TRANSMISSION AND HOST SPECIFICITY 



It has long been assumed that, if ingested, 

 the spores taken directly from infected trout 

 will infect other trout (Plehn, 1904; SchMperclaus, 

 1931, 1954). As previously discussed, we were 

 not able to do this experimentally at Leetown, 

 and to our knowledge no one else has . Therefore, 

 all knowledge concerning transmission and life 

 cycle has come from studies on material collect- 

 ed during epizootics. 



Trout fry can be infected by exposing them 

 to water containing the silt, and presumably the 

 spores, of ponds from a hatchery epizootic 

 (Schaperclaus, 1931). One assumption is that 

 the spores are ingested accidentally, but the 

 possibility of an invertebrate transport host has 

 not been ruled out. Another assumption is that 

 spores are freed from infected fish when they 

 decompose or are crushed. Uspenskaya (1957) 

 has found isolated spores in various organs of 

 the fish and suggests that they may be carried 

 away from the site of infection by blood or lymph 

 and be deposited in other organs . If this in- 

 cludes the intestine, they could be shed while the 

 fish is still alive. However, it has not been 

 determined whether fish can be infected by this 

 method. Apparently the freed spores accumulate 

 in the ponds (particularly earthen ponds) and the 

 severity of the epizootic depends on the number 

 so accumulated. Small trout up to four months 

 are most severely affected. The disease can be 

 controlled therefore, but perhaps not eliminated, 

 by keeping the trout in spore -free water until 

 they are four months or more of age. Older fish 

 may become infected, but are usually not serious- 

 ly affected because ossification of the skeleton 

 prevents massive infection. Such fish, however, 

 may act as "carriers". 



On the basis of epidemilogical evidence 

 the spores are apparently very resistant to dry- 

 ing, freezing, and survive a long period of time 

 (Plehn. 1904, 1924; Schaperclaus, 1931, 1954). 

 We have kept 2 vials of spores for 3 years, one 

 at room temperature, the other at about 6° C. 

 At the end of 22 months all spores appeared 

 normal, but at 3 years the sporoplasm has com- 

 pletely disappeared from 85 percent and did not 

 appear normal in the remaining 15 percent. We 

 believe they were 100 percent non-viable. 



It is likely that the spores can be carried 

 from pond to pond or hatchery to hatchery on 

 boots and other equipment. Schaperclaus (1931) 

 found myxosporidean spores in the feces of 

 kingfishers at an affected hatchery and believes 

 that the disease can be spread in this manner. 



Most myxosporidean species show varying 

 degrees of specificity for certain species or 

 closely related species of fish . They are also 

 usually specific for a certain organ or tissue. 

 Myxosoma cerebraUs is no exception- -it has 

 been found in rainbow trout (Salmo gairdneri ); 

 eastern brook trout ( Salvelinus fontinalis ); brown 

 trout (Salmo trutt a) and recently in salmon 

 (Salmo salar) (Uspenskaya, 1957), grayling 

 (Volf, 1957), and in Salvelinus leucomaenis, 

 S. malma, Oncorhynchus keta and O. masu 

 (Bogdanova, 1960). Rainbow trout are most 

 seriously affected by the disease, brook trout 

 somewhat less severely, and brown trout show 

 no symptoms at all but may act as "carriers". 

 Likewise, any symptom -free but infected rainbow 

 or brook trout may be serious "carriers". The 

 initial infection in a fish is always in cartilage, 

 but loss of cartilage and proliferation of tissue 

 may leave the spores outside of the skeleton in 

 little cyst-like structures. 



LIFE CYCLE 



The complete life cycle of M3rxosoma 

 cerebralis ( Lentospora c .) has never been 

 determined experimentally (fig. 4). We know 

 of no one who has demonstrated the experimental 

 life cycle of any Myxosoma or related Myxobolus 

 or Henneguya species. These are all histozoic 

 parasites. Plehn (1904, 1924), SchSperclaus 

 (1954), and Uspenkaya (1957) assume that the 

 spores are ingested, the sporoplasm leaves the 

 spore, penetrates the intestinal mucosa and 

 migrates to the cartilage. However, this has 

 never been verified experimentally. Kudo (1930), 

 p. 313, reviews experimental infections and cites 

 two workers who successfully infected fish with 

 three coelozoic m yxospori deans- - Myxidium, 

 Chloromyxum , and Leptotheca; but none of the 

 histozoic Myxosoma, Myxobolus , or Henneguya 

 are mentioned. 



The various tissue stages from hatchery 

 epizootics have been described by Plehn (1904) 



