Healthcare Infection Prevention: Wounded soldiers hit by Acinetobacter infections

Wounded soldiers hit by Acinetobacter infections

Infection control and the fog of war

The fog of war is making it difficult to get a clear epidemiologic picture of why so many soldiers wounded in Iraq and Afghanistan are developing highly resistant Acinetobacter baumannii infections.

First the good news: Though the pathogen is highly drug resistant and certainly contributes to morbidity, the soldiers are generally surviving infections that could be fatal in more immune compromised patients. In a published account focusing on 23 soldiers at Walter Reed Army Medical Center in Washington, DC, investigators note that mortality rates associated with nosocomial Acinetobacter infection typically are in the range of 19%-54%.¹ Rather than excessive virulence, the prime driver of the death rate for the infections is treatment failure due to high levels of antibiotic resistance. Yet all of the 23 infected soldiers survived.

"None of the patients in this series failed therapy, and none died because of Acinetobacter infection," the investigators reported. "Such is not the case in outbreaks among immunocompromised or intensive care patients, in whom Acinetobacter infection leads to increased mortality. The successful outcomes in this case series may be a reflection of the youth and general good health of the soldiers."

However, the soldiers have an increased risk for recurrent Acinetobacter infections, meaning some may be dealing with the problem intermittently for many years to come. Meanwhile, epidemiologists are trying to determine the source of the pathogen. The prevailing theory has been that it sprung from the sand and dust of Iraq’s ubiquitous desert climate. Yet environmental sampling is yielding few isolates. Some epidemiologists have wondered whether it is a pathogen common to Iraqi hospitals that now is colonizing American soldiers. That was one of the questions that went unanswered at an update on the situation recently in Chicago at the annual meeting of the Society for Healthcare Epidemiology of America (SHEA).

"At this point, many unanswered questions remain, including what is the source of the infections," said Paul Scott, MD, MPH, an epidemiologist at the Walter Reed Army Institute of Research. "There are several theories that this could be an environmental bug that is occurring upon injury. Because this is a well-known nosocomial organism, is that the source of the outbreak? Could it be both?"

First cases right after combat

At a SHEA session on the situation, Scott reviewed the beginning of the outbreak and updated control efforts. "In March 2003, the combat phase of Iraqi Freedom began," he said. "Two days later, the first Acinetobacter isolate was obtained from a patient at Landstuhl Regional Medical Center evacuation hospital in Germany."

The case count grew from there, with the first big cluster identified on the U.S. Comfort naval hospital ship stationed in the Persian Gulf. In April 2003, an active surveillance program began at Walter Reed to look for incoming cases.

"The first thing we did was to confirm that it was in fact an outbreak," Scott said. "From surveillance network data, we would have expected that 1% to 2% of all wound infections — consistent with other similar facilities — would have been Acinetobacter."

The number of infections occurring immediately verified the outbreak suspicions, as military hospitals were running well beyond baseline rates for the pathogen. "In 2003 at Landstuhl, there were a total of three Acinetobacter isolates, and at Walter Reed there were 11," he said. "In just six weeks after combat began in Iraq, there were 12 at Landstuhl and 41 at Walter Reed. We looked back in the literature to see if this had been a similar problem in the first Gulf War in 1991, and it had not."

For the most part, the infected soldiers are seriously wounded combat casualties requiring multiple invasive interventions. "Of the isolates we have collected, the most common site was wounds in the extremities, followed by airway isolates, blood and urine," Scott said. "These were very resistant organisms. Seven percent were resistant to all antibiotics tested and 26% were sensitive to carbapenem [antibiotics] only. These patients had been treated at multiple field hospitals at Iraq and Kuwait as well as our military hospitals in the United States."

Investigators went to the seven field hospitals in Iraq and neighboring nations, searching for isolates in the health care settings and surrounding environment. They also looked at outpatients to see if soldiers were colonized on the skin before they entered the military health care system.

"We were able to collect 37 Acinetobacter isolates from out environmental sampling [of hospitals]," he said. "The majority of them were obtained from critical care treatment areas including operating room equipment, the intensive care unit and the emergency department. We found a couple in sinks in the radiology section, and bedrails in a sick hall area."

However, very few isolates were recovered from the surrounding soil, which was considered the most likely source since soldiers are heavily exposed in the field and during sandstorms. Meanwhile, cases began appearing at Walter Reed in patients with no link to war, demonstrating that nosocomial transmission now was occurring.

"This appeared to be a hospital associated outbreak throughout our entire health care system and the outbreak source is probably multifactorial," Scott said. "Clearly we have environmental contamination of our health care facilities. We have demonstrated nosocomial transmission in our health care facilities, and skin colonization is present in our soldiers. Soil contamination has not been ruled out because we did find some Acinetobacter in the soil, although it was very rare."

Though nosocomial transmission is occurring, the timing of infection onset suggests pre-hospital exposures. "More than 50% of the bloodstream infections occurred within the first 48 hours of their hospitalization," Scott said. "So they often arrived well into their infections."

Infection control measures adopted at Walter Reed to deal with the outbreak include:

• All injured soldiers admitted to the facility returning from the war are placed in contact isolation.
• Screening cultures of the axilla, groin, and any open wound are completed to assess for colonization with Acinetobacter.
• If cultures taken on admission are negative, the soldier is then removed from contact isolation. Soldiers with wound infection or osteomyelitis caused by Acinetobacter are kept in contact isolation for the duration of hospitalization.

"These infections do appear to be associated with adverse outcomes," Scott told SHEA attendees. "The whole investigation really underscored the need for infection control measures that work throughout the casualty treatment and evacuation system. This is the only way we are going to control Acinetobacter. The question that remains is how to do that? You saw the [slide of] dust blowing around our field hospitals. Keeping the environment out of our hospitals is very difficult. Then in evacuation, these patients go on aircraft where they are stacked several high. There is very small amount of space between patients."

Reference

1. Davis KA, Moran KA, McAllister CK. Multidrug-resistant Acinetobacter extremity infections in soldiers. Emerg Infect Dis 2005; 11:1,218-1,224.