The cases of nine Polish patients with diagnosed cystic echinococcosis (CE) were examined. A total of nine isolates obtained postoperatively were investigated using PCR and sequencing. The mitochondrial region of nad1 gene was amplified. This PCR and sequencing analysis revealed the presence of Echinococcus canadensis G7 in seven patients and E. granulosus G1 in two patients. These data demonstrate that E. canadensis is the predominant causative agent of human cystic echinococcosis in Poland. E. granulosus G1 detection in Polish patients suggests that the parasite was imported; however it does not exclude the possibility that these cases could have been of Polish origin.
Trichinella spiralis larvae were examined in TEM to identify calcareous corpuscles in the outer part of parasite capsule. The microroentgenographic analysis of calcareous corpuscles mainly demonstrated the presence of phosphorus and calcium. The physiological importance of calcareous corpuscles, as well as their significance in decay of T. spiralis larvae were discussed.
Behavioral flexibility is subserved by the prefrontal cortex and the basal ganglia. Orbitofrontal cortex (OFC) and dorsomedial striatum (DMS) form a functional frontocorticostriatal circuit crucial for the mediation of flexibility during reversal learning via dopamine (DA) neurotransmission. The regulatory control in maintaining DA homeostasis and function is provided by the dopamine transporter (DAT), which therefore likely plays a significant role in controlling the influence of DA on cognitive processes. Here we used a gene knockout mouse model to investigate the role of DAT in the performance on the Attentional Set-Shifting Task (ASST) stages dependent upon the OFC and the DMS. Additionally, behavior of mice after repeated administration of selective DAT inhibitor, GBR 12909, was examined.The animals were treated with the inhibitor to elicit a compensatory DAT up-regulation following withdrawal. Learning was slower and the number of errors during reversal learning and intra-dimensional shift stages was higher in DAT+/− mutant mice than in WT mice. GBR 12909-treated mice had deficits in reversal stages of the ASST. Neuronal activation in the OFC and DMS during the ASST was examined with early growth response proteins 1 and 2 (egr-1, egr-2) immunohistochemistry. Density of egr-2 labeled cells in the OFC was lower in mutant mice than in wild-types during reversal learning and the expression of the egr-1 was lower in mutant mice in the OFC and DMS during reversal and intra-dimensional shift stages. Mice with decreased DAT levels displayed behavioral difficulties that were accompanied by a lower task-induced activation of neurons in brain regions involved in the reversal learning. Altogether, these data indicate the role of the DAT in the behavioral flexibility.
Trichinella spiralis and Toxocara canis larvae migrated through the lung and induced many alterations in the lung parenchyma. Using electron microscopy, we identified and described the histopathological changes. These changes resulted from mechanical damage or from local inflammatory reactions provoked by larvae. The pattern of changes was described between 6 and 12 days post-infection (DPI) with T. spiralis larvae, and between 21 and 28 DPI with T. canis. The ultrastructural studies demonstrated that T. spiralis larvae migrating through the lungs evoked mainly destruction of type I epithelial cells, destruction of lamellar bodies of epithelial cells or extracellular alveolar lining layer. The severity of these changes was dependent on the number of infective larvae (400 or 800 T. spiralis larvae) and possibly the result of mechanical damage in the lung parenchyma. In contrast, infection with T. canis larvae initiated mainly eosinophilic perivasculitis and vasculitis as well as macrophage accumulation in the lung, which were additionally impacted by numerous crystalloid inclusions in macrophages. Trichinella spiralis larvae and T. canis larvae induced different pathological changes in the lungs of infected mice.
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