Mass mortality of hatchery-reared milkfish (Chanos chanos) and mangrove red snapper (Lutjanus argentimaculatus) caused by Amyloodinium ocellatum (Dinoflagellida)
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Outbreaks of heavy infestation by the parasitic dinoflagellate Amyloodinium ocellatum in hatchery-reared milkfish (Chanos chanos) and mangrove red snapper (Lutjanus argentimaculatus) caused 100% mortality events in hatcheries in the Philippines. Parasites were recorded on the body surface in 14-day-old milkfish fry and on both skin and gills in 2-month-old snapper. Trophonts of A. ocellatum caused local erosions of fish skin and degeneration of epithelial cells at the sites of the parasite's attachment to the body surface. Separation and hyperplasia of gill epithelium and fusion of secondary lamellae at the distal parts of the gill filaments were common. High pathogenicity of A. ocellatum to fish may be attributed to the severe alterations of the fish gills, the disruption of the host's skin, and feeding of trophonts on hosts' epithelial cells. In-vivo treatments of A. ocellatum-infested snapper with a 1 h freshwater bath and 200 ppm H2O2 showed promising results. This is the first report of A. ocellatum infestation in milkfish and mangrove red snapper in the Philippines.
CitationCruz-Lacierda, E. R., Maeno, Y., Pineda, A. J. T., & Matey, V. E. (2004). Mass mortality of hatchery-reared milkfish (Chanos chanos) and mangrove red snapper (Lutjanus argentimaculatus) caused by Amyloodinium ocellatum (Dinoflagellida).
This study was done under the Regional Fish Disease Project of Government of Japan-Trust Fund. We acknowledge Dr. Yasuo Inui and Dr. Kazuya Nagasawa for technical guidance, Albert Gaitan and Angelo Marte of Aquaspec Hatchery and Marietta Duray and Jhozine Damaso of SEAFDEC Fish Hatchery for providing the fish samples, the Microtechnique Service Laboratory of SEAFDEC Aquaculture Department for assistance in histological processing of the samples, and Dr. Evelyn de Jesus for editing an earlier draft of the paper.
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Conference paperLV Benitez - In RD Fortes, LC Darvin & DL de Guzman (Eds.), Fish and crustacean feeds and nutrition : Proceedings of the seminar-workshop on fish and crustacean feeds and nutrition held on 25-26 February 1985 at UPV, Iloilo City, 1989 - Philippine Council for Aquatic and Marine Research and DevelopmentThis paper reviews recent work on milkfish nutrition. Substantial progress had been made towards understanding the digestive physiology of milkfish. Major enzaymes envolved in the digestions of carbohydrates, protein and lipids had been detected in the pyloric caece, intestines and pancreas of milkfish. The most active carbohydrates were involved in the hydrolysis of α - glocosidic bonds. Intestinal amylase activity consistently reached the peak at about noon when milkfish gut was full. This confirms that milkfish is s daytime feeder. No cellulase activity was detected in any region orf the digertive treat although the fish relies heavily algae and other plant source for food. Trypsin, chymotrypsin and general proteases were also detected in milkfish digestive tract. A powerful milkfish trypsin inhabitor was detected in the filementous algae, Chaetomorpha brachygona which is predominant species in lumot. Lipass in the pancreas and intestines had two pH optima, suggesting a physiologic versatility for lipid digestion in milkfish. There is a limit information on the nutrient requirement of milkfish. Most studies showed that milkfish fry has a dietary requirement of 40% protein, and 7-10 lipid. Studies on the protein-energy requirement of fingerlings suggested that 30-40% protein, 10% fat and 25% carbohydrates are required. Subsequent studies showed an optimum protein energy to total metabolizable energy ratio of 44.4%. Amino acid test diets for milkfish had been formulated to contain white fish meal, gelatin and approprate amino acid mix.
