The major causes of mortality of seabass fry in the nursing period are cannibalism, stocking density, uneven growth and disease infection.
Seabass is highly cannibalistic especially in the early stages when the individuals tend to congregate at high density in a certain place. This offers an opportunity for the stronger fry to take their prey. Upon its first success to prey on its kind, a seabass fry will exhibit increasing vigour and urge to feed mainly through its cannibalistic behaviour.
Chan (1982) observed that while the bigger individual readily takes the smaller fry, it is also not uncommon for one to take another of the same size. The cannibalistic behaviour is most pronounced at dawn and dusk when light intensity is low and also when flow rate of culture medium is minimal. The cannibalistic behaviour of the species is also pronounced when the fry congregate in high densities, fighting for feed during feeding time.
The cannibalistic rate increases with increasing stocking density, clarity of water, and the number of feeding sessions per day. It also increases with decreasing percentage satiation per feeding, the number of feeding sessions per day, and the intensity of light.
High stocking density is another common cause of high nursery mortality especially in the absence of stock management measures. Chan (1982) observed that in the absence of stock management initial stocking density of fry size ranging between 2.0 and 2.2 cm TL at 375 fry/m3 would be reduced to about 200 fish or by 47 percent after 25 days of culture. The remaining stock is much more even in size, comprising roughly 2% of 6.7 cm TL, 88% of 4.5 cm TL and 10% of 2.5–3.0 cm TL. Of this remaining stock, the lowest size group similarly exhibits a contrasting colour pattern signifying a state of stress while the highest size group is also silvery except when disturbed.
As stocking density increases about this level, the percentage of mortality accordingly increases for the same culture period. Thus, high stocking density is definitely another common cause of high nursery mortality.
Under confinement conditions, the uneven growth of the fish promotes competition among the individuals for feed, space and other essentials for survival. The resulting additive effects of stresses on the smaller and weaker fry, are witnessed by the dark to black colour, making them much more susceptible to being preyed upon and contracting disease.
If such a stock is not properly managed, uneven growth as an indirect cause of nursery mortality can be rather significant. The uneven growth could be due to the cannibalistic behaviour of the species. It is important to note that in each batch of fry, there are the normal and the subnormal fry in terms of growth and other biological characteristics, which cannot be detected until later. Dietary and environmental factors may also be responsible.
Disease infection is another major cause of nursery mortality posing the principal constraint to confront the future development of seabass culture. (The term “disease” generally refers to viruses, bacteria, fungi, protozoans and other harmful pathogens.)
Based on visual observations, the most common symptoms of diseased seabass fry are:
loss of desire to feed;
immediately followed by increasing production of melanin cells making the fry almost uniformly dark grey to, in extreme cases, black, and coupled with complete loss of desire to feed;
simultaneously, the ventral profile of the fry becomes concave, and the body sub-normally compressed suggesting a noticeable decline in condition;
concurrent with (b) and (c) fry show loss of skin typically dorsal on the frontal-supraoccipital area and on the side of the body, sometimes with skin flaps still attached to these parts;
either before or after (d), a very long string of faeces typically whitish-grey attached to the anal opening trailing behind the fry as it swims sluggishly with head up and tail down, and
initial fungal infection on the skinless parts becoming thick white patches.
As the number of these symptoms increases, the fry show a distinctly poor condition, a complete loss of appetite, a uniformly black colour, and a gradual loss of orientation. Death normally begins two to three days after the appearance of symptoms (e). The rate at which these symptoms develop from (a) to (f) varies from four to six days. Generally, the higher the stocking density, the faster will be the rate of advancement of these symptoms.
Chan (1982) found that such disease-affected fry showing symptoms (a) and (b) are affected by concentrations of protozoans on the gills. On immersion of the fry in a medium at a reduced salinity of 15–20 ppt with a concentration of 2 ppm formalin for several hours, the expression of the other symptoms can be deterred. On immersion in a medium of reduced salinity of 10–15 ppt with a concentration of 2 ppm of terramycin for more than 2 hours with aeration in a closed recirculating system, nearly all fry resume the normal intensity of their ground colour and also their desire to feed.
