HELENA (AP) - Researchers at a Montana laboratory helped determine how a new tick-spread disease manages to survive one of the most effective disease-killing assaults the human body can muster.
Scientists at Rocky Mountain Laboratories in Hamilton and at the University of Minnesota showed that the bacteria actually reproduces after it has been gobbled up by a front-line immune cell called a neutrophil.
A paper on their research was published this month in the online edition of the Journal of Immunology.
Despite its alarmingly clever avoidance of the body's immune system, the bug in question is not a very serious disease. It usually causes fever, muscle aches and nausea and can be easily treated with everyday antibiotics. It's not known to exist in Montana.
''It's just unusual that this is a pathogen that survives,'' said Frank DeLeo, who led the Montana research.
Neutrophils, the most common immune system cells, kill pathogens by ingesting them, he said. Once inside the neutrophil, the pathogen is almost always kept in a special part of the disease-killing cell where the neutrophil bombards it with bleach-like chemicals, destroying it. Then, the neutrophil self-destructs.
Not so with human granulocytic anaplasmosis or HGA.
This unusual, tick-borne disease actually seeks out neutrophils. And instead of going to the special germ-killing chamber, HGA is able to get into a different part of the cell where it cannot be touched by the body's homegrown disinfectant.
First cultured in people in 1996, the bug also manages to postpone the programmed self-destruction of the neutrophil. DeLeo said he doesn't know how long HGA is able to live inside the neutrophil, but long enough to reproduce.
''Between 36 to 48 hours,'' he said. ''It definitely replicates inside the cell.''
The young HGA bacteria then somehow escape, through a means not yet clear, to infect other cells.
The way it manipulates the immune system for its own survival is unique, DeLeo said. The bug doesn't even have to be alive to play its game with neutrophils. DeLeo thinks there must be some kind of protein on the outside of the bacteria that enable it to avoid the neutrophil death chamber and keep the immune cell from destroying itself.
''On a global scale, it was very striking that this bacteria did not trigger what we typically see,'' DeLeo said.
