, bacteriologists were simply wrong about the way that
bacteria respond to a challenge.
Bacteria will try anything. Bacteria don’t draw hard and fast
intellectual distinctions between their own DNA, a partner’s DNA, DNA
from another species, virus DNA, plasmid DNA, and food.
This property of bacteria is very alien to the human experience. If
your lungs were damaged from smoking, and you asked your dog for a
spare lung, and your dog, in friendly fashion, coughed up a lung and gave
it to you, that would be quite an unlikely event. It would be even more
miraculous if you could swallow a dog’s lung and then breathe with it just
fine, while your dog calmly grew himself a new one. But in the world of
bacteria this kind of miracle is a commonplace.
Bacteria share enormous amounts of DNA. They not only share
DNA among members of their own species, through conjugation and
transduction, but they will encode DNA in plasmids and transposons and
packet-mail it to other species. They can even find loose DNA lying
around from the burst bodies of other bacteria, and they can eat that DNA
like food and then make it work like information. Pieces of stray DNA can
be swept all willy-nilly into the molecular syringes of viruses, and
injected randomly into other bacteria. This fetid orgy isn’t what Gregor
Mendel had in mind when he was discovering the roots of classical genetic
inheritance in peas, but bacteria aren’t peas, and don’t work like peas, and
never have. Bacteria do extremely strange and highly inventive things
with DNA, and if we don’t understand or sympathize, that’s not their
problem, it’s ours.
Some of the best and cleverest information-traders are some of the
worst and most noxious bacteria. Such as Staphylococcus (boils).
Haemophilus (ear infections). Neisseria (gonorrhea).
Pseudomonas (abcesses, surgical infections). Even Escherichia, a very
common human commensal bacterium.
When it comes to resisting antibiotics, bacteria are all in the effort
together. That’s because antibiotics make no distinctions in the world of
bacteria. They kill, or try to kill, every bacterium they touch.
If you swallow an antibiotic for an ear infection, the effects are not
confined to the tiny minority of toxic bacteria that happen to be inside
your ear. Every bacterium in your body is assaulted, all hundred trillion
of them. The toughest will not only survive, but they will carefully store,
and sometimes widely distribute, the genetic information that allowed
them to live.
The resistance from bacteria, like the attack of antibiotics, is a
multi-pronged and sophisticated effort. It begins outside the cell, where
certain bacteria have learned to spew defensive enzymes into the cloud of
slime that surrounds them — enzymes called beta-lactamases,
specifically adapted to destroy beta-lactam, and render penicillin useless.
At the cell-wall itself, bacteria have evolved walls that are tougher and
thicker, less likely to soak up drugs. Other bacteria have lost certain
vulnerable porins, or have changed the shape of their porins so that
antibiotics will be excluded instead of inhaled.
Inside the wall of the tank car, the resistance continues. Bacteria
make permanent stores of beta-lactamases in the outer goo of periplasm,
which will chew the drugs up and digest them before they ever reach the
vulnerable core of the cell. Other enzymes have evolved that will crack
or chemically smother other antibiotics.
In the pump-factories of the inner cell membrane, new pumps have
evolved that specifically latch on to antibiotics and spew them back out
of the cell before they can kill. Other bacteria have mutated their interior
protein factories so that the assembly-line no longer offers any sabotage-
sites for site-specific protein-busting antibiotics. Yet another strategy
is to build excess production capacity, so that instead of two or three
assembly lines for protein, a mutant cell will have ten or fifty, requiring
ten or fifty times as much drug for the same effect. Other bacteria have
come up with immunity proteins that will lock-on to antibiotics and make
them useless inert lumps.
