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THE INVISIBLE ENEMY IN IRAQ: ACINETOBACTER
BAUMANNII -- As Iraq War veterans enter VA
hospitals, older veterans already in the
system become the primary target
of the deadly bacteria.

The operating room at Ibn Sina
Hospital in Baghdad, an Army facility implicated in the spread of
Acinetobacter baumannii.
(photo: Peter Van AGTMAEL/POLARIS) |
Some background here...
http://www.vawatchdog.org/old%20
newsflashes%20JAN%2006/newsflash01-01-2006-3.htm
and here...
http://www.vawatchdog.org/old%20
newsflashes%20MAR%2006/newsflash03-25-2006-4.htm
Today's story here...
http://www.wired.com/news/
wiredmag/0,72532-0.html?tw=wn_index_1
Story below:
---------------
The Invisible Enemy in Iraq
By Steve Silberman
A homemade bomb exploded under a Humvee in Anbar province, Iraq, on
August 21, 2004. The blast flipped the vehicle into the air, killing two
US marines and wounding another - a soft-spoken 20-year-old named
Jonathan Gadsden who was near the end of his second tour of duty. In
previous wars, he would have died within hours. His skull and ribs were
fractured, his neck was broken, his back was badly burned, and his
stomach had been perforated by shrapnel and debris.
Gadsden got out of the war zone alive because of the Department of
Defense's network of frontline trauma care and rapid air transport known
as the evacuation chain. Minutes after the attack, a helicopter touched
down in the desert. Combat medics stanched the marine's bleeding,
inflated his collapsed lung, and eased his pain. He was airlifted to the
31st Combat Support Hospital in Baghdad, located in an old health care
facility called the Ibn Sina, which had formerly catered to the Baathist
elite. Army surgeons there repaired Gadsden's cranium, removed his
injured spleen, and pumped him full of broad-spectrum antibiotics to
ward off infection.
Three days later, he was flown to the Landstuhl Regional Medical Center
in Germany, the largest American military hospital in Europe. He was
treated for his burns, and his spine was stabilized for the 18-hour
flight to the US. Just a week after nearly dying in the desert, Gadsden
was recuperating at the National Naval Medical Center in Bethesda,
Maryland, with his mother, Zeada, at his bedside.
The surgeons, nurses, medics, and pilots of the evacuation chain have
saved thousands of lives. Soldiers wounded in Vietnam were six weeks of
transit time away from US hospitals, and one out of every four of them
died. By contrast, a soldier's odds of surviving battle injuries in Iraq
are nine out of 10. Unfortunately, this remarkable advance in
battlefield logistics has also resulted in an increase in the number of
traumatically injured patients who are particularly susceptible to
infections during their recovery. In Gadsden's case, from the moment he
was carried into the Ibn Sina, the injured marine was in the crosshairs
of an enemy he didn't even know was there.
At first, he did quite well. By early September, Gadsden was weaned off
his ventilator and breathing on his own. For weeks he gradually
improved. His buddies took him to a Washington Redskins game in his
wheelchair, and the next day he navigated 50 feet with a walker. Soon
Gadsden was transferred to a veterans' hospital in Florida called the
James A. Haley Medical Center, where he offered to serve as the eyes of
a fellow marine blinded in an ambush. The doctors told Zeada that her
son might be able to go home by the end of October.
But he still had mysterious symptoms that he couldn't shake, like
headaches, rashes, and intermittent fevers. His doctors gave him CT
scans, laxatives, methadone, beta-blockers, Xanax, more surgery, and
more antibiotics. An accurate evaluation of his case was difficult,
however, because portions of his medical records never arrived from
Bethesda. If they had, they would have shown a positive test for a kind
of bacteria called Acinetobacter baumannii.
In the taxonomy of bad bugs, acinetobacter is classified as an
opportunistic pathogen. Healthy people can carry the bacteria on their
skin with no ill effects - a process known as colonization. But in
newborns, the elderly, burn victims, patients with depressed immune
systems, and those on ventilators, acinetobacter infections can kill.
The removal of Gadsden's spleen and the traumatic nature of his wounds
made him a prime target.
