Modern medicine has made important strides in combating sleeping sickness: a debilitating and sometimes deadly parasitical disease. But treating human patients may not be enough to wipe it out completely, according to research published today. The study suggests that animals play a bigger role in transmitting sleeping sickness than previously thought, and suggests that they could form a natural reservoir from which sleeping sickness could bounce back even if it were defeated in humans. In fact, the researchers say, the loss of wildlife habitat in Africa—and not human treatment programs—could be the main reason that sleeping sickness disease, usually called human African trypanosomiasis (HAT), is now on the retreat.
HAT is caused by a single-celled parasite, Trypanosoma brucei, that enters the body through the bites of tsetse flies. The parasite later moves into the brain, where it causes drowsiness, confusion, and comas. An estimated 20,000 to 30,000 people in sub-Saharan Africa are infected every year and about 70 million are at risk. Left untreated, HAT is fatal.
About 2% of HAT cases are caused by a subspecies called T. brucei rhodesiense, which is found in eastern and southern Africa. It is considered a zoonosis: an infection that can be transmitted to humans from animals such as cattle. That means it will be almost impossible to eradicate, most scientists say.
Prospects seemed much brighter for the other subspecies, T. brucei gambiense, which is endemic in countries in Central and West Africa and causes the remaining 98% of cases. Although T. brucei gambiense has also been found in various wild and domestic animal species, these are usually considered sporadic, "dead-end" hosts, from which the disease isn't transmitted further. "The West African form of HAT is often thought of as an exclusively human disease," says Peter Hotez, an expert on neglected tropical diseases at Baylor College of Medicine in Houston, Texas. Hence the current strategy to eliminate it: finding human cases of HAT and treating them, with the hope that this will eventually get rid of the disease altogether.
But researchers at the London School of Hygiene & Tropical Medicine wondered whether animals might play a bigger role in transmitting HAT gambiense. To investigate that question, they used data collected between 1998 and 2004 in the Bipindi area in Cameroon. After doctors found a number of HAT cases in two villages there, French and Cameroon scientists visited the villages, sampling thousands of humans but also taking blood samples from pigs, goats, crocodiles, antelopes, and primates, which they tested for Trypanosoma DNA. They also caught tsetse flies and determined what species they had last fed on.
From these data the scientists built a model, calculating how likely one infected individual of a certain species was to infect another individual of the same and of another species. The results suggest that HAT gambiense cannot be sustained in a human population alone. "There really seems to be a whole mix of animals playing a role in transmission," says mathematical biologist Sebastian Funk, one of the authors of the study. "So there is a good chance that if you get rid of the disease in humans, it will continue to cycle in animals and come back to humans." In fact, the decline in HAT in countries such as Gambia and Nigeria may be mainly due to the reduction in wildlife habitats and populations in the last decades, the authors write today in PLOS Computational Biology.
The paper adds weight to the argument that animals are an important factor in HAT transmission, says Wendy Gibson, who researches HAT at the University of Bristol in the United Kingdom. "You cannot really test the idea that animal reservoirs are important other than building a model from the data available. And they used the best data we have."
The paper is "interesting and useful," Hotez says, but there is still too much uncertainty in the numbers to know whether targeting animals will be necessary to eliminate the disease. It might be possible, he says, that finding and treating humans patients alone will eventually cause it to peter out and disappear. "It is an important research question that needs to be looked at while elimination efforts are ongoing."