apparently of M. cerebralis disease, about a 

 year earlier. The source of infection may have 

 been in one lot of trout transferred from Lamar 

 to Kensington in 1959. 



To our knowledge whirling disease caused 

 by M. cerebralis has not been verified anywhere 

 else in North America. Dr. R. Bangham (pers. 

 comm.) recalls identifying M. cerebralis at a 

 northern Wisconsin hatchery about 1945 but no 

 specimens are available for our verification . 

 We have seen similar whirling at three other 

 hatcheries but could find no M_. cerebralis and 

 assume that some physiological disturbance or 

 other disease may also cause this symptom . No 

 other characteristic symptoms were present in 

 these fish. 



If the spreading of this disease is not 

 halted shortly, it can be expected to show up in 

 trout and salmon hatcheries where infected fish 

 are transferred and particularly those which 

 have earthen ponds, trout in spring water reser- 

 voirs or stream water supply. 



SYMPTOMS AND THE COURSE OF THE DISEASE 



The symptoms are thoroughly discussed by 

 Plehn (1904), SchMperclaus (1954) and Uspenskaya 

 (1957) but will be reviewed here because of the 

 lack of a previous English discussion. The 

 symptoms we have seen are identical with those 

 reported in Europe. 



Trout may beco me infected up to one year 

 of age (SchSperclaus, 1954) but usually become 

 infected during the first few weeks of life --the 

 earlier the infection, the more severe the 

 disease because of the greater amount of carti- 

 lage present in younger fish. As we have 

 pointed out, we were not able to prove that trout 

 become infected by ingesting the spores, but this 

 should be assumed until disproven. The disease 

 takes the following course: 



Period of "incubation" . After exposure to the 

 spores a lapse of 40-60 days ensues before the 

 symptoms of whirling disease are evident 

 (SchMperclaus, 1954). Our experimental fish 

 in which we were never able to demonstrate the 

 parasite exhibited symptoms in 12 to 16 days. 

 We mention it here because there may be other 



conditions which simulate M. cerebralis whirl- 

 ing disease. We do not know for certain whether 

 the disease causes mortalities during the 

 "incubation" period. The parasites are so small 

 during this period that histological verification 

 is probably impossible or extremely difficult and 

 mortalities might be attributed to other factors. 



Initial symptoms . The most obvious symptoms, 

 tail-chasing, whirling and black tail (fig. 1), 

 become evident at about 40 to 60 days and may 

 last about 1 year. The trophozoites have in- 

 vaded and eroded the cartilage of the developing 

 skeleton. Rather large "lesions" containing the 

 parasites and debris can be seen in histological 

 preparations. The cartilaginous capsule around 

 the auditory -equilibrium organ behind the eye is 

 usually invaded. Perhaps toxins released by the 

 parasite (Plehn, 1904) or simply weakening of 

 the capsule destroys the equilibrium of the fish 

 to such an extent that each time it is disturbed 

 or tries to feed it goes into a frantic tail-chasing 

 whirl. This tail-chasing type of whirling differs 

 from the horizontal spiraliqg of the fish along its 

 long axis which is characteristic of a virus 

 disease, infectious pancreatic necrosis (Snieszko 

 and Wolf, 1958) and possibly hexamitiasis 

 (octomitiasis) (Davis, 1953). Small fish, up to 

 3 months of age (about 2 inches long) may become 

 so exhausted that they fall to the bottom and re- 

 main on their sides until they regain their 

 strength. It is during this period that mortalities 

 are likely to occur. Other debilitating factors 

 such as other parasites, bacterial or viral 

 diseases or malnutrition will probably increase 

 mortalities. During the early part of this period 

 the whirling symptom is at its worst, but it tends 

 to subside gradually until it is only rarely seen 

 in fish one year post -infection. 



Very often the cartilage of the vertebral 

 column, posterior to the 26th vertebra, is 

 simultaneously affected (Plehn, 1904; Schaperclaus, 

 1954). The sympathetic nerves which control 

 the caudal pigment cells have their origin at about 

 the 26th vertebra. Apparently the weakened 

 skeleton at this point causes pressure on the 

 caudal nerves and pigment cell control is lost, 

 hence the black tail. The black tail tends to 

 dissappear earlier than the whirling symptoms. 

 One lot of about 4, 000 rainbows at Kensington 

 became infected when brought to the hatchery at 