On October 17, the marine was given a day pass to accompany his mother
to Wal-Mart, where he bought her a purse. Hours after returning to the
hospital, his condition deteriorated abruptly. His heart rate and blood
pressure were elevated, and his white blood cell count was spiking.
Nurses noted in his chart that he had become "disoriented to place,
time, and people - thinking he is at home - sitting up thinks he's lying
down." He struggled through occupational therapy the following morning,
shivering and complaining of the cold.
Gadsden had a seizure and a heart attack the next day. The neurology
team discovered that his cerebrum and cerebellum had swelled up
overnight; he was clinically brain-dead. His family and minister were
called to the hospital, and on October 22 he was taken off life support.
The Marine Corps public affairs office sent out the customary press
release attributing Gadsden's death to "injuries as a result of enemy
action." But then a few weeks later, Zeada's dentist told her a Florida
newspaper was reporting that her son had died of bacterial meningitis.
Aided by US representative Bill Young, Zeada - who works as a
cardiac-care technician in South Carolina - demanded an investigation.
She discovered that an autopsy was performed shortly after her son's
death. The coroner recorded the "manner of death" as "homicide
(explosion during war operation)" but determined the actual cause of
death to be a bacterial infection. The organism that killed Gadsden,
called Nocardia, had clogged the blood vessels leading to his brain. But
the acinetobacter had been steadily draining his vital resources when he
could least afford it. For weeks, it had been flourishing in his body,
undetected by the doctors at Haley, resisting a constant assault by the
most potent antibiotics in the medical arsenal.
"No one said that my son had anything like that," Zeada says. "I never
had to wear gloves or a mask, and none of the nurses did either. No one
had any information."
Since OPERATION Iraqi Freedom began in 2003, more than 700 US soldiers
have been infected or colonized with Acinetobacter baumannii. A
significant number of additional cases have been found in the Canadian
and British armed forces, and among wounded Iraqi civilians. The Armed
Forces Institute of Pathology has recorded seven deaths caused by the
bacteria in US hospitals along the evacuation chain. Four were unlucky
civilians who picked up the bug at Walter Reed Army Medical Center in
Washington, DC, while undergoing treatment for other life-threatening
conditions. Another was a 63-year-old woman, also chronically ill, who
shared a ward at Landstuhl with infected coalition troops.
Behind the scenes, the spread of a pathogen that targets wounded GIs has
triggered broad reforms in both combat medical care and the Pentagon's
networks for tracking bacterial threats within the ranks. Interviews
with current and former military physicians, recent articles in medical
journals, and internal reports reveal that the Department of Defense has
been waging a secret war within the larger mission in Iraq and
Afghanistan - a war against antibiotic-resistant pathogens.
Acinetobacter is only one of many bacterial nemeses prowling around in
ICUs and neonatal units in hospitals all over the world. A particularly
fierce organism known as MRSA - methicillin-resistant Staphylococcus
aureus - infects healthy people, spreads easily, and accounts for many
of the 90,000 fatal infections picked up in US hospitals each year.
Another drug-resistant germ on the rise in health care facilities,
Clostridium difficile, moves in for the kill when long courses of
antibiotics have wiped out normal intestinal flora.
Forerunners of the bug causing the military infections have been making
deadly incursions into civilian hospitals for more than a decade. In the
early 1990s, 1,400 people were infected or colonized at a single
facility in Spain. A few years later, particularly virulent strains of
the bacteria spread through three Israeli hospitals, killing half of the
infected patients. Death by acinetobacter can take many forms:
catastrophic fevers, pneumonia, meningitis, infections of the spine, and
sepsis of the blood. Patients who survive face longer hospital stays,
more surgery, and severe complications.
Nevertheless, the bug makes an unlikely candidate for the next mass
plague. It preys exclusively on the weakest of the weak and the sickest
of the sick, slipping into the body through open wounds, catheters, and
breathing tubes. Colonization poses no threat to people who aren't
already ill, but colonized health care workers and hospital visitors can
carry the bacteria into neighboring wards and other medical facilities.
Epidemiologist Roberta Carey at the Centers for Disease Control and
Prevention calls acinetobacter the Rodney Dangerfield of microorganisms:
"It doesn't get a lot of respect because it's not out there bumping off
normal, healthy people." But lately the bacteria has been getting its
due, because it is rapidly evolving resistance to all of the antibiotics
that used to keep it in check.
