Taratuto A L, Venturiello S M
Department of Neuropathology, Raul Carrea Institute for Neurological Research, Buenos Aires, Argentina.
Brain Pathol. 1997 Jan;7(1):663-72. doi: 10.1111/j.1750-3639.1997.tb01081.x.
Trichinosis is a worldwide zoonotic disease closely related to cultural and dietary habits caused by a nematode Trichinella spp. Human infection is acquired through ingestion of undercooked meat containing infective encysted larvae. There are two cycles of transmission, one domestic and the other wild. A complete life cycle develops in a single host harboring adult worms in the small intestine, from which newborn larvae migrate and finally encyst in striated muscle. Traumatic and immunological alterations are responsible for the main clinical features, including diarrhea, febrile syndrome, myalgias, oculopalpebral signs and eosinophilia. Cardiovascular, lung and CNS involvement characterize severe trichinosis. CNS inflammatory infiltration and damage may result from larval migration and vascular obstruction, or from the effect of toxic parasite antigens, or eosinophil infiltration. Humoral and cellular immune host response are relevant both to protect against re-infection and for immunodiagnosis. DNA probes and PCR technology may help to identify Trichinella spp. Muscle biopsy may disclose T spiralis larvae coiled within a muscle fibre host nurse cell surrounded by a capsule. Inflammatory infiltration includes monocytes, plasma cells, eosinophils and T lymphocytes mainly of the suppressor/cytotoxic phenotype. Histological appearance and histochemical profile of the host nurse cell differ from that of striated muscle fibre and are partly indicative of regeneration. Our own histological and histochemical findings in experimental studies of infected mouse muscle support the concept that changes induced by the larva encysting within a single host skeletal muscle fibre which becomes a nurse cell are unique of Trichinella infection. Interestingly, no dystrophin could be detected within the host nurse cell-capsule interface. It has been advanced that larva-induced host muscle fibre changes may be regulated at muscle gene transcription level whilst host regulatory pathways governed by cell cycle phase may also contribute to larval development.
旋毛虫病是一种与文化和饮食习惯密切相关的全球性人畜共患病，由线虫旋毛虫属引起。人类通过摄入含有感染性包囊幼虫的未煮熟肉类而感染。有两个传播循环，一个是家庭内的，另一个是野生的。完整的生命周期在单个宿主体内完成，成虫寄生于小肠，新生幼虫从这里迁移，最终在横纹肌中形成包囊。创伤性和免疫性改变是主要临床特征的原因，包括腹泻、发热综合征、肌痛、眼睑体征和嗜酸性粒细胞增多。心血管、肺部和中枢神经系统受累是重症旋毛虫病的特征。中枢神经系统的炎性浸润和损伤可能是幼虫迁移和血管阻塞、有毒寄生虫抗原的作用或嗜酸性粒细胞浸润所致。体液和细胞免疫宿主反应对于预防再次感染和免疫诊断都很重要。DNA探针和PCR技术可能有助于鉴定旋毛虫属。肌肉活检可能会发现旋毛虫幼虫盘绕在被囊包围的肌纤维宿主滋养细胞内。炎性浸润包括单核细胞、浆细胞、嗜酸性粒细胞和主要为抑制性/细胞毒性表型的T淋巴细胞。宿主滋养细胞的组织学外观和组织化学特征与横纹肌纤维不同，部分表明有再生现象。我们在感染小鼠肌肉的实验研究中的组织学和组织化学发现支持这样一种观点，即幼虫在单个宿主骨骼肌纤维内形成包囊（该纤维成为滋养细胞）所引起的变化是旋毛虫感染所特有的。有趣的是，在宿主滋养细胞-被囊界面未检测到肌营养不良蛋白。有人提出，幼虫诱导的宿主肌纤维变化可能在肌肉基因转录水平受到调节，而由细胞周期阶段控制的宿主调节途径也可能有助于幼虫发育。
