The tissue response of carp Cyprjnus carpio to the coccidian parasite Goussia carpelli (Leger & Stankovitch, 1921) was investigated during a laboratory infection by histological and electron microscopical techniques. During merogonic and early gamogonic development severe damage to infected epithelia1 tissue was observed, resulting in extensive loss of epithelium and damage to the lamina propria. In heavily infected carp, the most severe damage was observed in late merogony and early gamogony at about Day 9 post exposure, when the epithelium was destroyed with the exception of some remnants deep between mucosa folds. As a repair mechanism of destroyed tissue, areas of naked propria became covered by broad, plain cells of a squamous epithelium within a few days. Enterocytes harbouring G. carpelli oocysts were observed to migrate into subepithelial tissue. Phagocytic activity was seen in all granulocyte types in the gut. Compared to coccidia of birds and mammals, the tissue damage caused by G. carpelli indicated high pathogenic capacity. The weak clinical symptoms of this coccidiosis might be explained by the rapid repair of destroyed tissue and thc dbsence of dehydration in freshwater fishes.
For several years now, pathological skin changes have been observed in tench Tinca tinca L. from northern Germany. Using light microscopy, numerous instances of the causative agent have been detected, cell-bound in macrophages and/or between altered tissue structures. The infection shows systemic spread, as the microorganisms, Sporozoon tincae, also appear in the spleen. Using electron microscopy, it was possible to depict numerous different features of the microorganism associated with the intracellular development and multiplication of the agent. The structures lacked a true cell nucleus, so the previous assignment of the organism to the Protozoa is no longer maintainable. Our findings demonstrate that S. tincae is not a eukaryotic organism. We suggest that S. tincae be classified as bacteria.
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