Until a few years ago, most strains could be dispatched with a wide
variety of drugs. For the most tenacious infections, doctors could rely
on a family of ultrabroad spectrum antibiotics called carbapenems. But
strains of acinetobacter are emerging now that are immune to every known
remedy. Multidrug - resistant pathogens are an epidemiologist's
nightmare - reminders of the dark ages when millions of people died
every year of runaway infections.
"We've been looking at acinetobacter in real time for years and years in
our lab," says John Quinn, scientific director of the Chicago Infectious
Disease Research Institute. "Then all of a sudden in 2005, we started
seeing more bugs that were resistant to the carbapenems. First one out
of 10 bugs, then four out of 10, and then almost all of the bugs. So
there's a new sheriff in town. That's a clinical disaster."
To battle these new strains, clinicians are being forced to dust off a
World War II-era relic called colistin, which is so toxic that it causes
kidney damage in as many as one in four patients who take it. In 2004,
the Infectious Diseases Society of America included acinetobacter on its
"bad bugs, no drugs" short list of pathogens that are "raising
significant public health concerns." According to a recent CDC study,
the new multidrug-resistant organisms are almost four times more deadly
than older strains.
And they're spreading fast. A major outbreak in Chicago two years ago
infected 81 patients, killing at least 14. Arizona health officials
tracked more than 200 infections in state hospitals early last year.
Doctors at Vanderbilt University Medical Center in Tennessee used to see
an infection or two every year; now it's one or more a month. "These
bacteria are developing very, very quickly," says CDC epidemiologist
Arjun Srinivasan, who has been consulting with the DOD about the
military outbreak. "The bad news is that we're many years away from
having new drugs to treat them. It should be a call to arms."
I VISITED WALTER REED in 2004 to write about anesthesia on the front
lines. As I spoke with an Army sergeant who had survived a brutal attack
in Najaf, US senator John McCain and talk-radio host Don Imus came into
the room to thank him for his service. When we walked out, McCain's
assistant whipped out a bottle of sanitizing gel and passed it around. A
nurse explained to me, "It's this bug that grows in the soil over there
and gets blown into their wounds by IEDs. These poor guys are covered
with it. Around here we call it Iraqibacter." Rumors were circulating at
the hospital that insurgents dosed their homemade bombs with the flesh
of dead animals.
Nearly four years into the war, the notion that deadly bacteria is
lurking in the Iraqi dirt is still proposed by DOD officials as the most
likely explanation for the military infections. In November, Duane
Hospenthal, an infectious-disease expert at Brooke Army Medical Center
in Texas and a consultant to the Army Surgeon General, said, "The
question really has been: Is it coming from these old facilities we're
using in Iraq? Is it coming from some of the Iraqi patients we have? Is
it normal flora for our deployed soldiers who have been there for a
while? Or is it being blown into them from shrapnel, dirt, and other
materials by these explosive devices?"
Hospenthal added that he believes there is little cause for concern.
"It's a low-grade, low-virulence pathogen that can be recovered from
soil and water. Without having it blasted into you or your being
immunocompromised, it's not going to hurt you. We still see
acinetobacter, but now that it's been recognized, people are less
excited about it here. It's hard for me to even understand if this is a
big issue."
It's true that many species of acinetobacter flourish widely in the
environment. Thriving colonies have been recovered from soil, cell
phones, frozen chicken, wastewater treatment plants, Formica
countertops, and even irradiated food all over the world. But the
particular species causing the military infections, baumannii, is almost
always found in just one environment - hospitals.
Lenie Dijkshoorn, a senior researcher at Leiden University Medical
Center in the Netherlands, has studied the bug since 1984. "My
colleagues and I have been looking for Acinetobacter baumannii in soil
samples for years, and we haven't found it," she says. "These organisms
are quite rare outside of hospitals."
In fact, they are supremely adapted to life in critical-care facilities.
They can survive for weeks on a stethoscope, a blood-pressure cuff, a
mattress, or a computer keyboard. The short, plump, rod-shaped bacilli
are so adept at mining nutrients from recalcitrant sources that Israeli
geneticists have engineered strains to bio-degrade oil spills. Even
before the bug evolved resistance to multiple antibiotics, it knew its
way around a sponge and bucket. A Norwegian microbiologist noted in 1973
that disinfectant used to clean catheters in a gynecologist's lab
contained "a veritable culture of the strain."
