SummaryHuman African Trypanosomiasis is caused by Trypanosoma brucei gambiense and T. b. rhodesiense. Historically, a treatment relapse rate of about 5% is observed in patients treated with melarsoprol, an arsenical derivative used for treatment of both gambiense and rhodesiense second stage sleeping sickness.More recently, relapse rates up to 30% are noted in gambiense sleeping sickness foci in Angola, Sudan and Uganda. Therefore, WHO established a Network on Treatment Failure and Drug Resistance in Sleeping Sickness. One of its objectives is to improve isolation of T. b. gambiense from relapsing cases for research on drug resistance mechanisms. Trypanosoma b. gambiense isolation techniques suffer from low success rates and long periods needed to adapt the parasite to its new host. Usually, rodents are inoculated with patient's blood or cerebrospinal fluid and sub-passaged until the strain becomes sufficiently adapted to yield high parasitaemia within few days after inoculation. Until now, the best recipient for T. b. gambiense is Mastomys natalensis, with a success rate of about 50%. In this study, Grammomys surdaster (former Thamnomys surdaster) was investigated as a potential recipient for isolation of T. b. gambiense. Comparative experimental infections of Swiss mice, Wistar rats and G. surdaster thicket rats with T. b. gambiense clearly show that this trypanosome grows faster in G. surdaster. Inoculation of the same rodent species with patient's blood and cerebrospinal fluid in Kinshasa (R.D. Congo) confirms the observation that the thicket rats are more susceptible to T. b. gambiense infection than typical laboratory rodents.