Natural Killers Degrade Brain Pathogen

By Philip Yam | May 19, 2011, scientificamerican.com:

Remember mad cow disease? In the 1980s, cattle in the U.K. had begun contracting a fatal brain ailment triggered by an infectious protein called a prion. The pathogen could spread to humans who ate contaminated beef. Officials brought the bovine epidemic under control with major changes in agricultural practices.


Unfortunately, the same cannot be said for a cousin of the sickness, one that targets deer, elk and moose in the U.S. Called chronic wasting disease (CWD), or "mad deer" disease, the ailment poses an unusual challenge in that it has spread among wild populations, not among herded animals. Wild animals go where they may, so you cannot institute controls the way you can for livestock. So it comes as good news that a naturally occurring disinfectant exists within common lichens and might actually be able to stop prions in the wild.


What has made prions difficult to control is their infamous durability. Boil water for a few minutes, and all the bacteria and viruses will be gone. Not so for the prion: it will be just fine, ready to infect. How does it fare in a dry heat of 600 degrees C? No problem there, either. How about ionizing radiation? Bring it on.


The prion's stubbornness caused many unfortunate medical mishaps in the days before researchers knew what they were dealing with. In the 1970s, electrodes used to treat epilepsy spread a human prion disease from one patient to another even though the electrodes had undergone standard sterilization and sat for 18 months before reuse. In a later test on monkeys, electrodes maintained their infectivity even after three bouts of sterilization. In the late 1980s, the processing of cadaver tissue—specifically, a brain lining called the dura mater that is sometimes used as a patch in neurosurgery—failed to inactivate prions from infected donors, leading to the transmission of a fatal brain disease to healthy recipients. (I recount these and other incidents in my 2003 book on prions.)


And the prion's resistance to inactivation is a big reason why mad cow disease spread: to save money, the makers of cattle feed, which spread the illness, had eliminated the use of solvents and extended heating that probably would have disabled the prion. In decontaminating an area that once harbored infected farm animals (such as sheep), U.S. officials spray down hard surfaces with a caustic solution such as sodium hydroxide (better known as plumber's lye), turn over several centimeters of soil to bury any prions on the surface and deem the land off-limits for years. Such draconian measures are one reason why farmers dread the diagnosis, even with government reimbursement for the loss.


Of course, such techniques won't work in wild animals, which spread prions via their urine, feces and saliva. First identified in the late 1960s, chronic wasting disease has been detected in deer, elk and moose in 19 U.S. states and two Canadian provinces (although much of that spread resulted from the transfer of animals for game ranches). Although no human has contracted CWD from eating venison or other cervid meat, the lessons from the mad cow epidemic led game officials to conduct massive culls and establish stricter butchering guidelines to prevent contamination from brain and spinal tissue, where infectious prions collect.


So news that a natural answer exists for prions is welcome. In a paper published May 17 in PLoS One , Christopher Johnson of the U.S. Geological Survey of the National Wildlife Health Center in Madison, Wisc., and his team describe experiments with lichens, symbiotic collections of algae, fungus and bacteria that casual observers might mistake for moss. Three common species of lichens, the team has found, exude an enzyme that breaks down the prion.


The scientists achieved the results in a test tube, but they suspect that lichen power will work in the wild. "While great caution must be exercised in extrapolating in vitro studies to environmental conditions, our data suggest lichens could contribute to prion degradation on the landscape," they wrote, noting that inactivation might occur when prions come into direct contact with the lichens or with nearby soil. The team plans to test the hypothesis and even see if animals are protected from CWD if they eat the lichens.