Mother Jones - May 01, 2018

(Michael S) #1

56 MOTHER JONES |^ MAY  JUNE 2018


THE BEST VIRAL NEWS YOU’LL EVER READ

in 1937, and d’Herelle died in 1949. Their in-
stitute dwindled, but it survived the collapse
of the Soviet Union in 1991 and the Georgian
civil war the following year. When the former
ussr opened up to the West, physicians in
the United States and Europe learned the
Eliava Institute was one of the few places
in the world where researchers were still
studying and administering phages. That
was fortunate timing, because antibiotics
in the West were losing their power under
the onslaught of antibiotic resistance.
Antibiotics began as natural com-
pounds, the chemical weapons that bac-
teria aim against each other to compete
for living space and food. For millennia
before humans arrived, bacteria countered
those attacks with mutations—and when
humans turned those natural weapons into
medicine, by taking them into laboratories
to synthesize and perfect them, bacteria

kept on adapting. The mutations they pro-
duced in response to antibiotics are what
we call antibiotic resistance.
Penicillin-resistant staph infections
swept the world not long after penicillin
came into use during World War II.
Methicillin- resistant staph (mrsa) immedi-
ately followed the 1960 debut of methicillin,
designed to replace some of penicillin’s lost
firepower. Over the decades, as each new
antibiotic arrived, resistant infections have
arisen to undermine them. In the United
States, the Centers for Disease Control and
Prevention estimated in 2013 that at least
23,000 people die each year from resistant
infections, and that 2 million are made sick
enough to go to a doctor’s oice or hospital.
Worldwide, the death toll is estimated at
700,000 people a year. And because resis-
tance is accelerating ahead of production
of new drugs to counter it, the death toll is
expected to rise to 10 million per year and
cost the world as much as $100 trillion in
lost economic activity by 2050.
Superbugs pervade health care, causing
grave infections after surgeries and in inten-
sive care units, and because antibiotics are

routinely added to livestock feed, they per-
meate the food supply. In 2015, for instance,
an fda project discovered that 47 percent
of salmonella bacteria samples found in
retail chicken were resistant to tetracycline,
as were 76 percent of the E. coli found in
ground turkey.
Phages’ vast biological diversity helps
them against the mutations that make up
disease organisms’ resistance defenses.
Plus, because phages kill only specific
strains of bacteria, they can quell infections
without inducing a terrible diarrheal dis-
ease from Clostridium dificile (usually
known as C. diff) that occurs when the bal-
ance of bacteria in the gut is disrupted by
antibiotics wiping out good bugs along
with the bad. The cdc estimates that in
2011 there were more than 450,000 cases
of C. diff infections in the United States,
leading to more than 15,000 deaths. It’s

possible that using phage therapy instead
of antibiotics could prevent some of them.
But for phage therapy to be deployed rou-
tinely in the United States, phages would
have to be approved as drugs by the fda. To
treat an American patient with them now
requires emergency compassionate- use
authorization—effectively an acknowledg-
ment that nothing with an fda license can
save the patient’s life. And Strathdee was
about to learn that because phages have no
such approval, awareness of them is scarce
and unevenly distributed, and finding the
right researchers and physicians requires
extraordinary luck.

strathdee directs ucsd’s Global Health
Institute and like her husband is a profes-
sor in the medical school. Decades earlier,
she had tinkered with phages in lab sci-
ence classes, using them as a tool to dif-
ferentiate bacteria. Before her husband
got sick, she had never heard they could
be used as treatments.
The physician whom she’d emailed—Dr.
Robert “Chip” Schooley, at the time ucsd’s
chief of infectious diseases, and an old

friend—knew a little more. Anyone who
works in infectious diseases is aware of the
peril of drug resistance, and the wish for
reliable alternatives to antibiotics is a con-
stant companion to that work. But phages
had no direct relevance for him because
his personal expertise is disease-causing
viruses—hiv and hepatitis—that phages
would not affect.
He knew the next step to take, though.
The fda maintains a hotline that lets phy-
sicians ask permission to use an unapproved
treatment on a single patient if every other
hope has been exhausted. The fda’s re-
viewer agreed to let the pair attempt phages.
Time was short, and the odds were against
Strathdee. She needed to find someone who
was conducting phage research, who had
already isolated phages that worked against
Acinetobacter, and who would be willing to
test those phages on Patterson’s infection
to see if there was a match.
She cast a wide net, sending about 10
emails to labs around the world, including
the Eliava Institute. Two and a half hours
later, she got a message from one of the few
phage research groups in the United States,
the Center for Phage Technology at Texas
A&M University, run by a biologist named
Ryland Young. Strathdee called Young and
talked at him for more than an hour.
“She has persuasive power,” Young re-
called. “And she has made herself probably
the most knowledgeable civilian in the
world on the use of phage therapy. She got
us mobilized.”
What happened next illustrates how
time-consuming it can be to try to use an
unapproved treatment. Young’s lab has
been isolating and testing phages since
2010 and has several hundred individual
viruses in its collection, but when Strathdee
called fewer than 10 of them were known
to work against Acinetobacter. Young put
out a call to the small worldwide network
of phage researchers, asking for contribu-
tions, and was sent some 35 new viruses. He
and his lab tested all of them on a sample
from Patterson’s infection, sent by Schooley.
None of Young’s phages made a dent. One
virus, sent by a company called AmpliPhi,
did kill cells from the infection. They would
need more to make a difference, so Young
and his team embarked on what he drawl-
ingly calls “a good old-fashioned phage
hunt.” To find a phage that worked against
Acinetobacter, Young reasoned, he would

“I always thought viruses were the bad
guys. Now I see that viruses may
actually be used for good, too.”
Free download pdf