Does presence of nitrates in urine diagnose malaria?
Q: Does the presence of nitrate in routine urine examination in case of high fever help in the diagnosis of malaria?
A:Gram-negative bacteria in the urine reduces dietary nitrate to nitrite, forming the basis of this test. Any degree of uniform pink to red color that appears on the test confirms the presence of nitrite, and indicates significant bacteriuria. Prolonged urinary retention in the bladder (at least 4 - 8 hours) is essential to obtain an accurate result. Sensitivity decreases with frequent micturition and/or increased diuresis; with insufficient dietary nitrate to convert to nitrite; when the bacteria causing the urinary tract infection does not contain the enzyme reductase, as well as urine with a high specific gravity. For accurate test results, antibiotics should have been discontinued/course completed for at least 3 days before the test is performed. Abnormal nitrite values may be indicative of a bacterial urinary tract infection caused by E. coli, Salmonella sps, Citrobacter sps, Proteus sps, Klebsiella sps, Enterobacter sps, etc. Check for the following if nitrites are found in urine: - leucocytes - pH - protein - blood/hemoglobin Send urine for microscopy and culture sensitivity. The routine urine test for nitrate has no bearing on the diagnosis of malaria. However, there is an interesting study, the details of which are given below, in which there was an inverse relationship between urinary nitrate and severity of malaria. ------ J Exp Med. 1996 Aug 1;184(2):557-67. Nitric oxide in Tanzanian children with malaria: inverse relationship between malaria severity and nitric oxide production/nitric oxide synthase type 2 expression. ------ Anstey NM, Weinberg JB, Hassanali MY, Mwaikambo ED, Manyenga D, Misukonis MA, Arnelle DR, Hollis D, McDonald MI, Granger DL. Division of Infectious Diseases & International Health, Duke University Medical Center, Durham, North Carolina 27710, USA. ------ Nitric oxide (NO)-related activity has been shown to be protective against Plasmodium falciparum in vitro. It has been hypothesized, however, that excess NO production contributes to the pathogenesis of cerebral malaria. The purpose of this study was to compare markers of NO production [urinary and plasma nitrate + nitrite (NOx)], leukocyte-inducible nitric oxide synthase type 2 (NOS2), and plasma TNF-alpha and IL-10 levels with disease severity in 191 Tanzanian children with and without malaria. Urine NOx excretion and plasma NOx levels (corrected for renal impairment) were inversely related to disease severity, with levels highest in subclinical infection and lowest in fatal cerebral malaria. Results could not be explained by differences in dietary nitrate ingestion among the groups. Plasma levels of IL-10, a cytokine known to suppress NO synthesis, increased with disease severity. Leukocyte NOS2 antigen was detectable in all control children tested and in all those with subclinical infection, but was undetectable in all but one subject with cerebral malaria. This suppression of NO synthesis in cerebral malaria may contribute to pathogenesis. In contrast, high fasting NOx levels and leukocyte NOS2 in healthy controls and asymptomatic infection suggest that increased NO synthesis might protect against clinical disease. NO appears to have a protective rather than pathological role in African children with malaria.