Abstract

In Egypt, the temperature of the water fluctuates drastically, reaching a daytime high of 25 °C and a nighttime low of 15 °C, respectively, in the spring and the fall. To understand the mechanism behind fish kill in fish farms, an indoor experiment was conducted wherein 240 Nile tilapia weighing 24 ± 2.5 g were stocked in 12 glass aquaria (20 fish/aquarium). Water temperature was regulated throughout the day at 27 ± 1.5 °C for 12 h from 8:00 a.m. to 8:00 p.m. and at 18 ± 1.5 °C for the remaining 12 h. Fish samples (mucus and tissues) were collected four times with a week interval. Proinflammatory tumor necrosis factor-α and interleukin (IL)-1β were decreased during the 4 weeks, while anti-inflammatory IL-10 was highly upregulated during the first week and then decreased compared to the control. Heat shock protein-70 was significantly raised, but IL-8 was unaffected. The gene expressions of antioxidant enzymes catalase and glutathione peroxidase were markedly elevated in the first week and then decreased linearly until they no longer differed from the control group. Mucus lysozyme significantly decreased in weeks 1 and 2 and then began to increase in weeks 3 and 4. Every week, Aeromonas hydrophila infection resulted in clinical signs that were delayed by over 2 days compared to the control group. The mortality rate increased from 35 to 40%, and bacteria were isolated at a rate of 61.54 to 75% from the surviving fish, compared to a rate of 41.67% in the control group. Fluctuations in water temperature suppress the immunity of Nile tilapia, making them vulnerable to bacterial infection.

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