While Trypanosoma congolense is mostly known to cause a chronic wasting disease in animals, a new mouse model shows that acute cerebral trypanosomiasis is triggered by parasite sequestration and infiltration of T helper cells in the brain parenchyma.

African trypanosomes residing within the skin of infected humans represent an important yet overlooked transmissible parasite population that may thwart efforts to eliminate African sleeping sickness.

Common kidney disease risk variants in African populations are associated with reduced susceptibility to deadly African trypanosomes.

Hypothemycin, which inhibits a number of protein kinases, kills the T. brucei parasites that cause sleeping sickness and reveals new therapeutic targets for the disorder.

According to experimental and field observations, stumpy forms appear to be the most adapted forms for African trypanosome transmission from the mammalian host to the tsetse fly in natural conditions.

A camelid single-domain antibody potently and specifically inhibits pyruvate kinases from trypanosomatids.

Two gene variants provide different levels of protection against sleeping sickness, but this comes with an increased risk of developing chronic kidney disease.

Transparent zebrafish, reveal the occurrence of foamy macrophages during an extracellular trypanosome infection and their association with an exacerbated inflammatory response.