Sometimes — rarely — a cell will come up with a useful mutation
entirely on its own. The theorists of forty years ago were right when they
thought that defensive mutations would be uncommon. But spontaneous
mutation is not the core of the resistance at all. Far more often, a
bacterium is simply let in on the secret through the exchange of genetic
Beta-lactam is produced in nature by certain molds and fungi; it was
not invented from scratch by humans, but discovered in a petri dish. Beta-
lactam is old, and it would seem likely that beta-lactamases are also very
Bacteriologists have studied only a few percent of the many
microbes in nature. Even those bacteria that have been studied are by no
means well understood. Antibiotic resistance genes may well be present
in any number of different species, waiting only for selection pressure to
manifest themselves and spread through the gene-pool.
If penicillin is sprayed across the biosphere, then mass death of
bacteria will result. But any bug that is resistant to penicillin will
swiftly multiply by millions of times, thriving enormously in the power-
vacuum caused by the slaughter. The genes that gave the lucky winner its
resistance will also increase by millions of times, becoming far more
generally available. And there’s worse: because often the resistance is
carried by plasmids, and one single bacterium can contain as many as a
thousand plasmids, and produce them and spread them at will.
That genetic knowledge, once spread, will likely stay around a while.
Bacteria don’t die of old age. Bacteria aren’t mortal in the sense that we
understand mortality. Unless they are killed, bacteria just keep splitting
and doubling. The same bacterial “individual” can spew copies of itself
every twenty minutes, basically forever. After billions of generations,
and trillions of variants, there are still likely to be a few random
old-timers around identical to ancestors from some much earlier epoch.
Furthermore, spores of bacteria can remain dormant for centuries, then
sprout in seconds and carry on as if nothing had happened. This gives the
bacterial gene-pool — better described as an entire gene-ocean — an
enormous depth and range. It’s as if Eohippus could suddenly show up at
the Kentucky Derby — and win.
It seems likely that many of the mechanisms of bacterial resistance
were borrowed or kidnapped from bacteria that themselves produce
antibiotics. The genus Streptomyces, which are filamentous, Gram-
positive bacteria, are ubiquitous in the soil; in fact the characteristic
“earthy” smell of fresh soil comes from Streptomyces’ metabolic products.
And Streptomyces bacteria produce a host of antibiotics, including
streptomycin, tetracycline, neomycin, chloramphenicol, and erythromycin.
Human beings have been using streptomycin’s antibiotic poisons
against tuberculosis, gonorrhea, rickettsia, chlamydia, and candida yeast
infection, with marked success. But in doing so, we have turned a small-
scale natural process into a massive industrial one.
Streptomyces already has the secret of surviving its own poisons.
So, presumably, do at least some of streptomyces’s neighbors. If the
poison is suddenly broadcast everywhere, through every niche in the
biosphere, then word of how to survive it will also get around.
And when the gospel of resistance gets around, it doesn’t come just
one chapter at a time. Scarily, it tends to come in entire libraries. A
resistance plasmid (familiarly known to researchers as “R-plasmids,”
because they’ve become so common) doesn’t have to specialize in just one
antibiotic. There’s plenty of room inside a ring of plasmid DNA for handy
info on a lot of different products and processes. Moving data on and off
the plasmid is not particularly difficult. Bacterial scissors-and-zippers
units known as “transposons” can knit plasmid DNA right into the central
cell DNA — or they can transpose new knowledge onto a plasmid. These
segments of loose DNA are aptly known as “cassettes.”
So when a bacterium is under assault by an antibiotic, and it
acquires a resistance plasmid from who-knows where, it can suddenly
find an entire arsenal of cassettes in its possession. Not just resistance
to the one antibiotic that provoked the response, but a whole Bible of
resistance to all the antibiotics lately seen in the local microworld.
Even more unsettling news has turned up in a lab report in the
Journal of Bacteriology from 1993. Tetracycline-resistant strains in the
bacterium Bacteroides have developed a kind of tetracycline reflex.
Whenever tetracycline appears in the neighborhood, a Bacteroides
transposon goes into overdrive, manufacturing R-plasmids at a frantic
rate and then passing them to other bacteria in an orgy of sexual
encounters a hundred times more frequent than normal. In other words,
tetracycline itself now directly causes the organized transfer of
resistance to tetracycline. As Canadian microbiologist Julian Davies
commented in Science magazine (15 April 1994), “The extent and
biochemical nature of this phenomenon is not well understood. A number
of different antibiotics have been shown to promote plasmid transfer
between different bacteria, and it might even be considered that some
antibiotics are bacterial pheromones.”
