Battling Resistance ■ 215to emerge, says Gilmore. He knew that once
vancomycin was widely used to kill staph, the
microbe population would evolve resistance
to the poison. The process by which a popula-
tion gains one or more alleles that enable it to
survive better than other populations is called
natural selection, as we saw in Chapter 11.
Darwin and Wallace were the first to propose
natural selection, and today we know that it is
the central driver of evolution.
During natural selection, individuals with
particular inherited characteristics survive and
reproduce at a higher rate than other individuals
in a population. Natural selection acts by favor-
ing some phenotypes over others (Figure 12.6).
For example, in an environment where bacteria
are exposed to vancomycin, the bacteria that
can resist the antibiotic will continue to live and
reproduce, while those that cannot will perish.
Although natural selection acts directly on the
phenotype, not on the genotype, of a population,
the alleles that code for a phenotype favored by
natural selection tend to become increasingly
common in future generations. Bacteria that
survive an antibiotic attack, for example, pass
on alleles that confer that resistance to their
offspring.
Natural selection acts on adaptive traits, and
therefore a population can become better suited
to survive and reproduce in its environment.
And unfortunately for us, natural selection is
the mechanism by which staph is adapting to
our use of vancomycin.
Because staph’s vancomycin-resistance adap-
tation is very recent, scientists are studying
the patterns of how natural selection gives rise
to VRSA. In nature we observe three common
patterns of natural selection: directional selec-
tion, stabilizing selection, and disruptive selec-
tion. All types of natural selection operate by the
same principle: individuals with certain forms
of an inherited trait have better survival ratesIf that highly resistant organism had the abil-
ity to spread rapidly, we’d have some very sick
people at risk in hospitals and other health care
settings,” says Sievert.
Yet it was not the end of VRSA. Since 2002,
there have been 13 additional cases of vanco-
mycin-resistant staph infections in the United
States: in the urine of a woman in New York
with multiple sclerosis, in the toe wound of a
diabetic man in Michigan, in the triceps wound
of a woman in Michigan, and more. So far,
each infection has been isolated; the microbe
has never been transmitted from person to
person, as MRSA has. VRSA, while dangerous,
doesn’t appear to spread through the human
population.
But that’s not to say it won’t evolve to do so.
When MRSA first emerged, it seemed restricted
to hospital settings. Today, however, clinicians
have been horrified to see cases of MRSA pop up
from simple scrapes on a playground, suggesting
that the microbe is out in the community, where
it can do widespread damage. In theory, the same
is possible for VRSA, raising the bone-chilling
specter of the superbug evolving into an “apoca-
lyptic bug,” as one reporter called it.
How did staph acquire vancomycin resistance
14 separate times? How likely is vancomycin
resistance to become more widespread? We can
find answers to these questions by understand-
ing four mechanisms of evolution:
- Natural selection
- Mutation
- Gene flow
- Genetic drift
Bacteria are ideal organisms for examining
these evolutionary mechanisms, for the same
reason that they are so dangerous: because they
evolve incredibly fast.
Rising Resistance
Harvard Medical School microbiologist
Michael Gilmore has long tracked the ways
that bacteria evolve antibiotic resistance.
After staph evolved widespread resistance
to methicillin in the 1980s and vancomycin
began to be used in hospitals, “we waited and
waited and waited” for vancomycin resistance
Michael Gilmore is a microbiologist at Harvard Medical
School. He and his laboratory uncovered the genetic
basis for the recent emergence of VRSA.MICHAEL GILMORE