MAY JUNE 2018 | MOTHER JONES 57have to go look for Acinetobacter in the wild.
So he sent his students hunting for envi-
ronmental samples, dipping into eluent
from sewage- treatment plants, pulling
water from ponds, and taking swabs of
pigs on ranches near the university. Among
the 126 samples obtained during the expe-
dition, the Texas lab identified three
phages that worked against Patterson’s
strain of Acinetobacter.
Now they had individual viruses that
might do the trick—but they needed
to grow enough of them to make up a
treatment. They let the bacteria from
Patterson’s infection reproduce under
lab conditions and then unleashed the
phages on them. The viruses worked the
way they had evolved to: They attached
to the bacteria, inserted their dna, copied
themselves, and exploded the pathogens.
The team fed the phages more and more
Acinetobacter. In 10 days, they had trillions
of copies. Young shipped them in a refrig-
erated box to Schooley, who meanwhile
had been explaining to the university’s
biohazard-safety committee why letting
a minimally tested living virus into an icu
full of very sick people would not be a risk.
(If the phage escaped, it would affect only
patients who happened to have the exact
same infection as Patterson, and no one
else there did.) Schooley had also found
another source of phages, in a lab main-
tained by the US Navy. In tests, four of the
Navy phages killed the bacterium from
Patterson’s infection as well.
The Texas phages arrived in San Diego
first, all four of them combined into a cock-
tail to increase the odds of success. They
had to be scrubbed of cellular toxins and
debris from the bacteria they had been
grown on, because those contaminants
could have sent Patterson into shock.
Schooley and his team infused the clean
solution into the drains that pierced Pat-
terson’s abdomen, hoping to sterilize the
cavities where the infection was lurking.
That was on a Tuesday. Patterson didn’t
get better, but he also didn’t get worse—
encouraging, given how rapidly he had
been slipping away. Two days later, the
Navy phages arrived, and the ucsd team
took a gamble and gave them to him in-
travenously, to chase the bacteria that had
found homes in his lungs and bladder and
blood. That was on a Thursday. On Satur-
day night, Patterson awoke from his coma
and recognized his daughter. The phages
had done their work.
He was not yet cured, not by a long shot.
His infection surged and he crashed back
into septic shock the next week, only to be
brought out of it with more phages. The
same thing happened again a month later,
and this time the Navy lab analyzed his in-
fection and tinkered with the phage cocktail.
The whole treatment process was a
scramble. “We had two people working lit-
erally 24/7 for six weeks to find and supply
phages to the clinical team at ucsd,” Young
said. “That is not sustainable.”
The effort was such an emergency, Young
added, that his group did not have time to
fully analyze the phages they sent. Later
they discovered that almost all the viruses
used in the first round of Patterson’s treat-
ment, both from Texas A&M and from the
Navy, targeted the same single attachment
point on the outside of the bacterium. It
was as if they were all the same drug, in-
stead of eight different ones. That meant
the bacterium had to make just one small
mutational change to defend itself against
them, producing phage resistance—a prob-
lem that appears in only a small number
of scientific papers about phages and that
medicine has not yet had to develop strat-
egies against, because phages have not been
a treatment in most of the world.
“If we had been able to do genetic and
molecular analysis of the phages, we could
have avoided that,” Young said. “The ideal
thing would be to have a walk-in cooler of
thousands of phages, each of which you
know everything about.”actually, two decades ago, someone
attempted to do just that. Alexander
Sulakvelidze, who holds a doctorate in
micro biology, is a native of Tbilisi, the
home of the Eliava Institute. Sulakvelidze
grew up experiencing phage treatments as
a routine part of medical care, off-the-shelf
products that doctors would prescribe like
Western physicians prescribe antibiotics.
Then he came to the United States to serve
a postdoctoral fellowship at the University
of Maryland School of Medicine. One day
during his fellowship, his supervisor, Dr.
J. Glenn Morris, announced that a patient
was gravely ill with a resistant bug called
vre and would likely die.
“I asked him, ‘Why can’t bacteriophages
get rid of the vre?’” Sulakvelidze recalls. “Ithought it was a naive question.” But later,
after the patient died, Sulakvelidze says he
realized, “Something very strange is going
on. Somebody just died in the most devel-
oped country in the world, from something
that could probably be very easily cured in
a country like Georgia.”
Out of that realization, Sulakvelidze and
Morris and a handful of other researchers
formed a company, Intralytix, in 1998. They
set out to license phage treatments for vre,
considered at the time the most dangerous
of the superbugs. It did not go as planned.
“The investors had no idea what the risks
are, the patentability, the return on invest-
ment,” he said. “The regulatory agenciesThe Resistance
Phages are viruses capable of infiltrating
and exploding bacterial cells that can cause
dangerous infection.Step 1
The phage
attaches
to the host
bacterial cell.Step 2
The phage
sends its
na into the
bacterial cell.Step 3
The phage
na replicates.
New proteins
are made.Step 4
New phages
are formed
inside the
bacterial cell.Step 5
The newly
made phages
burst out of
the bacterial
cell, killing it.
The process
repeats.