The disease in rainbow trout (S. gairdneri) known as the Egtved Disease was first described by Schaperclaus (1938) under the designation "Nierenschwellung" and later (1954) as "Infektiose Nierenschwellung und Leberdegeneration" (INuL). Other synonyms are: Bauchwassersucht, die neue Forellenkrankheit, Forellenseuche, la Lipoidosis Epatica, L'anemie infectieuse des truites, and L'anemie pernicieuse des truite.
Schaperclaus considered it to be a virus disease, whereas some later authors maintained various nutritional deficiencies, especially lack of vitamins (vitamins B1, B12 and E) to be the primary cause of the disease.
The authors has tested the various theories of nutritional deficiency as to their possible primary or secondary importance to the outbreak of the disease. Investigations have been carried out on the incubation period of artificial and natural infections and their relationship to temperature. Contributions have been given to the ways in which the infection can be spread, and some other salmonid species have been tested as to their susceptibility to artificial and natural infection and their possible importance as carriers of infection.
The results can be summarized as follows:
(1) It has nt been possible to find any primary connection between the disease and the food used. Based on the theories of the various authors a deficiency in vitamin E was sought by adding 20 percent cod liver oil to the normal food, and a deficiency in vitamin B12 by using a food artificially alkalized (pH about 9) by means of ammonia. No harmful effect on the stomach cells producing hydrochloric acid was found from the use of the last named food.
(2) By numerous experiments with artificial and natural infection it has been proved that the disease is caused by a primary factor. The period of incubation by artificial infection is generally two to three weeks, by contact infection one to two weeks longer.
(3) Results of the experiments on inoculation in healthy rainbow trout of pathological, bacteriologically sterile liver filtrate from diseased fish, and communication from the artificially infected to healthy rainbow trout, prove that the infectious factor must be a virus.
(4) Low water temperature favours the outbreak of the diseae, lengthens its duration, and increases the lethality.
(5) It has not been possible to obtain any protection against the disease by weekly intraperitoneally injections of vitamin B12 or vitamin E or a combination of the two. The same negative result was found from an addition of vitamins B1, E, and A to fish as well as meat food.
(6) It has not been possible to prove that food with a larger content of fat (herring) would favour the disease to a higher degree than a lean food (whiting).
(7) Experiments with addition of vitamin T-Goetsch to the food with or without a combined terramycin treatment have given no significantly favourable effect of these preparations. However, if such an effect be present, it is obvious from the results of the experiments that it must be to such a limited degree that the practical use may be doubted.
(8) It has been proved that brook trout (Salvelinus fontinalis) is susceptible to contact infection. The period of incubation in the experiment was more than eight weeks. It has been possible to communicate the disease to brown trout (Salmo trutta) by artificial infection but not by contact infection. The same holds for salmon (Salmo salar).
(9) Investigations on the dissemination of the disease have proved that the virus may be transported by water. Brown trout subjected to contact infection have not been able to communicate the disease to healthy rainbow trout. Experiments with artificial infection of rainbow trout by intraperitoneal injection of live filtrate from brown trout subjected to contact infection have given the same negative result.