Vos G J, Moloo S K, Gardiner P R
International Laboratory for Research on Animal Diseases, Nairobi, Kenya.
Parasitology. 1988 Feb;96 ( Pt 1):25-36. doi: 10.1017/s0031182000081634.
To determine if, as is the case with Trypanosoma brucei and T. congolense, serodemes of T. vivax could be distinguished on the basis of immunity to the metacyclic stages of the parasite, attempts were made to immunize goats by infection with infected tsetse, followed by chemotherapy or eventual 'self-cure'. Thirty goats were infected by tsetse with either clones or stocks of T. vivax from East or West Africa. Twenty-four goats were treated with diminazene aceturate (Berenil, Hoechst A.G.) 2-6 weeks after infection and 6 goats were allowed to self-cure. Infection, followed by treatment, induced immunity to a first homologous challenge by infected tsetse in only 2 of 24 goats (one immune to the East African stock, and the other to a clone of the West African stock). Immunity to a clone of the East African stock was induced in 3 or 4 animals after a second infection and treatment and in the fourth animal of the group following a third infection and treatment. One of 2 goats infected with the clone of the East African stock was immune to challenge at 16 weeks, following self-cure without treatment, and 1 of 4 goats infected with the parent stock was similarly immune when challenged at 40 weeks post-infection. Goats susceptible to infection with East African T. vivax showed evidence of partial immunity by delayed pre-patent periods and depressed parasitaemias after challenge. Goats infected with the relatively more virulent West African T. vivax were, however, completely susceptible to infection after homologous challenge, and showed only a slight delay in pre-patent period. A similar result was obtained in a further 8 goats primed and challenged by large numbers of tsetse (20 or 100 infected tsetse/goat) with the West African T. vivax. In further experiments using a very short treatment interval, infections following challenge were clearly shown to be the result of a lack of immunity rather than relapse following treatment. Lytic antibody activity to cultured metacyclic trypanosomes could not be detected during infection but such activity against bloodstream forms was detected after 2 weeks of infection. It is suggested that the primary reason for the erratic induction of immunity to T. vivax employing this methodology is the low number of metacyclics transmitted by infected tsetse, and thus poor antigenic stimulus encountered by goats upon tsetse challenge.
为了确定，如布氏锥虫和刚果锥虫的情况一样，间日锥虫的血清型是否可以根据对该寄生虫循环后期阶段的免疫力来区分，研究人员尝试通过用感染的采采蝇感染山羊，随后进行化学疗法或最终的“自愈”来对山羊进行免疫。30只山羊被来自东非或西非的间日锥虫克隆或虫株感染。24只山羊在感染后2 - 6周用乙酰氨基阿苯达唑（贝尼尔，赫斯特股份公司）进行治疗，6只山羊任其自愈。感染后再进行治疗，仅24只山羊中的2只（一只对东非虫株免疫，另一只对西非克隆株免疫）对首次同源感染的采采蝇攻击产生了免疫力。在第二次感染和治疗后，3或4只动物以及该组的第四只动物在第三次感染和治疗后对东非克隆株产生了免疫力。2只感染东非克隆株的山羊中有1只在自愈未治疗的情况下，16周时对攻击具有免疫力，4只感染亲本虫株的山羊中有1只在感染后40周接受攻击时同样具有免疫力。易感染东非间日锥虫的山羊通过潜伏期延长和攻击后虫血症降低显示出部分免疫的迹象。然而，感染毒性相对更强的西非间日锥虫的山羊在同源攻击后完全易感染，仅潜伏期略有延长。在用大量采采蝇（20或100只感染的采采蝇/山羊）对8只山羊进行初次感染和攻击的进一步实验中，也得到了类似的结果。在使用非常短的治疗间隔的进一步实验中，攻击后的感染被明确证明是缺乏免疫力的结果，而不是治疗后复发。在感染期间未检测到针对培养的循环后期锥虫的溶细胞抗体活性，但在感染2周后检测到了针对血流形式的此类活性。有人认为，采用这种方法对间日锥虫免疫诱导不稳定的主要原因是感染的采采蝇传播的循环后期锥虫数量少，因此山羊在采采蝇攻击时遇到的抗原刺激不足。