If this is the case, then our most potent chemical weapons have been
changed by our lethal enemies into sexual aphrodisiacs.
The greatest battlegrounds of antibiotic warfare today are
hospitals. The human race is no longer winning. Increasingly, to enter a
hospital can make people sick. This is known as “nosocomial infection,”
from the Latin for hospital. About five percent of patients who enter
hospitals nowadays pick up an infection from inside the hospital itself.
An epidemic of acquired immune deficiency has come at a
particularly bad time, since patients without natural immunity are forced
to rely heavily on megadosages of antibiotics. These patients come to
serve as reservoirs for various highly resistant infections. So do patients
whose immune systems have been artificially repressed for organ
transplantion. The patients are just one aspect of the problem, though;
healthy doctors and nurses show no symptoms, but they can carry strains
of hospital superbug from bed to bed on their hands, deep in the pores of
their skin, and in their nasal passages. Superbugs show up in food, fruit
juices, bedsheets, even in bottles and buckets of antiseptics.
The advent of antibiotics made elaborate surgical procedures safe
and cheap; but nowadays half of nosocomial infections are either surgical
infections, or urinary tract infections from contaminated catheters.
Bacteria are attacking us where we are weakest and most vulnerable, and
where their own populations are the toughest and most battle-hardened.
From hospitals, resistant superbugs travel to old-age homes and day-care
centers, predating on the old and the very young.
Staphylococcus aureus, a common hospital superbug which
causes boils and ear infections, is now present in super-strains highly
resistant to every known antibiotic except vancomycin. Enterococcus is
resistant to vancomycin, and it has been known to swap genes with
staphylococcus. If staphylococcus gets hold of this resistance
information, then staph could become the first bacterial superhero of the
post-antibiotic era, and human physicians of the twenty-first century
would be every bit as helpless before it as were physicians of the 19th. In
the 19th century physicians dealt with septic infection by cutting away
the diseased flesh and hoping for the best.
Staphylococcus often lurks harmlessly in the nose and throat.
Staphylococcus epidermis, a species which lives naturally on human
skin, rarely causes any harm, but it too must battle for its life when
confronted with antibiotics. This harmless species may serve as a
reservoir of DNA data for the bacterial resistance of other, truly lethal
bacteria. Certain species of staph cause boils, others impetigo. Staph
attacking a weakened immune system can kill, attacking the lungs
(pneumonia) and brain (meningitis). Staph is thought to cause toxic shock
syndrome in women, and toxic shock in post-surgical patients.
A 1994 outbreak of an especially virulent strain of the common
bacterium Streptococcus, “necrotizing fasciitis,” caused panic headlines
in Britain about “flesh-eating germs” and “killer bugs.” Of the fifteen
reported victims so far, thirteen have died.
A great deal has changed since the 1940s and 1950s. Strains of
bacteria can cross the planet with the speed of jet travel, and populations
of humans — each with their hundred trillion bacterial passengers —
mingle as never before. Old-fashioned public-health surveillance
programs, which used to closely study any outbreak of bacterial disease,
have been dismantled, or put in abeyance, or are underfunded. The
seeming triumph of antibiotics has made us careless about the restive
conquered population of bacteria.
Drug companies treat the standard antibiotics as cash cows, while
their best-funded research efforts currently go into antiviral and
antifungal compounds. Drug companies follow the logic of the market;
with hundreds of antibiotics already cheaply available, it makes little
commercial sense to spend millions developing yet another one. And the
market is not yet demanding entirely new antibiotics, because the
resistance has not quite broken out into full-scale biological warfare.
