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MICROBIOLOGY NOTES
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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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