Studies on the Pathogenesis of Leptospirosis

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Abstract
Summary Histochemical studies on kidney and liver sections from guinea pigs experimentally infected with Leptospira icterohemorrhagiae (LT-351) demonstrated a pronounced decrease in enzymatic activity for succinic, isocitric, glutamic, and glucose-6-phosphate dehydrogenases and, to a lesser extent, for lactic and malic dehydrogenases. These changes first appeared as patchy areas of diminished enzymatic activity in tissues from animals killed on the fifth day of infection and became widespread in tissues of sixth-day animals. The patchy distribution of lesions and the involvement of mitochondria strongly suggest a hypoxic mechanism as the cause of renal lesions in leptospirosis. Histochemical lesions were less apparent in liver sections than in kidney sections, although a marked decrease in activity was also observed especially for succinic and isocitric dehydrogenases. Biochemical assays of serum and kidney and liver homogenates, on the other hand, did not show variations from those observed in normal animals, although a decrease in activity was noted for isocitric dehydrogenase in sixth-day animals. The decrease in isocitric dehydrogenase is probably due to the decrease in number of mitochondria. Serum determinations of the various oxidative enzymes and of glutamic-oxaloacetic and glutamic-pyruvic transaminases gave values which were within the normal range of variation and which correlate well with the scarcity of necrotic lesions observed on histologic examination. It is suggested that determination of these enzymes in patients with jaundice will afford valuable information in the differential diagnosis of leptospiral vs. viral hepatitis.

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