Though African sleeping sickness—formally known as human African trypanosomiasis—likely has been present in East Africa for many centuries, the first recorded descriptions of the disease date to the late 19th century, when European powers began their conquest and colonization of much of the continent. The disease spread along with the upheaval of colonialism: Forced African labor, as well as the construction of roads and railways, led people to move more quickly from region to region, making it easier for different strains of the disease to spread between far-flung rural villages.
The first major reported epidemic occurred around 1900, primarily in Uganda and the Congo Basin, affecting some 500,000 people. In 1903, British microbiologist David Bruce and his colleagues on the Royal Sleeping Sickness Commission to Uganda confirmed that sleeping sickness was transmitted via the tsetse fly. Though the fly is not born with the parasite that causes the disease (dubbed Trypanosoma brucei), it can ingest it after biting an infected person or animal.
Drug therapy, screening measures and insect control techniques such as pesticides largely brought the disease under control by World War II, and today there are fewer than 10,000 confirmed cases reported annually. However, African sleeping sickness tends to affect people in epidemics, and there were 300,000 cases reported as recently as 1998. Found only in Africa, the disease threatens millions of people in 36 countries. Sleeping sickness attacks the central nervous system and causes confusion, slurred speech, seizures and difficulty walking and talking, among other symptoms. Without treatment, which is long and arduous, it is always fatal. Currently, no vaccine exists because the parasite that causes sleeping sickness is able to evade mammals’ immune systems. The tsetse fly also spreads nagana, an animal form of trypanosomiasis that affects some 3 million cattle and other animals in sub-Saharan Africa each year, threatening food security and making entire regions of Africa inhabitable to livestock.
Over the past decade, more than 140 scientists representing 78 research institutions in 18 countries have worked to sequence the genome of Glossina morsitans, one of several tsetse fly species, in the hopes that a better understanding of the insect’s biology could lead them to new ways of combating it. In contrast to other flies, which lay hundreds of eggs, a female tsetse fly gives birth to a single larva that weighs as much as she does. The tsetse fly is also the only insect to nurse its young: The larva nurses on a milk gland inside the mother’s uterus, ingesting milk proteins that work in a similar way to those in human breast milk.
This week, the scientists announced that they had successfully sequenced the tsetse fly genome and found several areas that could lead to improved insecticides or repellents. Their findings were published in the journal Science, along with 11 companion papers in various Public Library of Science (PLOS) journals. In particular, they pinpointed a gene that controls milk production, as well as one that enables the fly to extract water from the animal or human blood it feeds on. Understanding these genes, they hope, will lead to the development of a chemical that could interfere with the fly’s reproduction or survival processes, helping to eradicate it altogether.
In addition to the challenges posed by the tsetse fly’s complicated biological profile, the sequencing of its genome took a long time because of a relative lack of funding. Serap Aksoy of the Yale School of Public Health, whose laboratory ran the project, told the New York Times that federal grants went first to mosquito-borne diseases, the major threat to Americans. In the end, the project was completed for only $10 million in funds that came mostly from the World Health Organization, the Wellcome Trust and the Ambrose Monell Foundation, while scientists from the United States, France, England, Japan and various African countries donated their time to the project.