And drug research is expensive and risky. A hundred million dollars of
investment in antibiotics can be wiped out by a single point-mutation in a
We did manage to kill off the smallpox virus, but none of humanity’s
ancient bacterial enemies are extinct. They are all still out there, and
they all still kill people. Drug companies mind their cash flow, health
agencies become complacent, people mind what they think is their own
business, but bacteria never give up. Bacteria have learned to chew up,
spit out, or shield themselves from any and every drug we can throw at
them. They can now defeat every technique we have. The only reason true
disaster hasn’t broken out is because all bacteria can’t all defeat all the
techniques all at once. Yet.
There have been no major conceptual breakthroughs lately in the
antibiotic field. There has been some encouraging technical news, with
new techniques such as rational drug design and computer-assisted
combinatorial chemistry. There may be entirely new miracle drugs just
over the horizon that will fling the enemy back once again, with enormous
losses. But on the other hand, there may well not be. We may already
have discovered all the best antibiotic tricks available, and squandered
them in a mere fifty years.
Anyway, now that the nature of their resistance is better
understood, no bacteriologist is betting that any new drug can foil our
ancient enemies for very long. Bacteria are better chemists than we are
and they don’t get distracted.
If the resistance triumphs, it does not mean the outbreak of
universally lethal plagues or the end of the human race. It is not an
apocalyptic problem. What it would really mean — probably — is a slow
return, over decades, to the pre-antibiotic bacterial status-quo. A return
to the bacterial status-quo of the nineteenth century.
For us, the children of the miracle, this would mean a truly shocking
decline in life expectancy. Infant mortality would become very high; it
would once again be common for parents to have five children and lose
three. It would mean a return to epidemic flags, quarantine camps,
tubercular sanatariums, and leprosariums.
Cities without good sanitation — mostly Third World cities —
would suffer from water-borne plagues such as cholera and dysentery.
Tuberculosis would lay waste the underclass around the world. If you cut
yourself at all badly, or ate spoiled food, there would be quite a good
chance that you would die. Childbirth would be a grave septic risk for the
The practice of medicine would be profoundly altered. Elaborate,
high-tech surgical procedures, such as transplants and prosthetic
implants, would become extremely risky. The expense of any kind of
surgery would soar, since preventing infection would be utterly necessary
but very tedious and difficult. A bad heart would be a bad heart for life,
and a shattered hip would be permanently disabling. Health-care budgets
would be consumed by antiseptic and hygienic programs.
Life without contagion and infection would seem as quaintly exotic
as free love in the age of AIDS. The decline in life expectancy would
become just another aspect of broadly diminishing cultural expectations
in society, economics, and the environment. Life in the developed world
would become rather pinched, wary, and nasty, while life in the
overcrowded human warrens of the megalopolitan Third World would
become an abattoir.
If this all seems gruesomely plausible, it’s because that’s the way
our ancestors used to live all the time. It’s not a dystopian fantasy; it
was the miracle of antibiotics that was truly fantastic. It that miracle
died away, it would merely mean an entirely natural return to the normal
balance of power between humanity and our invisible predators.
At the close of this century, antibiotic resistance is one of the
gravest threats that confronts the human race. It ranks in scope with
overpopulation, nuclear disaster, destruction of the ozone, global
warming, species extinction and massive habitat destruction. Although it
gains very little attention in comparison to those other horrors, there is
nothing theoretical or speculative about antibiotic resistance. The mere
fact that we can’t see it happening doesn’t mean that it’s not taking place.
It is occurring, stealthily and steadily, in a world which we polluted
drastically before we ever took the trouble to understand it.
We have spent billions to kill bacteria but mere millions to truly
comprehend them. In our arrogance, we have gravely underestimated our
enemy’s power and resourcefulness. Antibiotic resistance is a very real
threat which is well documented and increasing at considerable speed. In
its scope and its depth and the potential pain and horror of its
implications, it may the greatest single menace that we human beings
confront — besides, of course, the steady increase in our own numbers.
And if we don’t somehow resolve our grave problems with bacteria, then
bacteria may well resolve that population problem for us.