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 Acinetobacter Baumannii
by Steve Silberman
Left, the operating room at Ibn Sina Hospital in Baghdad, an Army facility implicated in the spread of Acinetobacter baumannii. (photo: Peter Van AGTMAEL/POLARIS)
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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