Histopathology survey of rainbow trout (Oncorhynchus mykiss) fry mortality syndrome in coldwater hatcheries and reared farms in Iran

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Zorriehzahra M . J
Hj. Mohd Daud H
Sharifpour I
Soltani M
Mehrabi M.R
Kies F
Sheikh Asadi M


An investigation was conducted in order to determine the etiological factors of Fry Mortality Syndrome (FMS) that causes a serious economical loss in rainbow trout’s farms in Iran and around the world. The increased number of farms and the improvement of culture techniques and facilities in Iran had boosted the annual production of trout from 280 tonnes in 1978 to more than 30,000 tones in 2004. But unfortunately, in recent years, the rate of fry and juvenile mortalities has increased dramatically in some provinces. During 15 months, from Nov.2001 till Feb.2003, 104 tissue specimens consisting of liver, kidney, spleen, pancreas, intestine, and gills from 59 diseased fry as well as 45 infected fingerlings and suspected adults fish from Mazandaran, Tehran, Fars, Markazy, Kordestan, Kohgiloyeh and Boyerahmad provinces were collected for histopathological study. The clinical signs of the affected fry were darkening of the body, exophthalmia, ascites, erratic swimming and whirling, lethargy, gathering near the outlet of the ponds and presence of the faecal casts. Sampled tissues were fixed in 10 % buffered formalin for a minimum of 24 hours. The fixed tissues were processed in an automatic tissue processor using standard method. Processed tissues were embedded in paraffin wax and 5 µm sections were then cut using a rotary microtome. The sections were stained using H & E staining and examined under a compound microscope. Microscopic examination of the tissues revealed marked changes as follows. There were congestion and inflammation of the basal membrane of secondary lamellae, hyperplasia and fusion of secondary lamellae, and clubbing. In the kidney, congestion of blood vessels, degeneration and necrosis of hematopoietic tissue and tubules, increased melanin pigments and inflammatory cells infiltration were observed. In the liver, congestion of blood vessels of parenchyma, vacuolating changes in hepatocytes, congestion and dilation of sinusoids with the increased presence of monocytes and melanomacrophage centres (MMC) and focal necrosis were seen. Bile duct neoplasia (cholangioma) was also present in some cases. Spleen showed congestion, hemosiderosis, the increased presence of MMC and necrosis in some cases. In the pancreatic tissues, congestion, degeneration and necrosis of acinar cells and Islets of Langerhans were observed. Congestion of submucosal layer, necrosis and detachment columnar and mucous epithelial layer were also observed in the intestinal tissue. From clinical and histopathological changes seen, it was postulated that the causative agent of the trout fry mortality is likely to be a viral agent and the pathological signs were similar to IHN disease.

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