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谢海侠, 高谦, 聂品. 强壮粗体虫寄生引起的鳜肠道病理[J]. 水生生物学报, 2005, 29(2): 137-141.
引用本文: 谢海侠, 高谦, 聂品. 强壮粗体虫寄生引起的鳜肠道病理[J]. 水生生物学报, 2005, 29(2): 137-141.
XIE Hai-Xia, GAO Qian, NIE Pin. INTESTINAL PATHOLOGY OF THE MANDARIN FISH SINIPERCA CHUATSI INFECTED NATURALLY WITH THE ACANTHOCEPHALAN HEBESOMEA VIOLENTUM[J]. ACTA HYDROBIOLOGICA SINICA, 2005, 29(2): 137-141.
Citation: XIE Hai-Xia, GAO Qian, NIE Pin. INTESTINAL PATHOLOGY OF THE MANDARIN FISH SINIPERCA CHUATSI INFECTED NATURALLY WITH THE ACANTHOCEPHALAN HEBESOMEA VIOLENTUM[J]. ACTA HYDROBIOLOGICA SINICA, 2005, 29(2): 137-141.

强壮粗体虫寄生引起的鳜肠道病理

INTESTINAL PATHOLOGY OF THE MANDARIN FISH SINIPERCA CHUATSI INFECTED NATURALLY WITH THE ACANTHOCEPHALAN HEBESOMEA VIOLENTUM

  • 摘要: 强壮粗体虫是鳜肠道最常见寄生蠕虫。通过光镜及电镜对自然感染强壮粗体虫的鳜肠道进行了组织病理观察。强壮粗体虫的寄生引起鳜肠上皮细胞脱落、肠固有膜层结缔组织增生及白细胞向病灶处浸润,并可观察到嗜酸性粒细胞附着在与肠上皮及固有膜接触的虫体的体壁及吻部。在虫体吻部与肠固有膜层接触处依次观察到纤维细胞、成纤维细胞、嗜酸性粒细胞等,其中嗜酸性粒细胞又可分为未成熟嗜酸性粒细胞、成熟的嗜酸性粒细胞及正在脱颗粒的嗜酸性粒细胞。另外在肠壁的固有膜层观察到包裹虫体的结缔组织纤维囊,囊壁由三层结构构成,同时在鳜肠壁相同的位置观察到被宿主细胞浸润了的组织空腔,推测其为结缔组织纤维囊退化所形成

     

    Abstract: Siniperca chuatsi carrying heavy infections of Hebesomea Violentum in the gut were obtained from Liangzi Lake, Hubei Province. For light microscopical examination, the gut were fixed overnight in MFAA (Mathanol∶Formalin∶Acetic acid=85∶ 10∶ 5). After embedding in Histowax, the tissues were serially sectioned at 5μm and stained with May-Grünwald Giemsa using standard techniques. For transmission electronic microscopical examination, small pieces of gut with attached parasites were immersed in ice-cooled fixative and minced in approximately 2mm 3 pieces and then they were fixed in 2.5% glutaraldehyde in phosphate buffered saline (PBS; 0.1 M; pH 7.2) for 4 hours at 4℃ and postfixed for 1h in 1% osmium tetroxide in the same buffer at 4℃, and embedded in Epson-812. Semithin sections were stained with 1% aqueous solution of toluidine blue to select the most suitable areas. Ultrathin sections were double-stained with uranil acetate and lead citrate, and observed in a JEOL JEM-1230 electron microscope at 80kV. The parasite-induced histopathology was related to the penetration of H. violentum proboscis in the intestine wall. The host responded to the parasites with connective tissue hyperplasia and with an infiltration of leukocytes, predominantly eosinophilic granulocytes. Eosinophils were accumulated in the epithelium and lamina propria of the infected gut and some adhere to the parasite tegument and proboscis attachment. These eosinophils were subdivided into immature eosinophils, mature eosinophils and degranulating eosinophils. Fibre cells, fibroblast cells, and eosinophils were orderly distributed at the interface of the parasite-host. In addition, H. violentum elicits the formation of nodule in tunica propria. These nodules comprised a tri-layered structure to wrap the H. violentum. Tissue cava infiltrated by host cells were observed in the lamina propria and they are presumed to be the degenerated nodules.

     

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