M. Hasby Saad, O. Safwat, D. El-Guindy, R. Raafat, D. Elgendy and E. Hasby
Idiopathic Parkinson’s (IP) is a neurodegenerative disease that is suspected to be due to exposure to infections during early life. Toxoplasmosishas been the only suspected parasitic infection in IP (Celik et al., 2010). Recently, some non-central nervous system bacterial and viral infections have been incriminated in IP (Çamcı & Oğuz, 2016). So in the current study, we tried to explore if the systemic infl ammatory reactions triggered by some helminths like Trichinella spiralis can induce Parkinsonian lesions in the brain, especially that the cerebral complications have been reported in 10-20% of Trichinella spiralis infected patients . An experimental study was designed to assess the neurodegenerative and biomolecular changes that may occur in Trichinella spiralis infected BALB/C mice in comparison to rotenone induced PD model and apparently healthy ones. The motor affection was significantly lesser in the Trichinella infected mice than the Parkinson’s model, but when the catalepsy score was calculated (through the grid and bar tests) it was found to be significantly higher in the infected mice than in the healthy ones. A significant increase in the blood advanced oxidative protein products (AOPP), IFN-γ, TGF-β, and brain DNA fragmentation was also detected in the Trichinella spiralis infected mice. After histopathological examination, a significant increase in the cortical apoptotic neurons and Lewy’s body were observed in the Trichinella infected and the rotenone induced Parkinson’s model sections. A significant decrease in the immunohistochemical expression of the tyrosine hydroxylase expression in the brain sections and the ELISA measured dopamine level in the brain homogenate was also reported in the infected mice group. This study findings may collectively suggest that the systemic inflammatory reactions and the oxidative stresses associated with some systemic helminthic infections like trichinellosis are possible to precipitate neurodegenerative lesions and biomolecular changes in the brain , and manifest with IPD later in life.
A. S. Amer, A. E. Saad, S. N. Antonios and E. A. Hasby
Intestinal parasites may cause symptoms similar to acute appendicitis. Moreover, the diagnosis of parasitic infections is only done by post-operative histopathological examination of the appendices. Therefore, our aims are to assess the prevalence of intestinal parasitic infections among patients who were be appendectomized at Tanta Hospitals, Egypt and to investigate the possible association between these parasitic infections and appendicitis. To achieve these objectives, we performed a cross-sectional study including 65 patients chosen randomly who had undergone appendectomy over a period of one year from Oct 2015 to Oct 2016. Demographic data were retrieved. Complete blood picture was done. Moreover, appendiceal faecolith were examined macroscopically then by direct smear examination, formol-ether concentration technique, modified Ziehl-Nelseen stain and rapid immunochromatographic test. Histopathological examination of resected appendices was done. We found that parasitic infections were detected in 24.6 % of examined cases. Most of parasitic infections were prevalent in patients belonging to the school age group. Different parasitic infections were detected in the faecolith specimens. Moreover, Enterobious vermicularis adult female and Schistosoma mansoni granuloma were detected in histopathological sections. Also, a spectrum of pathological changes in the appendices was found ranging from lymphoid hyperplasia to acute inflammation with peritonitis. In conclusion, intestinal parasites may cause clinical picture similar to that of acute appendicitis. Therefore, careful attention to clinical history, stool examination and high eosinophilia may aid diagnosis and avoid unnecessary appendectomy. Moreover, the presence of different parasitic stages in the narrow lumen of the appendix may have a role in the development of appendicitis and this needs further studies.