ABSTRACT
Swiss albino mice get Cyclospora infection after orally inoculated with sporulated oocysts. Two weeks post inoculation, most of them passed numerous acid fast immature oocysts in their stools. One week later, light microscopic examination of their intestinal H & E stained sections revealed parasitic stages in a supranuclear location within enterocytes. They were most prominent in the mucosal villi. Lamina propria was expanded by an inflammatory infiltrate. The combined parasitological and histopathological present studies helped in distinguishing Cyclospora which is often confused with Cryptosporidia in stool samples and with Isospora in intestinal sections. Electron microscopy demonstrated both sexual and asexual developmental stages of Cyclospora in ultrathin infected sections. Therefore, Cyclospora species require only a single host to complete its entire life cycle
Subject(s)
Cyclospora/physiology , Cyclosporiasis/pathology , Cyclosporiasis/parasitology , Disease Models, Animal , Animals , Cyclospora/classification , Cyclospora/growth & development , Cyclospora/ultrastructure , Cyclosporiasis/diagnosis , Feces/parasitology , Humans , Intestines/parasitology , Intestines/pathology , Intestines/ultrastructure , Mice , Oocysts/isolation & purification , Oocysts/physiology , Oocysts/ultrastructure , Spores, Protozoan/isolation & purification , Spores, Protozoan/physiology , Spores, Protozoan/ultrastructureABSTRACT
OBJECTIVE: To study Langerhans's cells (LCs) in cervical squamous cell carcinoma. STUDY DESIGN: The study was carried out in the Shatby University Hospital, Alexandria, Egypt. Thirty cases with squamous cell carcinoma, 10 cases with cervical intra-epithelial neoplasia (CIN) and 10 cases with normal exocervix were recruited. Sections from the exocervix were stained with gold chloride, immunostaining with S-100 protein antiserum, adenosine triphosphatase ATPase and electron microscopy. Statistical evaluation was done using the t-test. RESULTS: Gold chloride staining revealed significantly increased number of LCs in all cases of CIN compared to normal controls and with increasing grade of CIN (p < 0.001). No relationship between LCs number and the grade of carcinoma. Least branched LCs were predominant in the normal tissue while in neoplasia, these cells were of the most branched type, indicating a hyperactivity. S-100 protein positive LCs were almost absent in normal controls while their number were almost lower than the corresponding cases of CIN and invasive carcinoma after gold chloride or ATPase stainings. Signs of hyperactivity were evident in LCs of neoplastic cases after electron microscopy. CONCLUSIONS: Proliferation and increased number of LCs in CIN is an immune response, while such reaction is suppressed by invasive carcinoma.
