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Updated: Jan 11, 2026

Using Eggs from Schistosoma mansoni as an In vivo Model of Helminth-induced Lung Inflammation
Published on: June 5, 2012
Temporal evolution of neuropathological changes in the brain of Schistosoma mansoni-infected mice: A
Shimaa E Mohammed1, Hend M Hussein1, Noha A Elleboudy1
1Medical Parasitology Department, Faculty of Medicine, Ain-Shams University, Cairo, Egypt.
Abstract:
Cerebral schistosomiasis is a severe complication of chronic Schistosoma mansoni infection, yet the temporal relationship between parasitic burden and central nervous system pathology remains incompletely understood. This study investigated the temporal dynamics of worm burden and corresponding histopathological changes in experimental murine CNS schistosomiasis from 7 to 23 weeks post-infection. Adult worm counts (male, female, copula, and total) were determined at nine time points (weeks 7-23 post-infection) using hepatic portal perfusion. Histopathological evaluation of brain sections was performed using hematoxylin and eosin staining with a semi-quantitative scoring system (0-3). Total worm burden fluctuated significantly over time (H = 19.78, p = 0.011), peaking at week 11 (8.0 [7-9] worms). Histopathological scores exhibited a biphasic pattern: an acute inflammatory phase (weeks 7-13) with increasing gliosis and mononuclear infiltration, peaking at week 13 (score = 2.5), followed by a chronic phase (weeks 17-23) marked by vascular damage, neuronal degeneration, and fibrosis (score = 3.0 at week 17). Total worm burden correlated strongly with histopathological severity (rs = 0.724, p < 0.001), with the strongest associations observed during weeks 9-15. Murine cerebral schistosomiasis follows a predictable biphasic progression, with peak worm burden preceding maximal neuropathological damage. The mid-infection period (weeks 9-15) may represent a critical therapeutic window for intervention. These findings provide quantitative evidence for timing treatment strategies to mitigate CNS damage.