Sensitivity of fertilized milkfish (Chanos chanos Forsskal) eggs to mechanical shock and simulated transport GV Hilomen-Garcia -
Aquaculture, 1998 - ElsevierNaturally-spawned milkfish eggs are routinely subjected to physical manipulation during collection and transport. To avoid unnecessary mortalities, sensitivity of milkfish eggs to mechanical shock was determined at different times after fertilization. Shock sensitivity was assessed in terms of egg mortality within 8 h after a free fall over calibrated heights. The LD50 and LD10 (drop height resulting in 50% and 10% mortality) were estimated for 11 stages of embryonic development. The corresponding force (F) imparted to eggs on impact after a free fall was also computed. LD10 estimates (cm) and their corresponding F (erg per egg) showed that shock sensitivity of milkfish eggs was high during cleavage until the early segmentation stage, rapidly declined as segmentation proceeded until the head and tail started to separate from the yolk, but returned to high levels when the embryo begun twitching and the heart beating until near-hatching. To determine the sublethal effects of mechanical shock, C-shaped embryos were subjected to a free fall over varying heights and transported to a hatchery for further incubation and hatching. The effects of varying periods of simulated transport (mobile or stationary periods) were also examined. At C-shaped embryo stage, neither mechanical shock (F, 13–127 erg per egg) nor prolonged shaking (3–9 h) simulating mobile periods of egg transport affected hatching rate, larval mortality, and incidence of deformed larvae. Exposure to still water (unshaken) simulating stationary periods of egg transport, however, tended to lower hatching rate and significantly increased the incidence of deformed larvae and the combined mortalities and deformed larvae. These results indicate that the sensitivity of milkfish eggs to mechanical shock varies during incubation and that C-shaped embryos may be manipulated or transported with minimum risk of injury. Some recommendations are given regarding proper handling and transport of fertilized eggs.
The sulfide tolerance of milkfish and tilapia in relation to fish kills in farms and natural waters in the Philippines Fish kills of milkfish Chanos chanos and tilapia Oreochromis spp. now occur frequently in brackish, marine, and freshwater farms (ponds, pens, and cages) in the Philippines. Aquafarms with high organic load, limited water exchange and circulation, no aeration, and high stocking and feeding rates can become oxygen-depleted and allow sulfide from the sediments to appear in the water column and poison free-swimming fish. The sulfide tolerance of 2-5 g milkfish and 5-8 g O. mossambicus was determined in 25-liter aquaria with flow-through sea water (100 ml min-1) at 26-30 °C and sulfide stock solutions pumped in at 1ml min-1. Total sulfide concentrations in the aquaria were measured by the methylene blue method and used in the regression against the probits of % survival. Four experiments showed that the two species have similar sulfide tolerance. In sea water of pH 8-8.5, about 163 ± 68 μM or 5.2 ± 2.2 mg l-1 total sulfide (mean ± 2 se) or 10 μM or 313 μg l-1 H2S was lethal to 50% of the fish in 4-8 h, and 61 ± 3 μM total sulfide or 4 μM H2S in 24-96 h (to convert all sulfide concentrations: 1 μM = 32 μg l-1). Earthen pond bottoms had 0-382 μM total dissolved sulfide (mean ± sd - 54 ± 79 μM, n - 76); a tenth of the samples had >200 μM. The water column may have such sulfide levels under hypoxic or anoxic conditions. To simulate some of the conditions during fish kills, 5-12 g milkfish were exposed to an abrupt increase in sulfide, alone or in combination with progressive respiratory hypoxia and decreasing pH. The tests were done in the same flow-through set-up but with sulfide pumped in at 25 ml min-1. The lethal concentration for 50% of the fish was 197 μM total sulfide or 12 μM H2S at 2 h, but 28-53 μM sulfide allowed fish to survive 6-10 h. Milkfish in aquaria with no aeration nor flow-through sea water died of respiratory hypoxia in 5-8 h when oxygen dropped from 6 to 1 mg l-1. Under respiratory hypoxia with 30-115 μM sulfide, the fish died in 2.5-4 h. Tests with low pH were done by pumping a weak sulfuric acid solution at 25 ml min-1 into aquaria with flow-through sea water such that the pH dropped from 8 to 4 in 5 h. Under these conditions, milkfish died in 7-9 h when the pH was 3.5. When 30-93 μM sulfide was pumped in with the acid, the fish died in 2-6 h when the pH was still 4.5-6.3. Thus, sulfide, hypoxia, and low pH are each toxic to milkfish at particular levels and aggravate each other's toxicity. Aquafarms must be well oxygenated to prevent sulfide toxicity and fish kills.