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Antimicrobial

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Last year an event doctors had been fearing finally occurred. In three geographically sepa-
rate patients, an often deadly bacterium,
Staphylococcus aureus, responded poor-
ly to a once reliable antidote—the anti-
biotic vancomycin. Fortunately, in those
patients, the staph microbe remained
susceptible to other drugs and was erad-
icated. But the appearance of S. aureus
not readily cleared by vancomycin fore-
shadows trouble.

Worldwide, many strains of S. aureus
are already resistant to all antibiotics ex-
cept vancomycin. Emergence of forms
lacking sensitivity to vancomycin sig-
nifies that variants untreatable by every
known antibiotic are on their way. S.

aureus, a major cause of hospital-ac-
quired infections, has thus moved one
step closer to becoming an unstoppable
killer.

The looming threat of incurable S.
aureus is just the latest twist in an inter-
national public health nightmare: in-
creasing bacterial resistance to many an-
tibiotics that once cured bacterial dis-
eases readily. Ever since antibiotics
became widely available in the 1940s,
they have been hailed as miracle drugs—
magic bullets able to eliminate bacteria
without doing much harm to the cells
of treated individuals. Yet with each
passing decade, bacteria that defy not
only single but multiple antibiotics—and
therefore are extremely difficult to con-

trol—have become increasingly common.
What is more, strains of at least three

bacterial species capable of causing life-
threatening illnesses (Enterococcus fae-
calis, Mycobacterium tuberculosis and
Pseudomonas aeruginosa) already evade
every antibiotic in the clinician’s arma-
mentarium, a stockpile of more than
100 drugs. In part because of the rise in
resistance to antibiotics, the death rates
for some communicable diseases (such
as tuberculosis) have started to rise
again, after having declined in the in-
dustrial nations.

How did we end up in this worrisome,
and worsening, situation? Several inter-
acting processes are at fault. Analyses of
them point to a number of actions that

The Challenge of Antibiotic Resistance

The Challenge
of Antibiotic Resistance

Certain bacterial infections now defy all antibiotics. The resistance
problem may be reversible, but only if society begins to consider how

the drugs affect “good” bacteria as well as “bad”

by Stuart B. Levy

Staphylococcus aureus

Causes blood poisoning,
wound infections and pneumo-

nia; in some hospitals, more
than 60 percent of strains are
resistant to methicillin; some
are poised for resistance to all

antibiotics (H/C; 1950s)

Acinetobacter

Causes blood poisoning
in patients with compromised

immunity (H, 1990s)

Enterococcus faecalis

Causes blood poisoning and
urinary tract and wound

infections in patients with
compromised immunity; some
multidrug-resistant strains are

untreatable (H, 1980s)

Haemophilus
influenzae

Causes pneumonia, ear
infections and meningitis,
especially in children. Now

largely preventable by
vaccines (C; 1970s)

Neisseria gonorrhoeae

Causes gonorrhea;
multidrug resistance now

limits therapy chiefly to
cephalosporins (C; 1970s)

46 Scientific American March 1998

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Copyright 1998 Scientific American, Inc.

could help reverse the trend, if individu-
als, businesses and governments around
the world can find the will to imple-
ment them.

One component of the solution is rec-
ognizing that bacteria are a natural, and
needed, part of life. Bacteria, which are
microscopic, single-cell entities, abound
on inanimate surfaces and on parts of
the body that make contact with the
outer world, including the skin, the mu-
cous membranes and the lining of the
intestinal tract. Most live blamelessly. In
fact, they often protect us from disease,
because they compete with, and thus
limit the proliferation of, pathogenic
bacteria—the minority of species that
can multiply aggressively (into the mil-
lions) and damage tissues or otherwise
cause illness. The benign competitors
can be important allies in the fight
against antibiotic-resistant pathogens.

People should also realize that al-
though antibiotics are needed to control
bacterial infections, they can have broad,
undesirable effects on microbial ecolo-
gy. That is, they can produce long-lasting
change in the kinds and proportions of
bacteria—and the mix of antibiotic-re-
sistant and antibiotic-susceptible types—
not only in the treated individual but
also in the environment and society at
large. The compounds should thus be
used only when they are truly needed,

and they should not be administered for
viral infections, over which they have no
power.

