Scientist at Hamilton’s Rocky Mountain Laboratories makes breakthrough with research on Q fever

The genetic blueprint of an important disease-causing microbe has been deciphered and analyzed in a collaboration with scientists at Hamilton’s Rocky Mountain Laboratories.

By JENNY JOHNSON Staff Reporter
Ravalli Republic

The labs’ Robert Heinzen worked on the breakthrough with scientists at the Institute of Genomic Research in Rockville, Md. Basically the scientists unveiled the genetic blueprint for a bacteria that causes Q fever, a flu-like illness in humans.

The information opens a treasure trove of information that will allow scientists to develop a much higher resolution picture of the microbe’s biology and its ability to cause disease, according to John Heidelberg, who headed the project supported by the National Institute of Allergy and Infectious Diseases, an arm of the National Institutes of Health.

The microbe, named Coxiella burnetii, is a potential agent of bioterrorism and is named after Harold Cox, a former Rocky Mountain Laboratories scientist who discovered and isolated a strain of the germ in the mid 1930s.

Severe cases of Q fever are fatal. The bug is of concern as a potential bioterrorist threat because early diagnosis of the disease is difficult and the microbe is a hardy organism that can be aerosolized.

A report describing the sequencing project will be published online this week in the "Proceedings of the National Academy of Sciences" and will appear in the journal’s April 29 print edition.

"The Coxiella genome sequence is a major advance," Heinzen said. "Not only will it allow us to more easily study genes that may be involved in causing disease, it also should reveal targets for improved diagnostics and potential vaccine candidates."

The analysis found many genes that appear to be involved in the microbe’s virulence and interaction with its human or animal host. Although the organism does not cause obvious disease in most animals, infected livestock are the primary reserve of the bacteria, according to the science report.

The germ is difficult to manipulate genetically because it only replicates inside mammalian cells. It primarily resides in human immune cells called macrophages, known as indiscriminate microbe eaters. It is unusual because it has an uncanny ability to survive in the environment and resist being broken down, Heinzen said.

Heinzen, who has studied C. burnetii and related bacteria for about 20 years, helped the project leaders interpret what the genome revealed about the biology of the organism. Among the team’s findings, the Q fever microbe does not appear to be as dependent on its human or animal host as other intracellular pathogens that cause leprosy, typhus fever or chlamydia, for example, indicating that the bacterium developed the intracellular adaptation more recently. The research also suggests that the Q fever genome is less stable than the genomes of these other pathogens.

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