Department of Microbiology and Parasitology, Universidade Federal de Santa Maria, Brazil. aleksandro
Pathol Res Pract. 2012 Jan 15;208(1):39-44. doi: 10.1016/j.prp.2011.10.010. Epub 2011 Dec 15.
The aim of this study was to investigate whether rats infected with Trypanosoma evansi had neurological and locomotor signs, as well as histological lesions in the central nervous system (CNS) and pelvic muscles. To carry out this study, 52 rats were used and divided into two groups. The animals in Group A (n=40) were infected with T. evansi, and the rats in Group B (n=12) were used as negative controls (non-infected). Neurological examination was performed at Days 5, 15, 30 and 150 post-infection (PI) with eventual euthanasia of the rats. Samples of brain, spinal cord and skeletal muscle (biceps femoris and gastrocnemius muscles) were collected. The neurological tests evaluated motor capacity, balance and pain sensitivity. At Day 5 PI in Subgroup A1, the rats showed high parasitemia, became apathetic and presented with slow movements and signs of disorientation. After Day 15 PI in Subgroup A2 and Day 30 PI in Subgroup A3, no more clinical abnormalities were observed. Histologically, there was no damage to the CNS in these three subgroups, but within Subgroup A3, mononuclear infiltration of the muscle was observed. Rats chronically infected (Subgroup A4 - Day 150 PI) showed muscle atrophy, walking dysfunction and paralysis of the hind limbs. Mild mononuclear inflammatory infiltrates and perivascular cuffs were observed in the CNS of some of the animals in Subgroup A4. In these rats, severe muscle damage was observed in the skeletal muscle which included atrophy and loss of muscle fibers, multinucleated giant muscle cells, mononuclear myositis, Wallerian degeneration of the innervating fibers and mononuclear inflammatory infiltrate in the perineurium and adipose tissue. Based upon these findings, we conclude that infection by T. evansi in rats leads to muscle damage, which is probably the cause of the paralysis of hind limbs.
本研究旨在探讨感染伊氏锥虫的大鼠是否具有神经和运动体征,以及中枢神经系统(CNS)和骨盆肌肉的组织学病变。为此,本研究使用了 52 只大鼠,并将其分为两组。A 组(n=40)的动物感染了 T. evansi,B 组(n=12)的大鼠作为阴性对照(未感染)。在感染后第 5、15、30 和 150 天进行神经学检查,随后对大鼠进行安乐死。收集大脑、脊髓和骨骼肌(股二头肌和比目鱼肌)样本。神经学测试评估运动能力、平衡和疼痛敏感性。在 A1 亚组感染后的第 5 天,大鼠出现高寄生虫血症,变得冷漠,动作缓慢,出现定向障碍。在 A2 亚组感染后的第 15 天和 A3 亚组感染后的第 30 天,未观察到更多的临床异常。组织学上,这三个亚组的 CNS 没有损伤,但在 A3 亚组中观察到肌肉单核细胞浸润。慢性感染(A4 亚组 - 感染后第 150 天)的大鼠出现肌肉萎缩、行走功能障碍和后肢瘫痪。在 A4 亚组的一些动物的 CNS 中观察到轻度单核炎性浸润和血管周围袖套。在这些大鼠中,骨骼肌观察到严重的肌肉损伤,包括萎缩和肌纤维丧失、多核巨肌细胞、单核肌炎、支配纤维的沃勒变性和神经外膜和脂肪组织中的单核炎性浸润。基于这些发现,我们得出结论,感染伊氏锥虫会导致肌肉损伤,这可能是后腿瘫痪的原因。