85] LIFE HISTORY OF TREMA TODES—FA UST 85 



the Cercaria hiflexa infection of Physa gyrina (Fig. 159), where the cyst mem- 

 brane is moderately heavy, many ceca are uninjured, yet some betray the 

 marks of injury. One such injury is shown in the figure. In this case the 

 cells of the ceca have undergone only a little change. A comparison of this 

 condition with that of C. micropharynx infection in Lymnaea proxima (Fig. 



160) and C. gracillima infection in Physa gyrina (Fig. 161), shows a compara- 

 tively small injury in the former tissue and a severe injury in the latter tis- 

 sues. Both the latter cases show tissue degeneration. The chemical change 

 in Lymnaea proxima is evinced by 1) fatty bodies that have accumulated in 

 some of the cells (a), showing as highly refractive inter-cellular inclusions; 

 2) large vacuoles in the cells (6), especially around the nuclei; 3) cytolysis and 

 karyolysis (c, d), including a sloughing of the tissues in the region of the lumina 

 of the ceca. The condition of C. gracillima infection in Physa gyrina (Fig. 



161) pictures a further degeneration of the tissues. Fatty globules {b), are 

 common, usually accumulated as spherules within the wall. Vacuolization 

 {d) has progressed to an advanced stage. Cytolysis and karyolysis (a, c) 

 have gone so far that the outlines of the majority of the cells are indistinct 

 and no difference exists longer between the epitheUal and the lymphocytoidal 

 cells. An indefinite, irregular margin marks off the ceca from the interstices 

 in which the cercariae lie. A further change consists in the formation of 

 fibromata {e) and granulomata within the degenerating ceca. Finally the 

 epithehum surrounding the entire liver mass has been penetrated by sand 

 granules (/), and other foreign bodies have had access to the tissues. 



In the infection of Planorbis irivolvis with C. trisolenata the mass of the 

 worms was about twice that of the Uver tissue infected. The tissue was so 

 distended with the parasites that a prick of the needle was sufficient to cause 

 the liver membrane to burst, upon which the rediae and cercariae fairly poured 

 out of the tissue. 



The data on the effect of the trematode infection on the molluscan host 

 are significant. No infection is so light that mechanical and chemical injuries 

 are not inflicted. In the heavy infections such as are conmion to the moUusks 

 of the Bitter Root Valley, the injury is so heavy that it must alter appreciably 

 the Hfe of the host. The mechanical pressure tends to inhibit or increase the 

 functioning of the glandular organs and cramps the tissues within unusual 

 confines. The presence of foreign proteins in close association with the lymph 

 sinuses is sufficient to alter the vital economy of the host. The boring of the 

 worm destroys the tissues locally and in general irritates the mechanism, 

 exposing it to bacterial infection. The secretion of digestive juices by the 

 parasite, and of anti-thrombins and possibly specific poisons, upsets the 

 entire physiological equilibrium of the organism. 



