198 BULLETIN OF THE BUREAU OF FISHERIES. 



when the atrophy is hyahn, there are considerable clefts in the sarcoplasm. (Fig. 4, 

 pi. XX). These spaces may come to be more or less closely packed with erythrocytes or 

 leucocytes, or both, so that when the cytoplasm of the blood cells has degenerated a 

 third and common condition is encountered. The nuclei in various stages of degenera- 

 tion become densely packed and enlarged. They assume ama-boid shapes, large alveoli 

 appear in them, and eventually they fall a prey to the short bacillus (fig. 5 and 6, pi. xx) 

 elsewhere encountered. 



The conditions thus presented are such as to suggest an amceboid parasite which 

 has demoUshed a muscle fiber and simultaneously broken up into innumerable bacillus- 

 shaped spores by schizogony. (See fig. 10, pi. xx.) The connective tissue nuclei of the 

 flesh and integument and the nuclei of the gill epithelium give rise to the same degen- 

 eration phenomena. Such nuclei may be about equally hypertrophied and massed in 

 such a manner as to completely disguise their true nature. Both muscle and vascular 

 nuclei may occur in abnormal numbers under the sarcolemma of fibers which are in 

 almost any state of atrophy but without clefts. (Fig. 5, pi. xx.) 



In both fresh and stained muscle the evolution of a curious artifact was observed. 

 It appears as a dense hyalin body in the sarcolymph, between fibrillae. (Fig. 3, pi. xx.) 

 Assuming an amoeboid form it resembles a rapidly growing organism. (Fig. 2 and 7, 

 pi. XX.) But the regular distribution (fig. 2 and 3) and numerous variations toward a 

 crystalline rosette structure are conclusive evidence of their lifeless nature. 



Whatever the active cause of the degeneration of muscle fiber, be it bacteria or 

 Protozoa, the atrophy advances far into one or more muscle fibers without causing any 

 damage to the adjacent fibers. In cross sections of such tissues there may be a small 

 group of normal fibers cut in section amongst numerous others that are wholly degenerate. 

 Capillaries, arteries, veins, and sheets of connective tissue, entirely normal in appear- 

 ance, may also penetrate these necrotic masses. This is no doubt due to the restraining 

 influence of the sarcolemma upon either the parasite or toxin. As we have already 

 noted, the sarcolemma retains its normal relations in completely atrophied fibers. 



Restricting our statements to tissues known to be infected by Sporozoa, there are 

 but two kinds where their action has been observed, namely, muscle, and the connective 

 tissue of the gill. The pathological condition of the muscle tissue, in such cases, is 

 not distinguishable, as far as we know, from that which results from the action of 

 bacteria; but if the pathological changes are to be considered as characteristic of a 

 parasite when it is known to be the cause of the atrophy, a careful study of those cases 

 where bacteria are a negligible factor is important. The mj-xospores, which are the 

 most easily recognized stages of the Myxosporidia, are common only in smear prepara- 

 tions and only those which include more or less diseased muscle fibers. These same 

 smear preparations also contain cells identical in appearance to myxoplasms, pansporo- 

 blasts, and sporoblasts, which happen to be the only representatives of the Sporozoa that 

 we have encountered in sectioned material, thus suggesting their myxosporidian character. 



Several fragments of tissue, the integument of which was slightly diseased, were 

 sectioned. They give no evidence of myxospores, but the muscle fibers present prac- 

 tically the same degenerative changes to be seen elsewhere. The dermis contains 

 numerous minute unstained lens-shaped structures similar to those described on 

 page 197. These extend into the ends of the adjacent muscle fibers, becoming less 

 numerous in the deeper parts. Such fibers show obvious signs of atrophy. Elsewhere 



