Toxoplasmic Infection-induced Injury in the Ileal Myenteric Plexus in Rats Depends on the Dose of Toxoplasma gondii Oocysts

Introduction The present study evaluated the effects of different inocula of Toxoplasma gondii oocysts on the ileal myenteric plexus in rats. Materials and Methods Male Wistar rats, 60 days old, were distributed into four groups: control group (CG; which received saline solution) and groups that were infected with 100 (TG100), 1000 (TG1000), and 5000 (TG5000) T. gondii oocysts. Thirty days after infection, the rats were sacrificed, and the ileum was collected to make whole-mount preparations that were subjected to immunofluorescence staining to observe the general neuronal population (HuC/D), nitrergic neurons (nNOS), and enteric glial cells (S100). Morphometric and quantitative analyses of myenteric neurons were performed. Results The infections with different T. gondii inocula did not cause neuronal or glial loss, but cause neuronal hypertrophy in general population and nitrergic subpopulation in infected groups. Conclusion: Changes in neuronal morphology were observed in the TG5000 group, including the presence of vacuoles, translocation of Hu protein to the nucleus, and dendritic distortions, suggesting functional alterations in these cells.

A Case of Diffuse Neuronal Hypertrophy in Acute Appendicitis

We report a case of neuronal hypertrophy associated with acute appendicitis in which significant neuronal fibers and the number of ganglion cells increased in the absence of inflammatory cells. Differential diagnosis from diffuse ganglioneuromatosis by the pathologic findings of resected specimen was difficult. A 33-year-old Japanese female visited our hospital complaining of acute abdominal pain. The patient underwent appendectomy upon the diagnosis of acute appendicitis on the day of admission. Postoperative examinations found no neoplastic lesions in other organs or inherited disorders such as multiple endocrine neoplasia (MEN) type 2b and von Recklinghausen's disease (VRD). The pathologic diagnosis was neuronal hypertrophy of the appendix. Because the clinical outcomes of diffuse ganglioneuromatosis and neuronal hypertrophy of the gastrointestinal tract are quite different, clinical and pathologic examination should be carefully carried out for lesions in which significant proliferation of neuronal components is seen.

Neuronal changes caused by Trypanosoma cruzi: an experimental model

Define an experimental model by evaluating quantitative and morphometric changes in myenteric neurons of the colon of mice infected with Trypanosoma cruzi. Twenty-eight Swiss male mice were distributed into groups: control (CG, n=9) and inoculated with 100 (IG100, n=9) and 1000 (IG1000, n=10) blood trypomastigotes, Y strain-T. cruzi II. Parasitemia was evaluated from 3-25 days post inoculation (dpi) with parasites peak of 7.7 × 10(6) and 8.4 × 10(6) trypomastigotes/mL at 8th dpi (p>0.05) in IG100 and IG1000, respectively. Chronic phase of the infection was obtained with two doses of 100mg/Kg/weight and one dose of 250mg/Kg/weight of Benznidazole on 11, 16 and 18 dpi. Three animals from each group were euthanized at 18, 30 and 75 dpi. The colon was stained with Giemsa. The quantitative and morphometric analysis of neurons revealed that the infection caused a decrease of neuronal density on 30th dpi (p<0.05) and 75 dpi (p<0.05) in IG100 and IG1000. Infection caused death and neuronal hypertrophy in the 75th dpi in IG100 and IG1000 (p<0.05, p<0.01). The changes observed in myenteric neurons were directly related to the inoculate and the time of infection