Hospenthal also told me that the acinetobacter has been recovered from
the skin of those who have never been to war: "We've swabbed nondeployed
soldiers and found the bacteria in their toe webs and other parts of
their bodies." The study he was referring to, however, published last
July in the journal Infection Control and Hospital Epidemiology, pointed
out that those organisms were genetically very different from the
bacteria infecting men and women evacuated from Iraq. The Acinetobacter
baumannii colonizing new enlistees in Texas was still susceptible to
antibiotics; the organisms infecting veterans are highly resistant.
In Europe, multidrug-resistant acinetobacter is spreading through
civilian hospitals, precipitating a public health crisis. A 2003-2004
epidemic hit more than 50 hospitals and long-term care facilities in
France, making scores of patients sick and killing 34 people.
Thirty-nine infected patients died at St. Mary's Hospital in London two
years ago.
British health care officials are deeply concerned about a possible link
between the civilian outbreaks and coalition troops carrying the
bacteria home from Iraq. The UK's Health Protection Agency sent out a
notice in 2003 asking doctors to submit samples of acinetobacter - from
patients known to have returned from Iraq, or from patients on a ward
where there have been Iraq returnees - to a lab for genotyping. Three
months ago, a health official in England told The Independent that the
same strain of bacteria infecting troops had been implicated in at least
three civilian outbreaks. Prime minister Tony Blair recently announced
that a major civilian hospital will open a ward just for military
patients.
Bacteria that know how to disable or block the efficacy of multiple
drugs are highly educated organisms. They're typically the product of an
environment where antibiotics are in frequent use, and they have
downloaded genetic cheat codes from other resistant bacteria into their
own DNA. Multidrug-resistant staph, for example, hijacked genes from a
bug called Enterococcus that have made it resistant to vancomycin - the
drug of last resort. Once a strain acquires these upgrades, Darwin's
selective pressure weeds out the late adopters.
So where are these highly educated military bugs coming from? "It would
be very interesting," Dijkshoorn says, "to investigate the routing of
these patients."
THE FIRST NEWS that US troops had engaged an unforeseen enemy in Iraq
appeared on a physicians' email list called ProMED on April 17, 2003. A
communicable-disease expert in the Navy named Kyle Petersen posted a
request for information about unusual infections he was seeing aboard
the USNS Comfort, a 1,000-bed hospital ship off the coast of Kuwait.
The Comfort was taking in 50 new patients a day by helicopter, many of
them Iraqi civilians and prisoners of war. Petersen told the ProMED list
that he had seen "several cases of [multidrug-resistant] acinetobacter
amongst Iraqi natives wounded by gunshots, shrapnel, burns or motor
vehicle accidents." Reviewing the literature, he found reports of an
outbreak in Turkish hospitals after an earthquake in 1999, which
suggested to him that "acinetobacter species are fairly common pathogens
in traumatic wounds, especially if they are dirty." The bugs on the
Comfort, however, were more resistant than the Turkish strains. He
continued: "Can anyone familiar with the soil biology of Iraq or the
drug prescribing practices of the pre-regime medical system explain the
severe drug resistance pattern we are seeing among our trauma victims
medevaced from Iraq" Any comments would be greatly appreciated."
The bug's emergence on the Comfort made a tough job even tougher. In
infected burn victims, skin grafts failed. Two Iraqi patients died.
Luckily, the acinetobacter on the Comfort was still susceptible to
imipenem, one of the carbapenem-based "magic bullets" kept in reserve
for the day when nothing else works. The staff quickly ran through its
stock of the drug, firing off urgent requests for more. By isolating
carriers in an area of the ship nicknamed Acinetobacter Alley and maxing
out the imipenem, the medics finally brought the spread of the bacteria
under control.
