that the parasites tend to disappear at the onset of blackvvater— but 
not, we think, so conclusively as in this case; nor do we know of 
relapses without either Plasmodia or haemoblobinuria having been 
previously noticed. 
We should add (i) that no signs of any other parasites beside; 
Plasmodia were seen ; and (2) that the total elimination of urobilin 
from the 8th to the 15th day represents an amount of haemoglobin 
equal to that of all the patient’s corpuscles, the 25 per cent, of 
haemoglobin still remaining being probably contained in young 
corpuscles generated during the period referred to. The relation 
between the numbers of circulating corpuscles and the haemoglobin 
percentage appears to confirm this estimate. As the asexual 
parasites cannot live outside the red corpuscles, this enormous 
destruction of the latter probably causes an equally great destruction 
of the former, which may explain Panse’s law and the absence of 
parasites after the sixth day in our case; but it does not seem 
capable of explaining the fever. (3) The comparatively slight fall 
<>f haemoglobin during the third pyrexial period may be explicable 
on supposition that the red corpuscles were then probably younger 
and more resistant. (4) I he enlargement of the liver and the bilious 
vomiting might suggest derangement of the hepatic system, but they 
may also represent the hyperaemia of extreme activity. The fact 
lhat the liver eliminated, in its usual manner, such an enormous 
amount of blood pigment tends to confirm the latter hypothesis. 
(. 5 ) In conclusion, we would remark that haemoglobinuria seems to be 
merely a small overflow of the freed haemoglobin which the liver 
las not been able to deal with ; and that some other cause other than 
t ic toxin of the Plasmodia seems to produce both the special 
aemolysis and the special fever associated with it. 
