injury or otherwise, to the discharge of the immature ova into the lymph-stream, to their impaction in the vessels leading to the lymph glands, and to the complete obstruction, with its resulting lymph stasis, which ensues. In addition to this, it is maintained that lymph stasis alone does not produce elephantiasis—some injury in the area of lymphatic construction must take place; lymphangitis ensues, the inflammatory products cannot be completely absorbed owing to the stasis, and elephantiasis results. It is, therefore, recognised that an erysipelatoid inflammation frequently recurring is an essential feature in the production of elephantiasis arabum. This theory, then, takes up a somewhat different standpoint. In those we have already considered the adult worm is said to be situated in the proximal end of the lymphatics; in the present case it is situated in the peripheral part, and the obstruction is produced between the worm and the thoracic duct. It is, as you will realise, an absolutely different point of view.
Now, the possibility or even probability of the adult female filaria aborting occasionally, as other females do, especially if it is injured, must be admitted, and in that case the immature ova would be discharged into the lymph- stream, and they have been identified more than once by Sir P. Manson. That this does occur, and that the occasional blocking of some of the afferent vessels of a lymph gland may take place, must also be admitted. But when I come to examine the distribution of the lymphatics in the different situations in which elephantiasis occurs, I find a difficulty, from a mechanical point of view alone, of explaining how the obstruction which is necessary to produce a complete lymph stasis can occur. Looking again at the illustration of the superficial lymphatics of the leg, at what point in the limb can a single worm be situated so that the lymph-stream would carry the ova so as to obstruct the whole of the superficial inguinal glands? Or if the worm