Soon, however, the bug started popping up in other hospitals along the
evacuation chain. More than 70 patients at Walter Reed eventually
contracted acinetobacter infections of the blood. Other infected
patients and carriers surfaced at Landstuhl, Bethesda, and Balad Air
Base, the embarkation point for troops on their way out of Iraq. By
early 2005, nearly one-third of the wounded soldiers admitted to the
National Naval Medical Center had been colonized by the bacteria. Only a
handful of the early cases could be traced directly to the bugs on the
Comfort, because the ship steamed out of the Gulf three months into the
war. But almost all of the infected patients and carriers had received
medical care at field hospitals in Iraq.
Known as combat support hospitals or CSHs, these facilities had been
hastily erected in tents and other temporary structures, in keeping with
the Pentagon's goal of a lean and mobile fighting force. Maintaining
sterile conditions in the desert required creative efforts. Sand blew
through every available opening in the walls, and the 130-degree days
took their toll on drugs, power supplies, and diagnostic equipment. To
move trauma care closer to the action, the DOD deployed modified
shipping containers called ISO boxes as portable operating rooms. It was
standard procedure to have a dozen nurses, surgeons, and
anesthesiologists in each box crowded around two patients undergoing
surgery simultaneously - an infection risk in any hospital.
At the 28th CSH near Camp Dogwood - home to more than 4,000 US and
British soldiers - there was only one washer and dryer to launder all of
the linen, including the surgical scrubs. Army nurses reported to the
DOD that "sheets were more often than not soaked with blood and other
body fluids - linen that covered the patients who were transferred back
to Germany was not replaced." When hospital-grade disinfectants ran low,
which was often, the supply crew stocked up on bleach from a local
bazaar.
The derelict infrastructure of the Ibn Sina, where Jonathan Gadsden was
treated during his evacuation, bedeviled the staff's best
infection-control efforts. Rainwater dripped into operating rooms and
supply closets, and pigeons roosted in the ventilation system, wafting
the smell of droppings into the surgical suites. (A request was filed to
the Iraqi Ministry of Health in September 2003 to "eliminate bird feces"
from the air ducts.) Clean sheets and scrubs were scarce at the Ibn Sina
as well, because the civilian laundry contractor was apparently selling
them on the black market.
"When you're interested in immediate lifesaving, you can't be thinking
about every infection-control nuance," says microbiologist Roberta
Carey, branch chief of epidemiology at the CDC. "In any emergency room
that deals with trauma patients, there's a limit - if they get too many
patients from a car crash, they put the others on bypass and send them
to another institution. But there is no bypass in a war zone."
The most effective way to curtail the development of multidrug-resistant
bacteria is to limit the use of broad-spectrum antibiotics. But these
drugs were dispensed widely in the CSHs. For wounded soldiers en route
to Germany, they were employed as a kind of antimicrobial body armor to
forestall future infection. But injured Iraqis would linger on
antibiotic IV drips for weeks because the local medical facilities were
overwhelmed or under rubble.
In the summer of 2003, civilian patients started getting sick at the
Saarland University Hospital, one of the German facilities that admitted
US troops evacuated from Iraq. A few months later, an elderly woman
being treated for chronic lung disease at Landstuhl died suddenly of
antibiotic-resistant acinetobacter pneumonia and bacteremia. DOD
investigators found a perfect genetic match between the bug that caused
her death and one infecting a military patient down the hall.
Eventually, more than 30 civilian patients picked up acinetobacter
infections at Walter Reed.
The bacteria was spreading beyond the theater of war.
Meanwhile, families of wounded US and British troops were being told
-often in haphazard ways - that their loved ones were infected with an
obscure organism they had somehow picked up in the desert.
A contractor named Merlin Clark was clearing mines near Baghdad for a
company called Ronco Consulting when an IED took off the front of his
left leg and severed a nerve in his right arm. When he first arrived at
Walter Reed, his wife, Marcie, says, "They told us they had found
bacteria, which you would expect from a dirty wound. We were more
concerned that he might lose his leg."
Just before Marcie put her husband on a medevac to a hospital in
Orlando, Florida, a nurse handed her a folder, which she put in her
purse. "I went down to get Merlin's bags," Marcie recalls, "and the
soldier who brought me to the van told me, 'Put everything in the
laundry right away. Don't touch this stuff. Don't breathe around it.
It's got that bug the guys are bringing back from Iraq.'"