A Bad Combination

Although many factors can influence whether bacteria in a person or in
a community will become insensitive to
an antibiotic, the two main forces are
the prevalence of resistance genes (which
give rise to proteins that shield bacteria
from an antibiotic’s effects) and the ex-
tent of antibiotic use. If the collective
bacterial flora in a community have no
genes conferring resistance to a given
antibiotic, the antibiotic will successful-
ly eliminate infection caused by any of
the bacterial species in the collection.
On the other hand, if the flora possess
resistance genes and the community uses
the drug persistently, bacteria able to
defy eradication by the compound will
emerge and multiply.

Antibiotic-resistant pathogens are not
more virulent than susceptible ones: the
same numbers of resistant and suscepti-
ble bacterial cells are required to pro-
duce disease. But the resistant forms are
harder to destroy. Those that are slight-
ly insensitive to an antibiotic can often
be eliminated by using more of the
drug; those that are highly resistant re-
quire other therapies.

To understand how resistance genes
enable bacteria to survive an attack by
an antibiotic, it helps to know exactly
what antibiotics are and how they harm
bacteria. Strictly speaking, the com-
pounds are defined as natural substan-
ces (made by living organisms) that in-
hibit the growth, or proliferation, of bac-
teria or kill them directly. In practice,
though, most commercial antibiotics
have been chemically altered in the lab-
oratory to improve their potency or to
increase the range of species they affect.
Here I will also use the term to encom-
pass completely synthetic medicines,
such as quinolones and sulfonamides,
which technically fit under the broader
rubric of antimicrobials.

Whatever their monikers, antibiotics,
by inhibiting bacterial growth, give a
host’s immune defenses a chance to out-
flank the bugs that remain. The drugs
typically retard bacterial proliferation
by entering the microbes and interfer-
ing with the production of components
needed to form new bacterial cells. For
instance, the antibiotic tetracycline binds
to ribosomes (internal structures that
make new proteins) and, in so doing,
impairs protein manufacture; penicillin
and vancomycin impede proper synthe-
sis of the bacterial cell wall.

Certain resistance genes ward off de-
struction by giving rise to enzymes that

The Challenge of Antibiotic Resistance

ROGUE’S GALLERY OF BACTERIA features some types hav-
ing variants resistant to multiple antibiotics; multidrug-resistant
bacteria are difficult and expensive to treat. Certain strains of
the species described in red no longer respond to any antibiotics
and produce incurable infections. Some of the bacteria cause in-

fections mainly in hospitals (H) or mainly in the community (C);
others, in both settings. The decade listed with each entry indi-
cates the period when resistance first became a significant prob-
lem for patient care. The bacteria, which are microscopic, are
highly magnified in these false-color images.

Mycobacterium
tuberculosis

Causes tuberculosis;
some multidrug-resistant

strains are untreatable
(H/C; 1970s)

Pseudomonas
aeruginosa

Causes blood poisoning and
pneumonia, especially in

people with cystic fibrosis or
compromised immunity; some
multidrug-resistant strains are

untreatable (H/C; 1960s)

Escherichia coli

Causes urinary tract infections,
blood poisoning, diarrhea and

kidney failure; some strains that
cause urinary tract infections

are multidrug-resistant
(H/C; 1960s)

Scientific American March 1998 47

Shigella dysenteria

Causes dysentery (bloody
diarrhea); resistant strains have
led to epidemics, and some can

be treated only by expensive
fluoroquinolones, which are

often unavailable in developing
nations (C; 1960s)

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Streptococcus
pneumoniae

Causes blood poisoning,
middle ear infections,

pneumonia and meningitis
(C; 1970s)

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Copyright 1998 Scientific American, Inc.

degrade antibiotics or that chemically
modify, and so inactivate, the drugs. Al-
ternatively, some resistance genes cause
bacteria to alter or replace molecules
that are normally bound by an antibiot-
ic—changes that essentially eliminate
the drug’s targets in bacterial cells. Bac-
teria might also eliminate entry ports
for the drugs or, more effectively, may
manufacture pumps that export antibi-
otics before the medicines have a chance
to find their intracellular targets.

My Resistance Is Your Resistance

Bacteria can acquire resistance genesthrough a few routes. Many inherit
the genes from their forerunners. Other
times, genetic mutations, which occur
readily in bacteria, will spontaneously

produce a new resistance
trait or will strengthen an
existing one. And frequently,
bacteria will gain a defense
against an antibiotic by tak-
ing up resistance genes from
other bacterial cells in the vi-
cinity. Indeed, the exchange
of genes is so pervasive that
the entire bacterial world can
be thought of as one huge
multicellular organism in
which the cells interchange
their genes with ease.

