Image of a tsetse fly taken in Gorongosa National Park, Mozambique. Image Credit: Judy Gallagher (CC BY 2.0)
Human African Trypanosomiasis – also known as sleeping sickness – is a deadly disease caused by the single-celled parasite Trypanosoma brucei. The parasite has a complex life cycle that involves both humans and tsetse flies. When a tsetse fly bites an infected human, it can take up the parasite and pass it on to other people.
Inside the human host, T. brucei exists in two forms: a rapidly dividing ‘slender’ form, and a non-proliferative ‘stumpy’ form that emerges once a high enough density of parasitic cells has been reached. For decades, scientists thought that only the stumpy form can successfully spread from humans to tsetse flies. However, a 2021 study challenged this view, suggesting that the slender form might also be transmissible.
To investigate this further, Ngoune et al. examined whether, and under what conditions, the slender and stumpy forms of T. brucei could infect tsetse flies. The team grew both forms of the parasite in the laboratory and fed them to tsetse flies in an environment designed to resemble natural conditions. The midgut and salivary glands of the flies were then dissected four weeks later to assess the level of infection.
Ngoune et al. found that slender forms of the parasite were only able to infect one out of 24 batches of young tsetse flies – and only when each fly ingested up to 10,000 parasites. The slender forms also failed to infect adult flies entirely, likely because they have a more robust immune system. In contrast, stumpy forms of the parasite where much more readily transmitted, successfully infecting about 75% of all the tested fly batches, even when as few as 10 parasitic cells were ingested.
The study by Ngoune et al. reaffirms the longstanding view that the stumpy form of T. brucei is the primary stage at which the parasite is transmitted from humans to flies. While the slender form of T. brucei may be capable of infecting tsetse flies under certain conditions, these results suggest that it rarely makes this jump and is therefore unlikely to play a significant role in the spread of sleeping sickness.
