Bouteille Bernard, Buguet Alain
Laboratory of Parasitology, Dupuytren University Hospital of Limoges, France,
Polyclinic Marie-Louise Poto-Djembo, Pointe-Noire, Congo.
Res Rep Trop Med. 2012 Jun 11;3:35-45. doi: 10.2147/RRTM.S24751. eCollection 2012.
Human African trypanosomiasis (HAT) is caused by the injection of () or by , the tsetse fly. Three historical eras followed the exclusive clinical approach of the 19th century. At the turn of the century, the "initial research" era was initiated because of the dramatic spread of HAT throughout intertropical Africa, and scientists discovered the agent and its vector. Two entities, recurrent fever and sleeping sickness, were then considered a continuum between hemolymphatic stage 1 and meningoencephalitic stage 2. Treatments were developed. Soon after World War I, specific services and mobile teams were created, initiating the "epidemiological" era, during which populations were visited, screened, and treated. As a result, by 1960, annual new cases were rare. New mass screening and staging tools were then developed in a third, "modern" era, especially to counter a new epidemic wave. Currently, diagnosis still relies on microscopic detection of trypanosomes without (wet and thick blood films) or with concentration techniques (capillary tube centrifugation, miniature anion-exchange centrifugation technique). Staging is a vital step. Stage 1 patients are treated on site with pentamidine or suramin. However, stage 2 patients are treated in specialized facilities, using drugs that are highly toxic and/or that require complex administration procedures (melarsoprol, eflornithine, or nifurtimox-eflornithine combination therapy). Suramin and melarsoprol are the only medications active against Rhodesian HAT. Staging still relies on cerebrospinal fluid examination for trypanosome detection and white blood cell counts: stage 1, absence of trypanosomes, white blood cell counts ≤ 5/µL; stage 2, presence of trypanosomes, white blood cell counts ≥ 20/µL; HAT intermediate stage, between these still controversial thresholds. Our group has proposed the use of noninvasive ambulatory polysomnography to identify sleep-wake abnormalities characteristic of stage 2 of the disease. Only patients with abnormal sleep-wake patterns would then undergo confirmative lumbar puncture.
人类非洲锥虫病（HAT）是由 （） 或由采采蝇叮咬注入 引起的。继19世纪单纯的临床治疗方法之后，出现了三个历史阶段。在世纪之交，由于HAT在整个热带非洲急剧蔓延，“初步研究”阶段开始了，科学家们发现了病原体及其传播媒介。当时，两种疾病，即回归热和昏睡病，被认为是第一阶段血淋巴期和第二阶段脑膜脑炎期之间的连续过程。治疗方法也得以研发。第一次世界大战后不久，专门的服务机构和流动团队成立，开启了“流行病学”阶段，在此期间对人群进行走访、筛查和治疗。结果，到1960年，每年的新病例已很罕见。在第三个“现代”阶段，特别是为了应对新的疫情浪潮，又研发了新的大规模筛查和分期工具。目前，诊断仍依赖于显微镜检测锥虫，检测方法有无浓缩技术（湿血片和厚血片）或有浓缩技术（毛细管离心、微型阴离子交换离心技术）。分期是关键步骤。第一阶段的患者在现场用喷他脒或苏拉明治疗。然而，第二阶段的患者则在专门机构接受治疗，使用的药物毒性很强和/或给药程序复杂（美拉胂醇、依氟鸟氨酸或硝呋替莫-依氟鸟氨酸联合疗法）。苏拉明和美拉胂醇是仅有的对罗德西亚型HAT有效的药物。分期仍依赖于脑脊液检查以检测锥虫和白细胞计数：第一阶段，无锥虫，白细胞计数≤5/µL；第二阶段，有锥虫，白细胞计数≥20/µL；HAT中间阶段，介于这些仍有争议的阈值之间。我们小组提议使用非侵入性动态多导睡眠图来识别该疾病第二阶段特有的睡眠-觉醒异常。只有睡眠-觉醒模式异常的患者才会接受确诊性腰椎穿刺。
