596 MR JOHN RATTRAY ON ECTOCARPUS. 



in fig. 10. Here the host cell wall has ruptured, and the membrane of the 

 parasitic cell has swollen so much that a complete relief from internal pressure 

 has occurred without rupturing the latter. The result is that the smarmspores 

 are arranged in a retiform manner, forming meshes by adhering to each other 

 along certain lines. That this is a transitory stage is at once manifest, but that 

 it may be the final appearance, presented by the swarmspores generally just 

 before the rupture of their bounding cell membrane takes place, is not unlikely. 

 It indicates that, although the protoplasm contained in the parent Rhizophydium 

 divides by a simultaneous process into numerous spores, a final separation 

 is not effected at the same moment throughout the entire mass, but rather 

 along certain lines whose direction is in all probability determined by the lines 

 along which the force or forces that determine rupture act. 



Various causes operate in bringing about the rupture of the cell wall of the 

 host plant, as well as of the thinner and more elastic membrane of the endo- 

 parasite. These may be regarded as being (a) intrinsic and (b) extrinsic. Of 

 intrinsic causes there may be noted (1) internal tension, and (2) weakness 

 resulting from pathological changes. The former of these factors is no doubt 

 that of the greater significance. It originates in the developmental changes that 

 take place inside the endo-parasite. The volume of the latter is being slowly 

 increased, and while a certain amount of nutritive material must be removed from 

 the host cell to produce this result, so that tension strain would thus so far be 

 antagonised, the growth of the parasite that follows more than counterbalances 

 the changes effected, while at the same time a certain amount of carbonic acid 

 gas, resulting from protoplasmic oxidation, given out by the parasite, will tend 

 still further to increase the pressure. As already noted, that pressure causes, 

 first a bulging of the host cell into the surrounding medium chiefly, but also 

 partly into adjoining cells of the thallus when these are not similarly affected, 

 and finally it results in producing rupture at their weakest point. The ultimate 

 expansion and rupture of the parasitic cell wall are due to a similar tension 

 exerted by the ever-increasing swarmspores. 



(2) The weakness resulting from pathological changes, operates, though in a 

 less degree, in accelerating the bursting of the host cell wall. The full complement 

 of nutritive material no longer reaches this wall from its normal channel, viz., 

 its own cell protoplasm, so that the supply of new food molecules, to maintain 

 the oxidation consequent on vital activity, is partially checked. This may 

 result in pathological molecular transformations in the wall, producing areas of 

 weakness, where rupture becomes possible by the operation of internal pressure 

 and the other extrinsic causes. In confirmation of this view, it is to be 

 remarked that the host cell is not usually found to rupture at or towards an 

 angle of the cell," but, in most cases, opposite the middle of the cell lumen, 



* If ruplure occurs here, it is attributable to the action of extrinsic and purely accidental causes. 