She tossed the dusty clothes in a hotel washing machine and checked the
folder, where she saw the words Acinetobacter baumannii for the first
time. Frantic for more information about her husband's infection, she
found little advice on sites for Iraq war veterans. "We felt so alone,
having to figure out everything for ourselves," she says. (When
PDHealth.mil, a Web site for doctors who treat vets, finally added an
acinetobacter FAQ in 2005, it became one of the two most popular pages
on the site.)
A veterans' activist named Kirt Love helped Marcie create a Web site to
raise public awareness of the outbreak, which launched in 2004 at
www.acinetobacter.org. Email started pouring in. "After speaking with
other family members at Brooke, I discovered that almost all of their
sons and daughters, husbands and wives, had tested positive," wrote the
mother of one infected soldier. Another message read: "An apparently
healthy civilian registered nurse working in the ICU at the National
Naval Medical Center in Bethesda has a life-threatening acinetobacter
infection - Are other workers within the same environment equally at
risk?"
As the bacteria spread through hospitals in the US and Europe, the DOD
worked overtime to keep a lid on the rumors. In a PowerPoint
presentation about acinetobacter and pneumonia delivered at the US Air
Force School of Aerospace Medicine, a slide labeled "How to handle the
press" read: "Don't lie. Don't obfuscate. Don't tell them any more than
you absolutely have to."
Quietly, in spring 2004, a group of military doctors, infectious-disease
specialists, and microbiologists decided to find out what was really
going on with this bug. "My concern was that we were changing the
bacterial environment in our hospitals, and I wasn't seeing a whole lot
being done about it," says Tim Endy, the former communicable-disease
research director at Walter Reed. "And now there were infections in
patients who had never been to Iraq. The potential consequences to
health care and to the cost of health care are huge."
The bills for imipenem use were soaring at Walter Reed, and each dose of
the drug contributed to the snowballing resistance of the bacteria. Endy
drafted a paper that became the catalyst for a full-fledged
epidemiological consultation (an epicon, in military-speak) under the
authority of the Army Surgeon General. Dozens of infectious-disease
experts joined the investigation, along with academic researchers and
epidemiologists from the CDC.
The task force sent field teams into Iraq and Kuwait to gather soil
samples, swipe stretcher handles, and scour chow halls. When a storm
dumped sand onto the decks of the Comfort, they swabbed the gunwale. To
put the IED theory to the test, they took samples of bacteria from the
dirty wounds of soldiers as they were admitted to the Ibn Sina. They
also analyzed soil archived by the DOD before the war began.
The investigators did find acinetobacter in Iraq. It wasn't in the dirt
- except for a few bugs under a dripping air conditioner outside a
health care facility in Mosul - or in the fresh wounds, either. But
multidrug - resistant Acinetobacter baumannii was thriving in the
emergency rooms, ICUs, and operating rooms of the combat support
hospitals. As Paul Scott, one of the lead investigators, told a meeting
of civilian epidemiologists in Chicago last spring, "This appeared to be
a hospital-associated outbreak throughout our entire health care
system."
The wounded soldiers were not smuggling bacteria from the desert into
military hospitals after all. Instead, they were picking it up there.
The evacuation chain itself had become the primary source of infection.
By creating the most heroic and efficient means of saving lives in the
history of warfare, the Pentagon had accidentally invented a machine for
accelerating bacterial evolution and was airlifting the pathogens
halfway around the world.
To stem the outbreak at its source, the epicon team proposed sweeping
reforms throughout the combat zone. The CSHs had to be run more like
real hospitals, with frequent scrub-downs, stringent hand-washing, and
HEPA filters to clean the air. The dead tissue surrounding "frag?"
wounds turned out to be an ideal colonization site for the bugs, so it
had to be removed more aggressively up front. "If you don't have that
necrotic tissue, your own innate defenses help keep the wound clean,"
says Kim Moran, a tropical-disease specialist who assisted the
investigation when she worked at Walter Reed. Wound dressings needed to
be changed less often, so bacteria from the hospital environ-ment had
less opportunity to get in. And the broad-spectrum anti-biotics had to
be reserved for the treatment of identified bugs.
