Histopathology and Ultrastructure of Segmented Filamentous Bacteria–Associated Rainbow Trout Gastroenteritis

虹鳟 组织病理学 超微结构 生物 病理 微生物学 鱼 动物 解剖 医学 渔业
作者
Jorge Del‐Pozo,Margaret Crumlish,James Turnbull,H. W. Ferguson
出处
期刊:Veterinary Pathology [SAGE Publishing]
卷期号:47 (2): 220-230 被引量:16
标识
DOI:10.1177/0300985809359381
摘要

Rainbow trout gastroenteritis (RTGE) is an emerging syndrome linked to the presence of large numbers of the segmented filamentous bacterium "Candidatus arthromitus" within the intestine. The present study examined the histopathological changes of the digestive tract of 152 trout with gross lesions typical of RTGE. Histopathology showed that 129 of 152 fish (85%) affected with RTGE had segmented filamentous bacteria in the distal intestine and/or pyloric caeca. The presence and number of segmented filamentous bacteria were always significantly higher (P < .001) in pyloric caeca, thereby suggesting the preferred site for these bacteria. Histopathological changes included enterocyte detachment and congestion of the lamina propria and adventitial layers. Samples from 6 RTGE-affected trout were examined using scanning and transmission electron microscopy, revealing a close interaction of segmented filamentous bacteria with the mucosa of distal intestine and pyloric caeca, with the presence of bacterial attachment sites, and with associated morphological changes of the apical membrane of enterocytes. Despite these interactions, segmented filamentous bacteria were not always adjacent to the areas with pathological changes, suggesting that if these organisms play a role in the pathogenesis of RTGE, extracellular products may be involved. Ultrastructural changes included loss of microvillar structure, membrane blebbing, hydropic mitochondrial damage, and basal hydropic degeneration of enterocytes, which frequently resulted in disruption of tight junctions and enterocyte detachment. The resulting exposure of large areas of lamina propria probably resulted in the compromise of the host osmotic balance and the facilitation of the entry of secondary pathogens.
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