Saturday, August 9, 2008


n August, 2000, Dr. Roger Wetherbee, an infectious-disease expert at New York University’s Tisch Hospital, received a disturbing call from the hospital’s microbiology laboratory. At the time, Wetherbee was in charge of handling outbreaks of dangerous microbes in the hospital, and the laboratory had isolated a bacterium called Klebsiella pneumoniae from a patient in an intensive-care unit. “It was literally resistant to every meaningful antibiotic that we had,” Wetherbee recalled recently. The microbe was sensitive only to a drug called colistin, which had been developed decades earlier and largely abandoned as a systemic treatment, because it can severely damage the kidneys. “So we had this report, and I looked at it and said to myself, ‘My God, this is an organism that basically we can’t treat.’ ”

Klebsiella is in a class of bacteria called gram-negative, based on its failure to pick up the dye in a Gram’s stain test. (Gram-positive organisms, which include Streptococcus and Staphylococcus , have a different cellular structure.) It inhabits both humans and animals and can survive in water and on inanimate objects. We can carry it on our skin and in our noses and throats, but it is most often found in our stool, and fecal contamination on the hands of caregivers is the most frequent source of infection among patients. Healthy people can harbor Klebsiella to no detrimental effect; those with debilitating conditions, like liver disease or severe diabetes, or those recovering from major surgery, are most likely to fall ill. The bacterium is oval in shape, resembling a TicTac, and has a thick, sugar-filled outer coat, which makes it difficult for white blood cells to engulf and destroy it. Fimbria—fine, hairlike extensions that enable Klebsiella to adhere to the lining of the throat, trachea, and bronchi—project from the bacteria’s surface; the attached microbes can travel deep into our lungs, where they destroy the delicate alveoli, the air sacs that allow us to obtain oxygen. The resulting hemorrhage produces a blood-filled sputum, nicknamed “currant jelly.” Klebsiella can also attach to the urinary tract and infect the kidneys. When the bacteria enter the bloodstream, they release a fatty substance known as an endotoxin, which injures the lining of the blood vessels and can cause fatal shock.

Tisch Hospital has four intensive-care units, all in the east wing on the fifteenth floor, and at the time of the outbreak there were thirty-two intensive-care beds. The I.C.U.s were built in 1961, and although the equipment had been modernized over the years, the units had otherwise remained relatively unchanged: the beds were close to each other, with I.V. pumps and respirators between them, and doctors and nursing staff were shared among the various I.C.U.s. This was an ideal environment for a highly infectious bacterium.

It was the first major outbreak of this multidrug-resistant strain of Klebsiella in the United States, and Wetherbee was concerned that the bacterium had become so well adapted in the I.C.U. that it could not be killed with the usual ammonia and phenol disinfectants. Only bleach seemed able to destroy it. Wetherbee and his team instructed doctors, nurses, and custodial staff to perform meticulous hand washing, and had them wear gowns and gloves when attending to infected patients. He instituted strict protocols to insure that gloves were changed and hands vigorously disinfected after handling the tubing on each patient’s ventilator. Spray bottles with bleach solutions were installed in the I.C.U.s, and surfaces and equipment were cleaned several times a day. Nevertheless, in the ensuing months Klebsiella infected more than a dozen patients.

In late autumn of 2000, in addition to pneumonia patients began contracting urinary-tract and bloodstream infections from Klebsiella. The latter are often lethal, since once Klebsiella infects the bloodstream it can spread to every organ in the body. Wetherbee reviewed procedures in the I.C.U. again and discovered that the Foley catheters, used to drain urine from the bladder, had become a common source of contamination; when emptying the urine bags, staff members inadvertently splashed infected urine onto their gloves and onto nearby machinery. “They were very effectively moving the organism from one bed to the next,” Wetherbee said. He ordered all the I.C.U.s to be decontaminated; the patients were temporarily moved out, supplies discarded, curtains changed, and each room was cleaned from floor to ceiling with a bleach solution. Even so, of the thirty-four patients with infections that year, nearly half died. The outbreak subsided in October, 2003, after even more stringent procedures for decontamination and hygiene were instituted: patients kept in isolation, and staff and visitors required to wear gloves, masks, and gowns at all times.

“My basic premise,” Wetherbee said, “is that you take a capable micro√∂rganism like Klebsiella and you put it through the gruelling test of being exposed to a broad spectrum of antibiotics and it will eventually defeat your efforts, as this one did.” Although Tisch Hospital has not had another outbreak, the bacteria appeared soon after at several hospitals in Brooklyn and one in Queens. When I spoke to infectious-disease experts this spring, I was told that the resistant Klebsiella had also appeared at Mt. Sinai Medical Center, in Manhattan, and in hospitals in New Jersey, Pennsylvania, Cleveland, and St. Louis.

Of the so-called superbugs—those bacteria that have developed immunity to a wide number of antibiotics—the methicillin-resistant Staphylococcus aureus, or MRSA, is the most well known. Dr. Robert Moellering, a professor at Harvard Medical School, a past president of the Infectious Diseases Society of America, and a leading expert on antibiotic resistance, pointed out that MRSA, like Klebsiella, originally occurred in I.C.U.s, especially among patients who had undergone major surgery. “Until about ten years ago,” Moellering told me, “virtually all cases of MRSA were either in hospitals or nursing homes. In the hospital setting, they cause wound infections after surgery, pneumonias, and bloodstream infections from indwelling catheters. But they can cause a variety of other infections, all the way to bacterial meningitis.” The first deaths from MRSA in community settings, reported at the end of the nineteen-nineties, were among children in North Dakota and Minnesota. “And then it started showing up in men who have sex with men,” Moellering said. “Soon, it began to be spread in prisons among the prisoners. Now we see it in a whole bunch of other populations.” An outbreak among the St. Louis Rams football team, passed on through shared equipment, particularly affected the team’s linemen; artificial turf, which causes skin abrasions that are prone to infection, exacerbated the problem. Other outbreaks were reported among insular religious groups in rural New York; Hurricane Katrina evacuees; and illegal tattoo recipients. “And now it’s basically everybody,” Moellering said. The deadly toxin produced by the strain of MRSA found in U.S. communities, Panton-Valentine leukocidin, is thought to destroy the membranes of white blood cells, damaging the body’s primary defense against the microbe. In 2006, the Centers for Disease Control and Prevention recorded some nineteen thousand deaths and a hundred and five thousand infections from MRSA.

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