The effects of a sublethal dose of botulinum serotype e on the swimming performance of channel catfish fingerlings.

Abstract Visceral toxicosis of catfish (VTC) is a disease of cultured Channel Catfish Ictalurus punctatus in the Mississippi Delta region and surrounding states. The etiology of VTC is associated with botulinum serotype E (BoNT/E), which causes blockage of acetylcholine release at the neuromuscular junction, leading to weakness and paralysis of skeletal muscles (including those involved in swimming). This study attempted to determine if sublethal exposure to purified BoNT/E caused reductions in swimming performance and metabolism of Channel Catfish. Catfish swimming performance was assessed on stocker-sized Channel Catfish (mean weight ± SD, 62.35 ± 2.5 g) with 10 sham-injected fish and 10 fish injected with a sublethal dose of BoNT/E. A modified Blazka-type swim chamber was used to assess swimming performance. We injected Channel Catfish with either 0.015% trypsin or 400 pg purified BoNT/E digested with 0.015% trypsin intracoelomically, then acclimated an individual catfish in the swim chamber for 17 h prior to the swimming trial. Water temperature was maintained at ∼28°C, and dissolved oxygen (DO) was between 4 and 7 mg/L. A critical swimming speed (Ucrit) protocol was followed, and DO and temperature were monitored every 2 min throughout the swim trial. Cost of transport was calculated from the oxygen consumption at each test speed (10-70 cm/s). There was a statistical difference between the Ucrits (P = 0.0034), but no differences were found between the cost of transports (P = 0.67) of the sham-injected and BoNT/E groups. There was a difference in the cost of transport as it relates to the speeds tested (P < 0.0001), cost of transports being highest at low speeds and decreasing as speed increased. These results indicate that botulinum E interferes with the swimming speed of the catfish, which could contribute to the mortality from the disease of VTC and potentially make the fish more susceptible to predation. Received September 20, 2013; accepted February 14, 2014.