Institute of Biology, Federal University of Bahia, Salvador, BA, Brazil.
Rev Soc Bras Med Trop. 2010 Sep-Oct;43(5):504-7. doi: 10.1590/s0037-86822010000500006.
Septal fibrosis of the liver regularly develops in rats infected with the nematode Capillaria hepatica. Curative treatment of the infection prevents the development of septal fibrosis when intervention occurs up to postinfection day (PID) 15, but not later. The present investigation aimed to demonstrate which parasitic factors are present when the process of septal fibrosis can no longer be prevented by curative treatment.
Wistar rats were infected with 600 embryonated eggs of C. hepatica administered by gavage and treated with ivermectin and mebendazole in separate groups at PIDs 10, 12, 15, 17 or 20. Rats from each group and their nontreated controls, were killed and examined 40 days after the end of treatment.
Findings by PID 15 were compatible with the stage of complete maturation of infection, when worms and eggs were fully developed and a complex host-parasite multifocal necroinflammatory reaction showed greater intensity, but with no signs of septal fibrosis, which appeared from PID 17 onward.
Since the worms spontaneously died by PID 15, not only septal fibrosis production, but also its maintenance and further development appeared dependent on the presence of eggs, which were the only parasitic factor remaining thereafter.
感染毛细线虫(Capillaria hepatica)的大鼠常会出现肝间隔纤维化。在感染后 15 天(PID)内进行治疗性干预可以预防肝间隔纤维化的发生,但超过该时间则无效。本研究旨在探讨当治疗性干预不再能预防肝间隔纤维化时,哪些寄生虫因素仍然存在。
将 600 枚毛首线虫的孵化卵通过灌胃的方式感染 Wistar 大鼠,然后在 PID 10、12、15、17 或 20 时,将伊维菌素和甲苯咪唑分别用于不同的治疗组。每组大鼠及其未经治疗的对照组在治疗结束后 40 天被处死并进行检查。
PID 15 时的发现与感染完全成熟的阶段一致,此时蠕虫和虫卵完全发育,宿主-寄生虫多灶性坏死性炎症反应更加剧烈,但没有肝间隔纤维化的迹象,从 PID 17 开始出现肝间隔纤维化。
由于蠕虫在 PID 15 时会自然死亡,因此不仅肝间隔纤维化的产生,而且其维持和进一步发展似乎都依赖于虫卵的存在,此后虫卵成为唯一残留的寄生虫因素。