The young Army medic would not stop bleeding.
He had been put on a powerful regimen of antibiotics by doctors aboard the hospital ship Comfort in the Persian Gulf. But something was wrong.
He was in shock and bleeding from small pricks where nurses had placed intravenous lines. Red, swollen tissue from an active bacterial infection was expanding around his abdominal wound. His immune system was in overdrive.
How odd, thought Dr. Kyle Petersen, an infectious disease specialist. He knew of one injured Iraqi man with similar symptoms and a few days later encountered an Iraqi teenager with gunshot wounds in the same condition.
For The Record
Los Angeles Times Tuesday, October 02, 2007 Home Edition Main News Part A Page 2 National Desk 1 inches; 35 words Type of Material: Correction
Bacterium: An article in Sunday's Section A about infections among soldiers caused by a drug-resistant bacterium known as Acinetobacter said the name was derived from the Latin for "motionless." The word is derived from Greek.
For The Record
Los Angeles Times Sunday, October 07, 2007 Home Edition Main News Part A Page 2 National Desk 1 inches; 37 words Type of Material: Correction
Bacterium: An article in the Sept. 30 Section A about infections among soldiers caused by a drug-resistant bacterium known as Acinetobacter said the name was derived from the Latin for "motionless." The word is derived from Greek.
Within a few days, blood tests confirmed that the medic and the two wounded Iraqis were all infected with an unusual bacterium, Acinetobacter baumannii.
This particular strain had a deadly twist. It was resistant to a dozen antibiotics. The medic survived, but by the time Petersen connected the dots, the two Iraqi patients were dead.
It was April 2003, early in the Iraq war -- and 4 1/2 years later, scientists are still struggling to understand the medical mystery.
The three cases aboard the Comfort were the first of a stubborn outbreak that has spread to at least five other American military hospitals, including Walter Reed Army Medical Center in Washington and the Army's Landstuhl Regional Medical Center in Germany.
Hundreds of patients -- the military says it has not tabulated how many -- have been infected with the bacterium in their bloodstream, cerebrospinal fluid, bones or lungs. Many of them were troops wounded in Iraq or Afghanistan; others have been civilians infected after stays in military hospitals.
At least 27 people have died in military hospitals with Acinetobacter infections since 2003, although doctors are uncertain how many of the deaths were caused by the bacteria.
The rise in infections has been dramatic. In 2001 and 2002, Acinetobacter infections made up about 2% of admissions at the specialized burn unit at Brooke Army Medical Center in Texas. In 2003, the rate jumped to 6%, and then to 12% by 2005. Other military hospitals have reported similar increases.
In the early days of the war, there were so many infections in an intensive care unit on the Comfort that a nurse posted a sign: "Acinetobacter Alley." In two months, the bacterium was found in 44 of the 211 patients wounded in battle.
It was getting out of control. Petersen pleaded for help on an infectious disease mailing list.
"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?"
A persistent slacker
It was no surprise that Petersen knew little about Acinetobacter -- which has long been seen as the slacker of the bacterial world.
It's called Acinetobacter, from the Latin word for "motionless," because the bacterium lacks flagella or cilia to move.
"Organisms that are relatively wimpy pathogens . . . are not high on people's list," said Fred Tenover, a microbiologist at the Centers for Disease Control and Prevention in Atlanta.
The bacterium is persistent, however, and requires few nutrients. It lives naturally in soil and can survive for days on dry surfaces, such as doorknobs or hospital equipment.
Acinetobacter usually threatens only the weakest of the weak, those whose immune systems are compromised because of old age, trauma or disease. Even then, garden-variety Acinetobacter is easily controlled with common antibiotics.
But the situation started to change about two decades ago.
Acinetobacter followed an evolutionary path trod by numerous other bacteria since World War II, when antibiotics were introduced widely. Bacteria not killed by an antibiotic would pass on their resistance to later generations.
The process was quickened by the often profligate use of the drugs, which allowed more bacteria to develop resistance.
Today a host of diseases, such as tuberculosis and gonorrhea, have highly antibiotic-resistant strains.
"If we use antibiotics to kill off everything else, what is left standing is very, very drug resistant," said CDC epidemiologist Arjun Srinivasan. "Acinetobacter is one of those left standing."
Tenover first noticed a strain of Acinetobacter with some drug resistance in the mid-1980s while working at a veterans hospital in Seattle. Several years later, he met with Ghassan Matar, a visiting Lebanese scientist at the CDC, whose samples of Acinetobacter baumannii from patients in a Beirut hospital raised another red flag.
The infections were a legacy of years of fighting. Positive tests for Acinetobacter more than tripled at the hospital from 1983 to 1984 and stayed high for years after. The samples Matar brought were already resistant to two important classes of antibiotics.
In the following years, civilian hospitals in the U.S. and around the world reported sporadic outbreaks of drug-resistant Acinetobacter.