Anti-sleeping sickness drives may also need to target animals
Trying to eliminate the main form of sleeping sickness in Africa by only targeting humans may end in failure as the disease would soon return from its animal reservoir, according to a study published today (17 January).
Sleeping sickness is a deadly disease caused by Trypanosoma parasites transmitted by tsetse fly bites. It affects up to 30,000 people a year in 36 countries in Sub-Saharan Africa, where there are two variants of the disease.
The east African type is known to also infect cattle and wild species, but the west African variant that accounts for more than 95 per cent of human cases is believed to persist mainly because of human-to-human transmission.
- Animals could be vital hosts of the tsetse fly-transmitted sleeping sickness parasite
- Efforts to eradicate the disease must focus on animal reservoirs as well as human infections
- But some disease hotspots have been eliminated without targeting animals, says expert
Now, a modelling study in PLOS Computational Biology challenges the notion that the parasites, Trypanosoma brucei gambiense, do not spread in animal populations in the absence of human infection.
Researchers used human and animal case data from two screening campaigns conducted in 1998-1999 in Cameroon — one of the few efforts to link the presence of the parasite in different animal species to human cases.
They found that, if the disease were eliminated from humans, it would take less than a year for it to be reintroduced if more than one tsetse fly in every 1,000 switched between animal and human hosts. They added that this is realistic as flies are unlikely to restrict themselves to just one host.
Sebastian Funk, lead author of the study and a researcher at Princeton University, United States, says that the study shows the usual method of eliminating the disease — by treating infected patients with drugs — is insufficient.
"The main message of this study is that we need to keep the animal reservoir in mind and it's not enough just to focus on humans," he tells SciDev.Net.
Funk says that human case control "has worked very well", but that "there's a risk of the disease coming back" if elimination efforts focus just on that.
The study also raises an "intriguing hypothesis" that the decline from a high of around 40,000 reported cases of sleeping sickness in 1998 might have been driven by the wildlife habitat loss.
"The reduction in wildlife habitats could play a role in the reduction of sleeping sickness," says Funk, although he adds that the paper did not examine this link systematically.
But Pere Simarro, head of the human African trypanosomiasis programme at WHO, is sceptical.
He says the finding about the animal cycle's role in the disease is not "strongly supported" by evidence in the paper.
"There are several examples where [the west African] sleeping sickness foci have been eliminated without taking the animal reservoir into account," he says. "Other factors have a crucial role in sleeping sickness transmission other than the animal reservoir, such as land use, demography, climate change and economic development."
PLOS Computational Biology doi: 10.1371/journal.pcbi.1002855 (2012)