Blackwater fever like in murine malaria.

Blackwater fever (BWF) is the term used to designate the occurrence of hemoglobin pigments in the urine of patients infected with malaria parasites. BWF is more often associated with Plasmodium falciparum infection in man. The pathogenesis of BWF has not been explained satisfactorily. In the present study, the clinical and pathological observations made upon CD1 mice infected with Plasmodium yoelii yoelii lethal strain with clinical signs of hemoglobinuria and acute renal failure were evaluated. From the 40 P. yoelii yoelii-infected mice, 14 presented hemoglobinuria. In the observations, it was emphasized that hemoglobinuria occurred in the animals 1-2 days before they die. At 6 days post-infection, infected hemoglobinuric mice (HM) exhibited clinical signs such as dark red urine, apnea, and evident oliguria and hematuria; urine microscopical examination showed very few red blood cells. The entire non hemoglobinuric infected mice had a high parasitemia preceding the time of death, while the HM parasitemia was just detectable. In HM, marked hepatosplenomegaly, anemia, and renal and hepatic dysfunction were observed with the blood chemistry analysis at 6 days post-infection. Severe renal lesions were demonstrated in histopathological and scanning electron microscopy samples. Occlusion and necrosis of convoluted tubules were the main lesions found. The conditions required for the experimental production of hemoglobinuria in CD1 mouse infected by P. yoelii yoelii is still unknown. The clinical picture of a BWF, like in our rodents, was produced exclusively by the interaction between the parasite and its host. Results showed that hemoglobinuria in CD1 mice infected with P. yoelii yoelii and BWF in man infected with P. falciparum are similar in their pathogenesis.

[Tropical malaria in children in the Republic of Tajikistan].

The complications of tropical malaria were noted in 25 (9.4%) of 196 pediatric patients followed up. These included cerebral malaria in 8 (3%), severe hemolytic anemia in 15 (5.7%), hemoglobinuric fever in 1 (0.37%), and malarial hepatitis in 1 (0.37%). The occurrence of complications was associated with the late referral of patients to a health care facility and untimely treatment, as well as with preliminary misdiagnoses (acute respiratory viral infection, typhoid-parathyphoid fever, meningitis, acute enteric infection, viral hepatitis, sepsis). The main reasons for late diagnosis were the absence of malarial paroxysm at the onset of disease in infants and the wrong type of a temperature curve.

Case reports: pernicious complications of benign tertian malaria.

We describe 2 patients with complications of Plasmodium vivax malaria. Both patients developed marked intravascular haemolysis and haemoglobinuria despite normal levels of glucose-6-phosphate dehydrogenase activity in blood. One required mechanical ventilation because of life-threatening hypoxia due to acute respiratory distress syndrome.

Enhanced lipid peroxide levels in the erythrocytes of calves with haemoglobinuria.

Eight 6-9 month old calves, showing clinical signs of intermittent haemoglobinuria, even after treatment with an antipiroplasmal drug (4,4-diamidinodiazaminobenzene diaceturate), were examined for oxidative damage to their erythrocytes and the presence of hemoprotozoa in blood smears. Four calves without signs of haemoglobinuria served as controls. The blood smears from three of the eight calves contained piroplasms for Theileria annulata. Irrespective of the presence of piroplasms in their blood smears, the calves with haemoglobinuria had significantly (p < 0.01) lower haemoglobin concentrations (Hb) and packed cell volumes (PCV). The lipid peroxide level in the erythrocytes, but not in the plasma, of calves with red urine was significantly (p <0.05) higher than that for the controls. It is concluded that haemoglobinuria, irrespective of the presence of piroplasms in blood smears, is associated with oxidative stress to erythrocytes and peroxidation of polyunsaturated fatty acids of cell membrane.

Acute haemolysis in childhood falciparum malaria.

Acute haemolysis associated with clinical episodes of high-level Plasmodium falciparum parasitaemia was studied in 20 children from an holoendemic area (coastal Tanzania). The change in blood haemoglobin (Hb) concentration ranged from -46 to g/L during the 72-h observation period and was linearly related to maximum parasitaemia. Balance studies between loss of blood Hb, increase in plasma Hb and appearance of Hb in the urine indicated that extravascular clearance of red cells was the predominant mode of erythrocyte clearance. Most subjects, however, showed minor signs of intravascular haemolysis. The plasma Hb was << 1% of blood Hb and haemoglobinuria was detected in 14/20 children but the excretion of Hb in urine was < 0.5% of total Hb loss. Haemoglobinuria was, however, a marker of severe haemolysis, since the maximum blood Hb loss in children without haemoglobinuria was 10 g/L. Erythrocyte-bound opsonins known to induce erythrophagocytosis, i.e., complement C3c fragments and autologous IgG, were increased in all patients. In the patients with major haemolysis, the changes correlated to the haemolysis over time. Hence, a similar mechanism for predominantly extravascular erythrocyte clearance may be operative in acute malarial anaemia, normal erythrocyte senescence and other forms of acute haemolysis.

[Blackwater fever in adults with sickle cell anemia. Two fatal cases]. / Fièvre bilieuse hémoglobinurique chez l'adulte drépanocytaire. A propos de deux cas mortels.

Blackwater fever is characterized by severe intravascular hemolysis with renal failure caused by recurrent use of quinine for prophylaxis. Once described in European patients, sporadic cases have been reported more and more often in autochthonous Africans and Asians. Newer antimalarials including aminoalchohol mefloquine, and halofantrine have also been implicated in Blackwater fever. In this report we describe two cases of blackwater fever involving patients with sickle cell anemia (HbSS). Symptoms including fever, acute hemolytic anemia, emesis, back pain, and hemoglobinuria were characteristic of blackwater fever. Both patients died. Although the underlying mechanism of blackwater fever remains unclear, a likely explanation is an immunoallergic reaction to quinine. Association with glucose-6-phosphate dehydrogenase deficiency has often been reported. Our cases suggest that blackwater fever may also be correlated with hemoglobinopathy such as HbSS.