Joseph Gideon Ibrahim, Ibrahim Mohammed Auwal, Balogun Emmanuel Oluwadare
Department of Biochemistry, Ahmadu Bello University, Zaria, 810001, Kaduna, Nigeria; Africa Center of Excellence for Neglected Tropical Diseases and Forensic Biotechnology (ACENTDFB), Ahmadu Bello University, Zaria, Kaduna, 810001, Nigeria; Department of Biochemistry, Federal University of Technology, PMB 65, Minna, Nigeria; Africa Centre of Excellence for Mycotoxin and Food Safety, Federal University of Technology, PMB 65, Minna, Nigeria.
Department of Biochemistry, Ahmadu Bello University, Zaria, 810001, Kaduna, Nigeria; Africa Center of Excellence for Neglected Tropical Diseases and Forensic Biotechnology (ACENTDFB), Ahmadu Bello University, Zaria, Kaduna, 810001, Nigeria.
Exp Parasitol. 2025 Sep;276:109002. doi: 10.1016/j.exppara.2025.109002. Epub 2025 Aug 20.
African trypanosomes evade host immune response through antigenic variation and utilize other immune modulatory mechanisms to survive in the immunologically hostile mammalian bloodstream. However, indigenous African chicken (Gallus gallus domesticus) exhibits lower susceptibility to trypanosomes, suggesting unique resistance mechanisms; but the exact factor(s) of resistance remains elusive. This study aims to elucidate the mechanisms underlying the observed resistance of indigenous African chickens to T. brucei brucei infection, and to assess their potential role as cryptic reservoirs in zoonotic transmission. Non-immunosuppressed and immunosuppressed chickens were intravenously inoculated with ∼2.5 × 10 parasites, and parasitemia was monitored using microscopy, xenodiagnosis, and PCR. Rats served as controls and were intraperitoneally infected with 10 parasites. Haematological parameters in both chickens and rats were assessed using standard methods. Furthermore, in vitro anti-Trypanosoma activity of normal and infected chicken blood components was evaluated. The results reveal that chickens displayed no microscopic parasitemia beyond 9 h post-infection (pi) and survived beyond 60 days, whereas rats passaged with over 10-folds less trypanosomes developed parasitemia at day 5, which progressed and killed the rats between days 10-19. Further, while there were no significant haematological alterations over a 4-week observation period in the chicken, infected rats presented significant reductions in packed cell volume, haemoglobin, and red blood cell counts at peak infection, indicating anaemia sequelae. Additionally, infected rats exhibited neutropenia, lymphocytosis, increased hemolysis and mortality. Intriguingly, despite the observed trypanosomes suppression in chickens, incubation of trypanosomes with chicken blood, serum, or plasma revealed no intrinsic anti-Trypanosoma activity. But blood collected from infected chickens at 1- and 7-days post-infection successfully initiated infection in rats through xenodiagnosis, confirming transmissibility despite the absence of detectable parasitemia in chickens revealing a covert but potentially infectious state. Similarly, PCR detection at 7 dpi, indicated covert/suppressed infection. These findings suggest that indigenous African chickens, while resistant to overt trypanosomiasis, may act as cryptic reservoirs for Trypanosoma spp., potentially facilitating parasite zoonotic transmission.
非洲锥虫通过抗原变异逃避宿主免疫反应，并利用其他免疫调节机制在免疫环境恶劣的哺乳动物血液中存活。然而，非洲本土鸡（家鸡）对锥虫的易感性较低，这表明存在独特的抗性机制；但确切的抗性因素仍不清楚。本研究旨在阐明非洲本土鸡对布氏布氏锥虫感染所表现出的抗性背后的机制，并评估它们在人畜共患病传播中作为隐匿宿主的潜在作用。对未免疫抑制和免疫抑制的鸡静脉接种约2.5×10个寄生虫，使用显微镜检查、异种接种诊断和聚合酶链反应监测虫血症。大鼠作为对照，腹腔感染10个寄生虫。使用标准方法评估鸡和大鼠的血液学参数。此外，评估了正常和感染鸡血液成分的体外抗锥虫活性。结果显示，感染后9小时（pi）后鸡未出现显微镜下可见的虫血症，并存活超过60天，而接种锥虫数量少10倍以上的大鼠在第5天出现虫血症，病情进展并在第10至19天之间死亡。此外，在4周的观察期内，鸡的血液学没有明显变化，而感染的大鼠在感染高峰期红细胞压积、血红蛋白和红细胞计数显著降低，表明出现贫血后遗症。此外，感染的大鼠表现出嗜中性粒细胞减少、淋巴细胞增多、溶血增加和死亡率上升。有趣的是，尽管观察到鸡体内锥虫受到抑制，但将锥虫与鸡血、血清或血浆一起孵育未发现内在的抗锥虫活性。但是，在感染后1天和7天从感染鸡采集的血液通过异种接种诊断成功地在大鼠中引发了感染，证实了尽管鸡体内未检测到虫血症，但仍具有传染性，揭示了一种隐匿但潜在的感染状态。同样，在感染后7天的聚合酶链反应检测表明存在隐匿/受抑制感染。这些发现表明，非洲本土鸡虽然对显性锥虫病具有抗性，但可能是锥虫属的隐匿宿主，有可能促进寄生虫的人畜共患病传播。