Bacteria have evolved several ways to
share their resistance traits with one an-
other [see “Bacterial Gene Swapping in
Nature,” by Robert V. Miller; Scien-
tific American, January]. Resistance
genes commonly are carried on plas-

mids, tiny loops of DNA that can help
bacteria survive various hazards in the
environment. But the genes may also
occur on the bacterial chromosome, the
larger DNA molecule that stores the
genes needed for the reproduction and
routine maintenance of a bacterial cell.

48 Scientific American March 1998 The Challenge of Antibiotic Resistance

The Antibacterial Fad:
A New Threat

Antibiotics are not the only antimicro-bial substances being overexploit-
ed today. Use of antibacterial agents—
compounds that kill or inhibit bacteria
but are too toxic to be taken internally—

has been skyrocketing as well. These compounds, also known as
disinfectants and antiseptics, are applied to inanimate objects or
to the skin.

Historically, most antibacterials were used in hospitals, where
they were incorporated into soaps and surgical clothes to limit
the spread of infections. More recently, however, those sub-
stances (including triclocarbon, triclosan and such quaternary
ammonium compounds as benzalkonium chloride) have been
mixed into soaps, lotions and dishwashing detergents meant for
general consumers. They have also been impregnated into such
items as toys, high chairs, mattress pads and cutting boards.

There is no evidence that the addition of antibacterials to such
household products wards off infection. What is clear, however,
is that the proliferation of products containing them raises pub-
lic health concerns.

Like antibiotics, antibacterials can alter the mix of bacteria:
they simultaneously kill susceptible bacteria and promote the
growth of resistant strains. These resistant microbes may include
bacteria that were present from the start. But they can also in-
clude ones that were unable to gain a foothold previously and
are now able to thrive thanks to the destruction of competing

microbes. I worry particularly about that second group—the in-
terlopers—because once they have a chance to proliferate,
some may become new agents of disease.

The potential overuse of antibacterials in the home is trou-
bling on other grounds as well. Bacterial genes that confer resis-
tance to antibacterials are sometimes carried on plasmids (cir-
cles of DNA) that also bear antibiotic-resistance genes. Hence, by
promoting the growth of bacteria bearing such plasmids, an-
tibacterials may actually foster double resistance—to antibiotics
as well as antibacterials.

Routine housecleaning is surely necessary. But standard soaps
and detergents (without added antibacterials) decrease the
numbers of potentially troublesome bacteria perfectly well. Sim-
ilarly, quickly evaporating chemicals—such as the old standbys
of chlorine bleach, alcohol, ammonia and hydrogen peroxide—
can be applied beneficially. They remove potentially disease-
causing bacteria from, say, thermometers or utensils used to pre-
pare raw meat for cooking, but they do not leave long-lasting
residues that will continue to kill benign bacteria and increase
the growth of resistant strains long after target pathogens have
been removed.

If we go overboard and try to establish a sterile environment,
we will find ourselves cohabiting with bacteria that are highly re-
sistant to antibacterials and, possibly, to antibiotics. Then, when
we really need to disinfect our homes and hands—as when a
family member comes home from a hospital and is still vulnera-
ble to infection—we will encounter mainly resistant bacteria. It is
not inconceivable that with our excessive use of antibacterials
and antibiotics, we will make our homes, like our hospitals,
havens of ineradicable disease-producing bacteria. —S.B.L.

ANTIBIOTIC

ANTIBIOTIC

ANTIBIOTIC-
RESISTANCE
GENES

PLASMID

ANTIBIOTIC

ANTIBIOTIC-
ALTERING

ENZYME
BACTERIAL

CELL

CHROMOSOME

ANTIBIOTIC-
DEGRADING
ENZYME

ANTIBIOTIC-
EFFLUX PUMP

b

a

c

ANTIBIOTIC-RESISTANT BACTERIA owe their drug insensitivity to re-
sistance genes. For example, such genes might code for “efflux” pumps that
eject antibiotics from cells (a). Or the genes might give rise to enzymes that
degrade the antibiotics (b) or that chemically alter—and inactivate—the
drugs (c). Resistance genes can reside on the bacterial chromosome or, more
typically, on small rings of DNA called plasmids. Some of the genes are in-
herited, some emerge through random mutations in bacterial DNA, and
some are imported from other bacteria.

