Büscher Philippe, Bin Shamamba Stomy Kahremere, Ngoyi Dieudonne Mumba, Pyana Pati, Baelmans Rudy, Magnus Eddy, Van Overmeir Chantal
Department of Parasitology, Institute of Tropical Medicine, Antwerpen, Belgium.
Trop Med Int Health. 2005 Sep;10(9):850-5. doi: 10.1111/j.1365-3156.2005.01468.x.
Human 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.
人类非洲锥虫病由布氏冈比亚锥虫和布氏罗德西亚锥虫引起。从历史上看，使用美拉胂醇（一种用于治疗冈比亚型和罗德西亚型第二阶段昏睡病的砷衍生物）治疗的患者中，观察到约5%的治疗复发率。最近，在安哥拉、苏丹和乌干达的冈比亚型昏睡病疫源地，复发率高达30%。因此，世界卫生组织建立了昏睡病治疗失败与耐药性网络。其目标之一是改进从复发病例中分离布氏冈比亚锥虫，以研究耐药机制。布氏冈比亚锥虫的分离技术成功率低，且需要很长时间使寄生虫适应新宿主。通常，将患者的血液或脑脊液接种到啮齿动物体内并传代，直到菌株充分适应，在接种后几天内产生高寄生虫血症。到目前为止，布氏冈比亚锥虫的最佳受体是南非多乳鼠，成功率约为50%。在本研究中，对粗尾侏鼠（原称非洲侏鼠）作为分离布氏冈比亚锥虫的潜在受体进行了研究。用布氏冈比亚锥虫对瑞士小鼠、Wistar大鼠和粗尾侏鼠进行的比较实验感染清楚地表明，这种锥虫在粗尾侏鼠体内生长更快。在金沙萨（刚果民主共和国）用患者的血液和脑脊液对同一啮齿动物物种进行接种，证实了灌丛鼠比典型的实验啮齿动物对布氏冈比亚锥虫感染更敏感的观察结果。
