Bunnajirakul S, Steinhagen D, Hetzel U, Körting W, Drommer W
Fish Disease Resarch Unit, School of Veterinary Medicine, Hannover, Germany.
Dis Aquat Organ. 2000 Feb 9;39(3):221-9. doi: 10.3354/dao039221.
The tissue response of common carp Cyprinus carpio to the kinetoplastid blood parasite Trypanoplasma borreli Laveran & Mesnil, 1901 was investigated during a laboratory infection of a highly susceptible carp line. With the development of the parasitaemia an increased proliferation of the lymphoid renal interstitial tissue was induced, which resulted in a progressive depression and deterioration of renal tubules. In heavily infected carp at Days 20 to 28 post inoculation (PI), a tubulonephrosis, a glomerulitis caused by a massive accumulation of leukocytes in glomerular capillaries, and large numbers of trypanoplasms in blood vessels and renal interstitium were observed. Corresponding with rising T. borreli numbers in the peripheral blood, splenic lymphocytes showed increasing proliferation rates, and the capillaries of the liver, gills, heart and intestine were infiltrated with lymphocytes and trypanoplasms. In heavily infected carp, congestion of liver sinusoids, focal necroses of hepatic tissue, extensive accumulations of erythrocytes in the spleen and in the blood marked anaemia were observed. These carp often showed abdominal distension, exophthalmus and swimming disorders described as 'sleeping sickness of carp'. Proliferation of cells from the interstitial lymphoid tissue of the kidney, which bears a close resemblance to the bone marrow of higher vertebrates, is considered a normal immune response of fish to antigen challenge. We here describe the unique case of a severe but ineffective immune reaction which results in the destruction of excretory renal structures. This has to be considered a severe disturbance of osmoregulation in affected carp, which, together with a decrease in oxygen uptake due to anaemia, is likely a major cause of death in these carp.
在对一个高度易感鲤系进行实验室感染期间，研究了鲤（Cyprinus carpio）对动基体血液寄生虫伯氏锥虫（Trypanoplasma borreli Laveran & Mesnil, 1901）的组织反应。随着寄生虫血症的发展，诱导了淋巴样肾间质组织的增殖增加，这导致肾小管逐渐萎缩和退化。在接种后第20至28天的重度感染鲤中，观察到肾小管坏死、肾小球肾炎（由肾小球毛细血管中白细胞大量积聚引起）以及血管和肾间质中有大量锥虫。随着外周血中伯氏锥虫数量的增加，脾淋巴细胞的增殖率升高，肝脏、鳃、心脏和肠道的毛细血管中有淋巴细胞和锥虫浸润。在重度感染鲤中，观察到肝血窦充血、肝组织局灶性坏死、脾脏和血液中红细胞大量积聚导致明显贫血。这些鲤常表现出腹部膨胀、眼球突出和被称为“鲤昏睡病”的游泳障碍。与高等脊椎动物的骨髓非常相似的肾间质淋巴样组织细胞的增殖，被认为是鱼类对抗抗原挑战的正常免疫反应。我们在此描述了一个严重但无效的免疫反应的独特案例，该反应导致排泄性肾结构的破坏。这必须被视为受影响鲤中渗透调节的严重紊乱，这与贫血导致的氧气摄取减少一起，可能是这些鲤死亡的主要原因。
