212 ■ CHAPTER 12 Mechanisms of Evolution
EVOLUTION
D
awn Sievert vividly remembers June 14,
2002—the day disaster struck. Sievert is
an epidemiologist, or “disease detective”—
someone who studies the patterns and causes of
human disease. At the time, she was working at
the Michigan Department of Community Health,
monitoring reported cases of antibiotic-resistant
bacteria, a major health care concern. Sievert
spent a significant amount of her time inves-
tigating outbreaks of an increasingly common
and worrisome microbe called MRSA, short for
“methicillin-resistant Staphylococcus aureus.”
S. aureus, commonly known as “staph,” is
a small, round bacterium that usually lives
benignly in our nostrils and on our skin. But on
rare occasions, staph slips beneath the surface
of a burn or cut and causes an infection, which
can be especially dangerous for individuals with
suppressed immune systems, such as the elderly
and patients on chemotherapy.
Staph is one of the most common causes of
hospital infections today, and it is treated with anti-
biotics, drugs that kill bacteria but not human cells.
Penicillin (Figure 12.1) was the first antibiotic used
against staph, but the wily microbe evolved resis-
tance to penicillin even before the drug became
commercially available to the public in the 1940s.
When penicillin stopped working against
staph, doctors switched to an antibiotic called
methicillin. Methicillin worked for about 20
years, until populations of staph evolved wide-
spread resistance to that antibiotic as well. To
the chagrin of doctors and patients everywhere,
bacteria are able to adapt rapidly to new anti-
biotics, thanks to their short generation time
and ability to share resistance genes among
themselves. (See Chapter 15 for more on bacte-
ria.) These tiny microbes are the Navy SEALs of
evolution—the best of the best at evolving.
As we saw in Chapter 11, biological evolution
is a change in the frequencies of inherited traits
in a population over generations. Staph adapted
to the presence of methicillin: Only bacteriawith genetic traits protecting the microbe from
the antibiotic survived. These traits were passed
among populations and down from one genera-
tion to the next until methicillin resistance was
frequent across staph populations (Figure 12.2).
Today, MRSA is rampant in hospitals, so
doctors have been forced to turn to one of medi-
cine’s last lines of defense against the superbug.
Vancomycin, a strong, blunt antibiotic that was
first isolated from the mud of the Borneo jungle,
is considered one of the “drugs of last resort” for
fighting these serious infections—which brings
us back to June 14, 2002, and Dawn Sievert.
On that day, a lab technician at a dialysis
center in Detroit, Michigan, took two swabs of
an infected foot ulcer belonging to a 40-year-old
diabetic woman (Figure 12.3). The patient had
previously suffered from numerous foot infec-
tions, including MRSA, which had been treated
with vancomycin for 6∏ weeks. The swabs of this
latest infection were sent to a local laboratory,
where technicians grew the bacteria in a dish to
test its susceptibility to various antibiotics.
When the results of the first test came in,
the laboratory staff immediately picked up the
phone and called Sievert’s office. The bacteria,
they told Sievert and the health department,
appeared to be resistant to vancomycin. “First,
we needed laboratory confirmation and had toFigure 12.1
Penicillin, produced by mold, kills bacteria
The mold Penicillium, the fuzzy white growth with
blue spores growing on this petri dish, secretes
the antibiotic penicillin into the agar medium,
killing the red bacteria surrounding it.Dawn Sievert is an infectious disease epidemiologist
who worked for the Centers for Disease Control
and Prevention until 2016. While at the Michigan
Department of Community Health previously, Sievert
investigated the first-ever VRSA infection.DAWN SIEVERT