supported by the Overseas Development Administration. We are very grateful
to our coleagues Ren6 Haller and John Balarin for their help with this
program and Mr. I.H. MacRae, Dr. R.L. Oswald and Staff of the Institute
for assistance with preparation of the manuscript. Dr. nan Paperna and Mr.
Shmuel Sarig have also been very helpful to us in providing information from
their long experience of tilapia culture in Israel.DiscussionLOVSHIN: I don't think you mentioned anything about myxosporidian parasites. In
cage culture in the Ivory Coast, they have just about had to stop using Sarotherodon
niloticus because myxosporidians wipe them out. They are changing to a local species, S.
melanotheron (T. heudelotii).
ROBERTS: I did mention those in terms of pond culture, but I have only just learned of
the example which you quote.PULLIN: Dr. Roberts, can you say anything more on the reasons why cold temperatures
always seem to bring disease problems, because this is not just so with tilapias, but for
many different fish.ROBERTS: Perhaps Dr. Avtalion could comment on this?AVTALION: We have not performed a comprehensive study of this problem in tilapia,
as we did in carp. We know that cold temperatures inhibit the immune response, namely,
the ability to respond to different antigens. We found that the inhibitory threshold for
antibody production was between 16 and 18OC in tilapia and 16OC in carp. At these low
temperatures, both activities of bacteria and immune system are considerably inhibited.
When spontaneous increase of environmental temperature occurs, the bacteria multiply
faster than the immune system could react. Thii seems to be different when viral and
parasitic diseases are considered.
ROBERTS: I think that it is temperature change that is a problem. If you have specific
pathogen-free tilapia or carp or salmon or trout and if you can reduce the temperature
very slowly, you can usuallq get away with it. Going down in temperature, each pathogen
seems to have an optimum temperature range and you go through those ranges for
particular strains or species of micro-organisms. At the same time your fish, particularly
warmwater species like tilapias have to switch enzyme systems on and off at different
temperatures and it would appear that for fishes in general the ability to do this is a little
slower than the ability of micro-organisms to adjust and take advantage of the situation.
Fishes also have a very nice mechanism for repairing skin damage. If we damage
our skin, then the cells round about proliferate and fill the hole. Fish have to use a
different system since at low temperatures their rate of metabolism and therefore rate of
cell multiplication is so low. In fish, the epidermis which is a thick layer, donates cells
which migrate from a wide surrounding area to cover the lesion. This happens even at low
temperatures within a few hours. In two or three hours, a reasonably small lesion will be
completely covered by a layer one cell thick. This is probably important to both fresh-
water and marine fish, including carps. A problem remains, however, that if aeromonads
and pseudomonads are deposited in the middle of a large lesion, then the epidermal cells
come in a certain distance and then stop. Presumably, therefore, there is a secondary
defense mechanism against such microorganisms for large lesions and for situations where
fish are not able to make their cell migration system work fast enough (e.g. at the bottom
of their temperature range). With large lesions, the whole skin gets very thin.