The T.b. gambiense parasite is truly a menace. It causes African sleeping sickness — a disease that attacks the nervous system and brain, disrupting sleep, causing rapid mood swings and confusion, essentially driving people mad before it kills them.
Researchers have been studying the parasite for years, looking for leads to help them develop a vaccine or drugs that would wipe it out.
So far, no luck. But now they’ve found a juicy tidbit that could lead to the critter’s undoing: it’s been thousands of years since T.b. gambiense last had sex.
See, sexual reproduction shuffles up an organism’s DNA, creating genetic diversity that helps a species adapt and survive. “But rather than reproducing through sex, this particular parasite has been cloning itself — making carbon copies of itself,” explains William Weir, a bioinformatician at the University of Glasgow who led the research, which was published Tuesday in the online journal eLife.
That makes the parasite especially vulnerable to attack — some good news in the long-running battle against sleeping sickness.
Efforts to control tsetse flies — whose bites are responsible for transmitting the parasite to humans — have helped cut down the number of cases since the last sleeping sickness outbreak, which subsided in the 1990s. Around 7,000 cases were reported in 2012, but the World Health Organization estimates that the actual number is closer to 20,000.
In their research, Weir and a team of researchers collected and analyzed the blood samples of 75 people across sub-Saharan Africa. They found that the parasites in all the samples were genetically identical. “In fact they can all be traced back to a single parasite that lived thousands of years ago,” Weir says. “There’s no parasite that I know of that operates quite like this one.”
The parasite that causes sleeping sickness, just like the parasite that causes malaria, is a single-celled protozoan capable of reproducing sexually and asexually. “What happens with these sorts of organisms is if they find a niche they’re particularly well adapted to, they will suddenly go crazy and make clones very fast,” Weir notes.
The malaria parasite continually switches back and forth between asexual multiplication (which is quicker and easier) and sexual reproduction (which drives evolution). But the sleeping sickness parasite seems to have found its ideal environment in human hosts — it hasn’t needed to evolve.
The cloning process isn’t perfect, so tiny but potentially harmful mutations have been accumulating in the parasite’s population over the years, Weir says. And if the parasite carries on its celibate lifestyle, the mutations will build up and eventually lead to its extinction.
“That could take forever, and I don’t think we can really sit and wait for that to happen naturally,” says Marilyn Parsons, a microbiologist at the Center for Infectious Diseases in Seattle, Washington, who was not involved in the research.
“But this discovery makes me hopeful,” she notes. “If we get develop a good drug, it’s more likely to work against all the parasites.”
There are currently some treatments for the disease, but the chemicals used have dangerous side-effects. Early stages are easier to treat, but difficult to diagnose. The infection can lie dormant for years before symptoms start to develop.
So with the recent insights into the parasite’s sex life (or lack thereof), scientists have a golden opportunity develop a drug that can defeat it for good — as long as the bugger sticks to no sex.