In a new study published in the journal Science, researchers from the Oklahoma Medical Research Foundation and Columbia University have found clues as to why the bacteria that cause Legionnaires’ disease can escape from their natural hosts before killing them. Scientists hope this information will provide a better understanding of the potentially fatal disease, which strikes an estimated 8,000 to 18,000 Americans each year.
The first known outbreak of the disease occurred in 1976, when scores of people attending an American Legion convention in a Philadelphia hotel fell mysteriously ill with a pneumonia-like infection. Ultimately, 221 people were infected and 34 died in this mysterious outbreak, later labeled Legionnaires’ disease. Scientists eventually determined that bacteria (known as Legionella pneumophila) growing in the hotel’s cooling tower caused the outbreak.
For the Science study, scientists at Columbia University created a mutant strain of the bacteria that lacked a pair of key proteins. After marking the bacteria with fluorescent proteins, researchers at OMRF observed what happened when amoebas consumed the altered strain.
“Typically, the bacteria would survive and replicate in these hosts, then escape,” said OMRF’s Margaret Clarke, Ph.D., an author of the study. “When the mutant bacteria were taken up by the amoeba, they survived and replicated normally, but they could not escape.” Without the ability to escape, she said, the multiplying bacteria would eventually cause the amoebas to burst, killing them.
These latest observations are important because they closely resemble what happens when Legionella bacteria enter a person’s system. “In humans, cells called macrophages can kill most types of bacteria,” Clarke said. “But certain pathogens, including the bacteria that cause Legionnaires’ disease, can survive and replicate inside of macrophages, eventually breaking them open and spreading the infection.”
According to Clarke, these new findings help to clarify why the bacteria are more destructive to human cells than they are to the single-celled organisms in which they normally grow. “The more we understand about how these bacteria interact with the cells they infest, the better our chances of learning how to alter these interactions in a therapeutic way,” she said.
Although certain antibiotics have been effective at fighting Legionnaires’ disease, the infection still poses a deadly risk to people with suppressed immune systems – including the elderly, infants, eczema sufferers and those undergoing chemotherapy – and kills 5 to 30 percent of those it strikes. The bacteria’s abundance in environments both natural (creeks, ponds) and man-made (air-conditioning and water systems) ensures that it will continue to threaten human health.
Howard A. Shuman, Ph.D., a professor of microbiology at Columbia University in New York, is the senior author on the paper, which appears in the Feb. 27, 2004 issue of Science.
OMRF (
www.omrf.org) is a nonprofit biomedical research institute dedicated to understand and curing human disease. Its scientists focus on such critical research areas as Alzheimer’s disease, cancer, and cardiovascular disease. OMRF is home to Oklahoma’s only Howard Hughes Medical Institute investigator and only member of the National Academy of Sciences in the area of biomedical research.
