met with. Blood corpuscles may be entirely absent, or very few in number. With the hæmoglobin there is also an escape of the serum-globulin of the blood, for the urine, in many cases, turns almost solid on boiling; the coagulum so formed carries down with it as it subsides the dissolved and suspended hæmoglobin, leaving a pale-yellow supernatant urine. For some days after the urine has regained a normal appearance it will still contain albumin, though in gradually diminishing amount. Spectroscopic examination gives the characteristic bands of hæmoglobin, sometimes those of methæmoglobin.
Mortality.— This varies greatly in different epidemics, in the same and in different places, and even under the same treatment. Some cases are so mild and transient, amounting, perhaps, to a single emission of hæmoglobinous urine, with little or no fever, that they are unattended with risk; on the other hand, a practitioner may encounter a run of severe cases in which nearly all die. Some old residents in Africa have passed through ten or more attacks with impunity. Taking one with the other, the case -mortality in blackwater fever may be put down at about 25 per cent.
Post-mortem appearances. The kidneys.— If the kidneys of a fatal case are examined at an early stage of the disease, they are seen to be enlarged and congested, the tubules blocked with hæmoglobin infarcts, the cells laden with yellow pigment grains, and the capillaries most probably with a certain amount of malarial pigment. If the case survive for three or four weeks and then die of uræmia, the appearances are those of large white kidney.
The spleen is enlarged, congested, and usually contains malarial pigment.
The liver is enlarged, soft, of a dark -yellow colour. Microscopically it reveals evidence of cloudy swelling with a large amount of hæmosiderin in the liver cells. Hæmozoin may or may not be present.
Diagnosis.— The diseases with which blackwater fever might be confounded are— 1, paroxys-