At first, these reforms ran into a major obstacle: Each link in the
evacuation chain was owned by a different branch of the DOD. "There was
no coordination among the services about infection-control policy," Endy
says. "No coordination about what kinds of antibiotics to use, no
communication within the services about infectious disease problems. So
it was almost impossible to coordinate any kind of broad policy
changes." But then the task force phoned Donald Jenkins, a
quick-thinking trauma surgeon at Balad who had already taken stock of
the situation and tightened infection control in his own hospital.
Jenkins briefed Elder Granger, head of the medical command throughout
the region. "We basically tried to initiate a policy change from the
bottom up, rather than the top down," Endy recalls. "And it worked."
Back in Washington, the DOD ramped up its medical surveillance networks
to track the enemy as it moved instead of waiting for reports of
full-blown infections. Epidemiological data across the armed services
was logged in a central database for the first time. To pinpoint the
particular strains causing the military infections, the investigators
shipped more than 200 samples of acinetobacter to a biotech firm called
Isis Pharmaceuticals, which has developed a new system for genetically
fingerprinting unknown pathogens. For purposes of comparison, the
Institut Pasteur in France also sent samples gathered during outbreaks
in European hospitals years before the war.
"Lo and behold, most of the bacteria from the military hospitals were
the same as the isolates from Europe - the same molecular signatures,
the same patterns of antibiotic resistance," says Isis microbiologist
David Ecker. "So my hypothesis became that there was a contamination of
the US military health care system from organisms circulating in Europe,
which happened somewhere along the path of the wounded soldiers."
The task force concluded that Camp Dogwood and Ibn Sina Hospital were
likely the first links in the chain where the bugs took hold. At the
epidemiologists' meeting in Chicago last spring, Paul Scott said that
some of the medical equipment used at the two facilities was originally
packed in Germany and may have been contaminated before it was shipped
to Iraq. But the "index case" that set the whole process in motion may
never be known.
It's not over. Acinetobacter is now a difficult part of daily life in
many military hospitals, as it is in civilian ICUs and burn wards
worldwide. And the rise of many other types of multidrug-resistant
bacteria will make things even more difficult in the next few years,
because there are few new antibiotics coming down the pipeline.
"The bugs are outpacing us, and these drugs are not the kind that bring
in incredible profits," says Robert Guidos, director of public policy
for the Infectious Diseases Society of America. "We're planning for
bioterrorism and pandemic influenza, but what about the hundreds of
thousands of people dying each year from nontheoretical situations? We
need to think in longer terms."
One of the most unsettling long-term questions about the military
outbreak is how far the bugs of war will proliferate now that thousands
of Iraq veterans have entered the VA hospital system. Many of the older
vets who are already there - struggling with chronic conditions for
decades, in and out of nursing homes - fall into the bacteria's target
demographic.
Duane Hospenthal of the DOD downplays the possibility that acinetobacter
could become a problem in the wider population. "Mom comes to visit her
son," he says, "and everybody's dressed up in gowns and gloves and hats
and masks, and she wants to know, 'Is this something I'm going to drag
home to my 4-year-old?'" Those are the misconceptions I have to deal
with from day to day. I can easily tell the family, "No, this is
something we do to keep it from passing from patient to patient. If you
have it on your hands, it's not going to cause any disease.'"
Once acinetobacter makes itself at home in a health care facility,
however, it's hard to get rid of and easy to pass along. Before Roberta
Carey started working for the CDC, she spent months trying
unsuccessfully to eradicate the bug from a university hospital in
Illinois. "This organism requires many different assaults to get rid
of," she says. "We see the bacteria metastasizing to neighboring
institutions because medical personnel, students, families, and patients
go back and forth into the community and to other medical centers. So we
have to be vigilant."
When a team of geneticists unlocked the secret of the bug's rapid
evolution in 2005, they found that one strain of multidrug-resistant
Acinetobacter baumannii carries the largest collection of genetic
upgrades ever discovered in a single organism. Out of its 52 genes
dedicated to defeating antibiotics, radiation, and other weapons of mass
bacterial destruction, nearly all have been bootlegged from other bad
bugs like Salmonella, Pseudomonas, and Escherichia coli.
In the open source world of bacteria, everyone is working for the
resistance. Ramping up the immunity of any single organism, while
dramatically increasing the size of the population most susceptible to
infection, only helps the enemy. To an aspiring superbug, war is
anything but hell.
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Larry Scott
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