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Copyright 1998 Scientific American, Inc.

Often one bacterium will pass resis-
tance traits to others by giving them a
useful plasmid. Resistance genes can
also be transferred by viruses that occa-
sionally extract a gene from one bacte-
rial cell and inject it into a different one.
In addition, after a bacterium dies and
releases its contents into the environ-
ment, another will occasionally take up
a liberated gene for itself.

In the last two situations, the gene will
survive and provide protection from an
antibiotic only if integrated stably into
a plasmid or chromosome. Such inte-
gration occurs frequently, though, be-
cause resistance genes are often embed-
ded in small units of DNA, called trans-
posons, that readily hop into other DNA
molecules. In a regrettable twist of fate
for human beings, many bacteria play
host to specialized transposons, termed
integrons, that are like flypaper in their
propensity for capturing new genes.
These integrons can consist of several
different resistance genes, which are
passed to other bacteria as whole regi-
ments of antibiotic-defying guerrillas.

Many bacteria possessed resistance
genes even before commercial antibiot-
ics came into use. Scientists do not know
exactly why these genes evolved and
were maintained. A logical argument
holds that natural antibiotics were ini-
tially elaborated as the result of chance
genetic mutations. Then the compounds,

which turned out to elimi-
nate competitors, enabled
the manufacturers to survive
and proliferate—if they were
also lucky enough to possess
genes that protected them
from their own chemical
weapons. Later, these protec-
tive genes found their way
into other species, some of
which were pathogenic.

Regardless of how bacte-
ria acquire resistance genes

today, commercial antibiotics can select
for—promote the survival and propaga-
tion of—antibiotic-resistant strains. In
other words, by encouraging the growth
of resistant pathogens, an antibiotic can
actually contribute to its own undoing.

How Antibiotics Promote Resistance

The selection process is fairly straight-forward. When an antibiotic at-
tacks a group of bacteria, cells that are
highly susceptible to the medicine will
die. But cells that have some resistance
from the start, or that acquire it later
(through mutation or gene exchange),
may survive, especially if too little drug
is given to overwhelm the cells that are
present. Those cells, facing reduced
competition from sus-
ceptible bacteria, will
then go on to prolif-
erate. When confront-
ed with an antibiotic,
the most resistant cells
in a group will inevit-
ably outcompete all
others.

Promoting resis-
tance in known path-
ogens is not the only
self-defeating activity
of antibiotics. When
the medicines attack
disease-causing bac-

teria, they also affect benign bacteria—
innocent bystanders—in their path. They
eliminate drug-susceptible bystanders
that could otherwise limit the expansion
of pathogens, and they simultaneously
encourage the growth of resistant by-
standers. Propagation of these resistant,
nonpathogenic bacteria increases the
reservoir of resistance traits in the bac-
terial population as a whole and raises
the odds that such traits will spread to
pathogens. In addition, sometimes the
growing populations of bystanders them-
selves become agents of disease.

Widespread use of cephalosporin an-
tibiotics, for example, has promoted
the proliferation of the once benign in-
testinal bacterium E. faecalis, which is
naturally resistant to those drugs. In
most people, the immune system is able
to check the growth of even multidrug-
resistant E. faecalis, so that it does not
produce illness. But in hospitalized pa-
tients with compromised immunity, the
enterococcus can spread to the heart
valves and other organs and establish
deadly systemic disease.

Moreover, administration of vanco-
mycin over the years has turned E. fae-
calis into a dangerous reservoir of van-
comycin-resistance traits. Recall that
some strains of the pathogen S. aureus

The Challenge of Antibiotic Resistance Scientific American March 1998 49

DEAD
BACTERIUM

RESISTANCE
GENE

BACTERIUM
RECEIVING
RESISTANCE
GENES

RESISTANCE
GENE

RESISTANCE
GENE

PLASMID DONOR PLASMID

Gene goes
to plasmid

or to
chromosome

VIRUS

BACTERIUM
INFECTED

BY A VIRUS

b
TRANSFER
BY VIRAL
DELIVERY

a
PLASMID
TRANSFER

c
TRANSFER
OF FREE
DNA

BACTERIA PICK UP RESISTANCE GENES from other bacterial cells in
three main ways. Often they receive whole plasmids bearing one or more
such genes from a donor cell (a). Other times, a virus will pick up a resis-
tance gene from one bacterium and inject it into a different bacterial cell (b).
Alternatively, bacteria sometimes scavenge gene-bearing snippets of DNA
from dead cells in their vicinity (c). Genes obtained through viruses or from
dead cells persist in their new owner if they become incorporated stably into
the recipient’s chromosome or into a plasmid.

