U.S. Department of Agriculture: Agricultural Research Service, Lincoln, Nebraska

 

Date of this Version

2006

Comments

Published in North American Journal of Aquaculture, 68:23–33, 2006. DOI 10.1577/A05-032.1

Abstract

A series of experiments were conducted to determine the toxicity, behavior, blood glucose stress response, and disease susceptibility in Nile tilapia Oreochromis niloticus following un-ionized ammonia (UIA) exposure. The acute toxicity of un-ionized ammonia to Nile tilapia was measured in a 96-h static test. The median lethal concentration (LC50) was 1.46 mg/L UIA at 24 and 48 h postexposure, 1.33 mg/ L at 72 h postexposure, and 0.98 mg/L at 96 h postexposure. No mortalities were noted in unexposed (0 mg/ L) control fish or fish exposed to 0.5 mg/L UIA. However, 93–100% mortalities were observed within 24 h among fish exposed to 2.0, 3.0, or 4.0 mg/L UIA. In additional UIA exposure experiments, Nile tilapia were exposed to sublethal concentrations (0.32–0.37 mg/L UIA) for 24 h and then administered an intraperitoneal injection with 750 colony-forming units (CFU) of Streptococcus agalactiae per fish. Mortalities of UIA-exposed and control fish were not significantly different 21 d postchallenge. Blood glucose levels were not significantly different between exposed and control fish 24 h after the beginning of UIA exposure or between preexposure fish and 24-h postexposure fish. Glucose levels in both groups increased significantly after UIA exposure and subsequent bacterial challenge, suggesting that Nile tilapia experienced handling or infection stress and not necessarily UIA exposure stress alone. During a time course study with 24-h UIA exposure, sequential blood glucose samples indicated acute stress responses 1–4 h postexposure that decreased by 24 h postexposure. The results of this study indicate that exposure to increased UIA concentrations alone had acute, transient effects on stress responses in Nile tilapia and that 24-h exposure to sublethal UIA concentrations up to 0.37 mg/L did not increase susceptibility to S. agalactiae.

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