Salama Amina M, Elgendy Dina I, Elmahy Rasha A, Eltantawy Asmaa F, Seleem Monira A, Elgohary Ahmed M, Docmac Omaima K, Al Mwafy Marwa E F, Almeldin Ahmed A, Sharaf Mahmoud S
Medical Parasitology Department, Faculty of Medicine, Tanta University, Tanta, Egypt.
Zoology Department, Faculty of Science, Tanta University, Tanta, Egypt.
Parasitol Res. 2025 Sep 4;124(9):98. doi: 10.1007/s00436-025-08528-7.
Human toxocariasis presents in several forms, including visceral larva migrans, ocular larva migrans, covert toxocariasis, and neurotoxocariasis. Although several studies suggest a potential link between toxocariasis and epilepsy, this link is still debated. Additional mechanistic and experimental studies in animal models are essential for a better understanding of this association. Our study aimed to explore the relationship between neurotoxocariasis and epilepsy in an animal model. In this study, 24 male Swiss albino rats were used. Rats were randomly assigned to three groups of eight: group I (normal control), group II (received pilocarpine hydrochloride in a single dose of 400 mg/kg body), and group III (infected with Toxocara canis). Several parameters were used to evaluate the possible link between toxocariasis and epilepsy, including clinical, histopathological, immunohistochemical, and biochemical studies. All rats in group III exhibited motor seizures 10 to 15 days post-infection, with no significant difference noticed regarding the maximum stage of seizures when compared with group II. Our study revealed definite structural and functional changes in the brain tissue, evidenced by the recorded histopathological changes, the increased GFAP, MMP2, and TNF-α expression, and the significant disturbances in neurotransmitter profile. Furthermore, a state of oxidative stress was noticed, with a significant increase in serum IL-6 levels. Our results indicate that the migration of Toxocara canis larvae to the central nervous system can result in significant structural changes and shifts in neurotransmitter levels, both of which may play a role in the development of epilepsy. Additionally, this research underscores the importance of oxidative stress and inflammatory cytokines in contributing to neuronal damage. These findings open avenues for future research aimed at identifying possible therapeutic targets and interventions to alleviate the neurological effects of toxocariasis.
人类弓蛔虫病有多种表现形式，包括内脏幼虫移行症、眼幼虫移行症、隐匿性弓蛔虫病和神经弓蛔虫病。尽管多项研究表明弓蛔虫病与癫痫之间可能存在联系，但这种联系仍存在争议。在动物模型中进行更多的机制和实验研究对于更好地理解这种关联至关重要。我们的研究旨在探讨动物模型中神经弓蛔虫病与癫痫之间的关系。本研究使用了24只雄性瑞士白化大鼠。大鼠被随机分为三组，每组8只：第一组（正常对照组）、第二组（接受单剂量400mg/kg体重的盐酸毛果芸香碱）和第三组（感染犬弓首线虫）。使用了多个参数来评估弓蛔虫病与癫痫之间的可能联系，包括临床、组织病理学、免疫组织化学和生物化学研究。第三组所有大鼠在感染后10至15天出现运动性癫痫发作，与第二组相比，癫痫发作的最大阶段没有显著差异。我们的研究揭示了脑组织中明确的结构和功能变化，记录的组织病理学变化、GFAP、MMP2和TNF-α表达增加以及神经递质谱的显著紊乱证明了这一点。此外，还注意到氧化应激状态，血清IL-6水平显著升高。我们的结果表明，犬弓首线虫幼虫向中枢神经系统的迁移可导致显著 的结构变化和神经递质水平的改变，这两者都可能在癫痫 的发生发展中起作用。此外，本研究强调了氧化应激和炎性细胞因子在导致神经元损伤中的重要性。这些发现为未来的研究开辟了道路，旨在确定可能的治疗靶点和干预措施，以减轻弓蛔虫病的神经学影响。