SPREAD OF RESISTANT BACTERIA, which occurs readily, can
extend quite far. In one example, investigators traced a strain of mul-
tidrug-resistant Streptococcus pneumoniae from Spain to Portugal,
France, Poland, the U.K., South Africa, the U.S. and Mexico.

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Copyright 1998 Scientific American, Inc.

BACTERIUM
SUSCEPTIBLE
TO ANTIBIOTICS

ANTIBIOTIC

SOMEWHAT
INSENSITIVE
BACTERIUM

SURVIVING
BACTERIUM

BACTERIUM
WITH INCREASED
RESISTANCE

DEAD
BACTERIA

are multidrug-resistant and are respon-
sive only to vancomycin. Because vanco-
mycin-resistant E. faecalis has become
quite common, public health experts
fear that it will soon deliver strong van-
comycin resistance to those S. aureus
strains, making them incurable.

The bystander effect has also enabled
multidrug-resistant strains of Acineto-
bacter and Xanthomonas to emerge and
become agents of potentially fatal blood-
borne infections in hospitalized patients.
These formerly innocuous microbes were
virtually unheard of just five years ago.

As I noted earlier, antibiotics affect

the mix of resistant and nonresistant
bacteria both in the individual being
treated and in the environment. When
resistant bacteria arise in treated individ-
uals, these microbes, like other bacteria,
spread readily to the surrounds and to
new hosts. Investigators have shown
that when one member of a household
chronically takes an antibiotic to treat
acne, the concentration of antibiotic-re-
sistant bacteria on the skin of family
members rises. Similarly, heavy use of
antibiotics in such settings as hospitals,
day care centers and farms (where the
drugs are often given to livestock for
nonmedicinal purposes) increases the
levels of resistant bacteria in people and
other organisms who are not being treat-
ed—including in individuals who live
near those epicenters of high consump-
tion or who pass through the centers.

Given that antibiotics and other anti-
microbials, such as fungicides, affect the
kinds of bacteria in the environment
and people around the individual being
treated, I often refer to these substances
as societal drugs—the only class of ther-
apeutics that can be so designated. An-
ticancer drugs, in contrast, affect only
the person taking the medicines.

On a larger scale, antibiotic resistance
that emerges in one place can often
spread far and wide. The ever increasing
volume of international travel has has-
tened transfer to the U.S. of multidrug-
resistant tuberculosis from other coun-
tries. And investigators have document-
ed the migration of a strain of
multidrug-resistant Streptococcus pneu-
moniae from Spain to the U.K., the
U.S., South Africa and elsewhere. This

bacterium, also known as the pneumo-
coccus, is a cause of pneumonia and
meningitis, among other diseases.

Antibiotic Use Is Out of Control

For those who understand that anti-biotic delivery selects for resistance,
it is not surprising that the international
community currently faces a major pub-
lic health crisis. Antibiotic use (and mis-
use) has soared since the first commer-
cial versions were introduced and now
includes many nonmedicinal applica-
tions. In 1954 two million pounds were
produced in the U.S.; today the figure
exceeds 50 million pounds.

Human treatment accounts for rough-
ly half the antibiotics consumed every
year in the U.S. Perhaps only half that
use is appropriate, meant to cure bacte-
rial infections and administered correct-
ly—in ways that do not strongly en-
courage resistance.

Notably, many physicians acquiesce
to misguided patients who demand an-
tibiotics to treat colds and other viral
infections that cannot be cured by the
drugs. Researchers at the Centers for
Disease Control and Prevention have
estimated that some 50 million of the
150 million outpatient prescriptions for
antibiotics every year are unneeded. At
a seminar I conducted, more than 80
percent of the physicians present admit-
ted to having written antibiotic pre-
scriptions on demand against their bet-
ter judgment.

In the industrial world, most antibi-
otics are available only by prescription,
but this restriction does not ensure
proper use. People often fail to finish
the full course of treatment. Patients
then stockpile the leftover doses and
medicate themselves, or their family and
friends, in less than therapeutic amounts.
In both circumstances, the improper
dosing will fail to eliminate the disease
agent completely and will, furthermore,

The Challenge of Antibiotic Resistance50 Scientific American March 1998

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b

a

c

d

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Copyright 1998 Scientific American, Inc.

