MICROBIOLOGY NOTES

 

   
BLACKWATER FEVER:

Blackwater fever is a disease, which is often associated with falciparum malaria and occurs usually in tropical countries. It has a wide geographical distribution, including tropical Africa, parts of Asia, the West Indies, the southern United States, and in Europe. Cases have been reported with fever, jaundice and haemoglobinuria or passing black urine throughout the history of medicine, dating as far back as to Hippocrates.

Clinical features:
Blackwater fever is called so because of passage of dark coloured urine. It is characterized by Hemolysis, hemoglobinemia, and the subsequent hemoglobinuria and hemozoinuria. Other features include noncardiogenic pulmonary edema, profound hypoglycemia (often occurs in young children and pregnant women), lactic acidosis (occurs when the microvasculature becomes clogged with P.falciparum), bleeding, hemolysis resulting in severe anemia and jaundice. After several bouts of falciparum malaria, particularly if there has been inadequate treatment, there is occasionally an abrupt onset of massive intravascular hemolysis with fever, chills, and prostration. The first urine is often red, and then turns dark brown. Vascular collapse is possible, followed by death of 20-30% of the patients.

Pathogenesis:
It is known to occur either spontaneously or after treatment with antimalarial drug quinine. Recently mefloquine and halofantrine have been recognized as possible triggers, although classical drug-induced haemolysis was not excluded in these cases. The exact pathogenic role of the parasite and the antimalarial drugs remains unclear. The hemoglobin escapes into the urine turning it black if the urine is acidic. Significant intravascular hemoglobin release causes hemoglobinuria and renal failure. Hemoglobinuria due to massive intravascular hemolysis can occur in non-immune or semi-immune individuals. The intravascular hemolysis can be due to non-immune destruction of parasitized red cells in case of high parasitemia or due to immune mediated destruction of parasitized as well as non-parasitized red cells. Patients with deficiency of glucose 6-phosphate dehydrogenase enzyme may develop hemolysis when treated with oxidant drugs like primaquine.

Laboratory diagnosis:
Diagnosis is more often made on clinical grounds and associated blood and urine tests. Thin and thick smears of peripheral blood usually do not reveal any malarial parasite.
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  Last edited in April 2024