The Genito-urinary System.—The dark colored urine is pathognomonic of the disease and gives it its name. The reddish to almost black color is due to haemoglobin and not to bile. Bile pigments do not appear in the urine. There is but rarely a red cell to be found in the granular débris with occasional haematoidin crystals which forms the urinary sediment, hence it is haemoglobinuria and not haematuria.
The urine resists decomposition for a long time. Albumin is present in large amount and comes on with the onset of haemoglobinuria. Casts are abundant and urobilinuria is marked. As a result of the blocking up of the renal tubules with haemoglobin casts pain over the loins and anuria may occur. There may be vesical tenesmus.
The Blood.—Cases have been reported where as many as 2,000,000 red cells have been destroyed within twenty-four hours, so that rapid and marked anaemia characterizes the disease. The blood is thin and the serum tinged. The degenerative changes of the red cells are not as commonly seen as one would expect but this is probably due to the fact that degenerated cells are first destroyed in the excessive haemolysis. Hb percentage reduction generally parallels the reduction in red cells. Melaniferous leucocytes may be found and during the leucopenia, which follows the paroxysm, the large mononuclears and transitionals may be increased to 20%. There is a reduction in the alkalinity and coagulability of the blood.
Diagnosis
Clinical Diagnosis.—An unusually asthenic prostrating paroxysm, similar to that of a malarial chill, but with more intense rigor, during which haemoglobinuria, early jaundice and marked bilious vomiting are features, makes for a diagnosis of blackwater fever.
The two diseases which are most likely to be confused with blackwater fever are yellow fever and bilious remittent malarial fever.
In infectious jaundice the jaundice does not appear for 48 to 72 hours, the pulse is slow, there is no haemoglobinuria, although there may be a haematuria, and we have a polynuclear leucocytosis.
A case of paroxysmal haemoglobinuria occurring in a blackwater district would be impossible to differentiate from a very mild case of blackwater fever. Chlorate of potash or carbolic-acid poisoning, or snake bite, or severe burns, may produce haemoglobinuria.
| Blackwater fever | Yellow fever | Bilious remittent | |
| Onset | Sudden but asthenic with marked rigor. | Sudden but asthenic for two or three days. | Comes on more slowly. |
| Urine | Haemoglobinuria. Pink foam to urine. Albuminuria from first day. | No blood in urine before 3d or 4th day and then haematuria. Albumin from 2d day. | Bile in urine. Yellow froth on shaking urine. Albuminuria slight and not common. |
| Icterus | Early and intense. Comes on in a few hours. | Does not appear before 3d day and gradually intensifies. | Jaundice develops slowly about 2d day. |
| Spleen | Somewhat enlarged and tender. | No enlargement of spleen. | Splenic enlargement is marked; may have ague cake. |
| Pulse | Rapid from start and becoming more so as disease progresses. | Stationary pulse with rising temperature or falling pulse with stationary temperature. (Faget’s law.) | Pulse not so rapid as in blackwater. |
| Vomit | Early marked bilious vomiting. | Mucus-like followed by black vomit about 4th day. | Bilious vomiting and gastric distress less than in blackwater. |
| Evidences of malaria | Usually present as parasites or melaniferous leucocytes or increased large mononuclear percentage. | Negative unless yellow fever occurs in a malarial case. | Some evidence at some time almost always obtainable. |
Laboratory Diagnosis.—Other than the noting of evidences of malarial infection, rapid reduction in red-cell count and haemoglobin percentage there is little information to be derived from the blood which is thin and shows delayed coagulation time. It is difficult to make good blood smears. In the urine we note the granular sediment of débris of red-cell destruction with at times haematoidin crystals. Spectroscopically we get absorption bands of methaemoglobin and more rarely oxyhaemoglobin.