HIGHLY
RESISTANT
POPULATION

encourage growth of the
most resistant strains, which
may later produce hard-to-
treat disorders.

In the developing world,
antibiotic use is even less
controlled. Many of the
same drugs marketed in the
industrial nations are avail-
able over the counter. Unfor-
tunately, when resistance be-
comes a clinical problem,
those countries, which often
do not have access to expen-
sive drugs, may have no sub-
stitutes available.

The same drugs prescribed
for human therapy are wide-
ly exploited in animal hus-
bandry and agriculture. More
than 40 percent of the anti-
biotics manufactured in the U.S. are
given to animals. Some of that amount
goes to treating or preventing infection,
but the lion’s share is mixed into feed to
promote growth. In this last application,
amounts too small to combat infection
are delivered for weeks or months at a
time. No one is entirely sure how the
drugs support growth. Clearly, though,
this long-term exposure to low doses is
the perfect formula for selecting increas-
ing numbers of resistant bacteria in the
treated animals—which may then pass
the microbes to caretakers and, more
broadly, to people who prepare and
consume undercooked meat.

In agriculture, antibiotics are applied
as aerosols to acres of fruit trees, for
controlling or preventing bacterial in-
fections. High concentrations may kill
all the bacteria on the trees at the time
of spraying, but lingering antibiotic
residues can encourage the growth of
resistant bacteria that later colonize the
fruit during processing and shipping.
The aerosols also hit more than the tar-
geted trees. They can be carried consid-
erable distances to other trees and food
plants, where they are too dilute to
eliminate full-blown infections but are
still capable of killing off sensitive bac-

teria and thus giving the edge to resis-
tant versions. Here, again, resistant bac-
teria can make their way into people
through the food chain, finding a home
in the intestinal tract after the produce
is eaten.

The amount of resistant bacteria peo-
ple acquire from food apparently is not
trivial. Denis E. Corpet of the National
Institute for Agricultural Research in
Toulouse, France, showed that when hu-
man volunteers went on a diet consist-
ing only of bacteria-free foods, the num-
ber of resistant bacteria in their feces
decreased 1,000-fold. This finding sug-
gests that we deliver a supply of resistant
strains to our intestinal tract whenever
we eat raw or undercooked items. These
bacteria usually are not harmful, but
they could be if by chance a disease-
causing type contaminated the food.

The extensive worldwide exploitation
of antibiotics in medicine, animal care
and agriculture constantly selects for
strains of bacteria that are resistant to
the drugs. Must all antibiotic use be halt-
ed to stem the rise of intractable bacte-
ria? Certainly not. But if the drugs are
to retain their power over pathogens,
they have to be used more responsibly.
Society can accept some increase in the

fraction of resistant bacteria when a
disease needs to be treated; the rise is
unacceptable when antibiotic use is not
essential.

Reversing Resistance

Anumber of corrective measures can be taken right now. As a start,
farmers should be helped to find inex-
pensive alternatives for encouraging an-
imal growth and protecting fruit trees.
Improved hygiene, for instance, could
go a long way to enhancing livestock
development.

The public can wash raw fruit and
vegetables thoroughly to clear off both
resistant bacteria and possible antibiot-
ic residues. When they receive prescrip-
tions for antibiotics, they should com-
plete the full course of therapy (to en-
sure that all the pathogenic bacteria die)
and should not “save” any pills for later
use. Consumers also should refrain from
demanding antibiotics for colds and
other viral infections and might consider
seeking nonantibiotic therapies for mi-
nor conditions, such as certain cases of
acne. They can continue to put antibi-
otic ointments on small cuts, but they
should think twice about routinely us-

Scientific American March 1998 51

ANTIBIOTIC
STOPS

SUSCEPTIBLE BACTERIA IN VICINITY

RESISTANT
POPULATION

DEAD CELLS
SUSCEPTIBLE
POPULATION

ANTIBIOTIC USE SELECTS—promotes the evolution and growth of—bacteria that
are insensitive to that drug. When bacteria are exposed to an antibiotic (a), bacterial
cells that are susceptible to the drug will die (b), but those with some insensitivity may
survive and grow (c) if the amount of drug delivered is too low to eliminate every last
cell. As treatment continues, some of the survivors are likely to acquire even stronger
resistance (d)—either through a genetic mutation that generates a new …

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