[Blackwater fever]

Blackwater fever is a clinical entity characterized by acute intravascular hemolysis classically occuring after the re-introduction of quinine in long-term residents in Plasmodium falciparum endemic areas and repeatedly using the product.

The symptomatology appears brutally with emission of porto-colored urine, icterus, pallor, nausea, fever and acute renal failure. The hemolytic-like anemia is immediately severe. Parasitemia is mild or absent. The mechanism of renal failure is tubular necrosis.

Well known at the start of the 20th century, blackwater fever has become exceptional since 1950, when quinine was replaced by chloroquine. The disease reappeared in 1990, following the re-utilization of quinine because of resistance to chloroquine. Thereafter, several cases have been described with halofantrine and mefloquine, two new molecules similar to quinine (amino-alcohol family). The physiopathogenesis of the disease is not well known, however it would appear that the concomitance of a double sensitivization of the red blood cells to the P. falciparum red blood cells and to the amino-alcohols is necessary to provoke the hemolysis.

The severity of the clinical picture often requires initial management in intensive care unit. Nowadays, however, prognosis is good and the disease usually regresses without after effects.