Crenosoma striatum is a species of parasitic nematodes from the family Crenosomatidae responsible for pathologic lung lesions in the hedgehog (Erinaceus europaeus). Infection with C. striatum can cause weight loss, dry cough, and bronchitis. In the present study, hedgehogs killed by road accidents, or trapped and found dead on farms in different parts of Mazandaran province (Iran), were transferred to the laboratory. After dissection, parasite samples collected from the lung were placed into 70% alcohol. After clarification with lactophenol and subsequent staining, the nematodes were identified as C. striatum according to previously published guidelines. For histopathologic examination, lung samples were collected. The tissues were fixed and following routine processing, sections were stained with hematoxylin and eosin. Microscopic diagnoses included hyperemia, eosinophilic bronchointerstitial pneumonia, thickening of the interstitium, and eosinophilic microabscesses in bronchial airways. Eosinophilic pneumonia was characterized by eosinophil and other mononuclear leukocyte infiltration within the lung interstitium. Crenosoma striatum can lead to mortality in hedgehogs.
Background: The application of nano-particles (NPs) in various industries is growing. Since their toxicity is not clearly understood, they can cause adverse effects on the environment. The aim of this study was to evaluate the histopathological effects of iron oxide nano-particles on the small intestine of common carp, Cyprinus carpio. Methods: Four experimental treatments were designed (15 fish/treatment). Treatment 1 was the controls while Treatments 2, 3 and 4 were experimental. The experimental groups were exposed to 50, 75 and the 100 mg/L of iron oxide NPs, respectively. On days 14, 21 and 28, the fish were randomly picked from each tank, samples of the small intestine were dissected, and were examined for both the accumulation of the iron NPs and the tissue histopathologies. Results: The highest concentration of iron accumulation was detected for Treatment 3 on day 21, compared to all other treatment groups (p<0.05). However, iron accumulation in the tissue declined unexpectedly after day 21 despite the continued treatments at 100 mg/L of the iron NPs. The histopathological examinations revealed that the treatment beyond 21 days caused damages to the intestinal epithelial cells, including enterocytes, villi and the goblet cells. Conclusion: This study demonstrated that the effect of iron oxide NPs on the small intestinal tissue was dependant on the dose and duration of exposure. We conclude that the iron accumulation in the small intestine declined despite increasing the iron oxide NPs concentration and the exposure duration secondary to damages caused to the intestinal epithelial cell layer.
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