A histopathological study of hearts and spleens of hamsters (Mesocricetus auratus) infected with Leptospira interrogans, serovar pyrogenes.

The effects of Leptospira interrogans on the heart and spleen of hamsters were studied histopathologically. Infected hamsters were sacrificed at 1 hour, 6 hours and on days 1, 2, 3, 4, 5 and 6 after inoculation with Leptospira interrogans serovar pyrogenes. The heart and spleen of each of the sacrificed animals were removed and processed for routine conventional light microscopy. Infected hearts showed degenerative change of the cardiac muscle cells composed of cellular swelling, condensation of chromatin granules, pyknotic nuclei and acidophilic cytoplasm. Congestion of the cardiac blood vessels and hemorrhagic areas were found. Necrosis of the cardiac muscle cells was surrounded by numerous inflammatory cells. In the spleen, cellular necrosis was found scattered throughout the splenic cord. The splenic sinusoids were dilated and congested with many hemorrhagic areas. Inflammatory cell infiltration was also noted in the splenic parenchyma and the splenic sinusoids.

A Microanatomical study of the organs of hamsters (Mesocricetus auratus) infected with Leptospira interrogans, serovar pyrogenes which caused an outbreak in Thailand 1999.

The effects of Leptospira interrogans on various organs of hamsters were studied microanatomically. Three infected hamsters were sacrificed at 1 hour, 6 hours and on days 1, 2, 3, 4, 5 and 6 after infection with Leptospira interrogans serovar pyrogenes. The kidneys, lungs, liver, gastrocnemius and hamstring muscles of all the sacrificed animals were removed and processed for routine conventional light microscopy. The microscopic change of the infected kidney showed degenerative changes of the renal tubular cells, including vacuolar degeneration, cellular swelling of proximal tubules, dilatation of the distal tubular lumen and necrosis. The glomeruli had many pathological appearances including congestion and swelling of the glomerular tuft, imflammatory cell infiltration, hemorrhage in the glomerular tuft and the urinary space. This phenomenon may have been related to glomerular damage. Congestion of the renal blood vessels was demonstrated in both the cortex and the medulla. There were many other hemorrhagic areas including the interstitium and the renal tubule. Interstitial nephritis and pyelonepritis were also found. In the lung, the alveolar and interalveolar capillaries were distended and engorged with red blood cells. A small number of alveoli were filled with inflammatory cells which represented bronchopneumonitis. Most areas of the lungs showed intersitital and intra-alveolar hemorrhage as well as thickening of the alveolar septum. The interalveolar septum was also thickened by accumulation of inflammatory cells which is a sign of interstitial pneumonitis. The infected liver showed enlarged and vacuolated hepatocytes being related to cloudy swelling the hepatocytes. Vascular and sinusoidal congestion, prominent Kupffer cells, and inflammatory cell infiltration in the hepatic parenchyma and hepatic sinusoids were also demonstrated. The portal area showed a number of inflammatory cells. Hepatocellular necrosis was found scattered throughout the hepatic lobules which is a sign of hepatocellular damage and disorganization of the liver structure and function. In the gastrocnemius and hamstring muscles, dilation and congestion of blood vessels was shown in some hamsters in the infected groups. The congestion of blood vessels is a sign of hyperemia. One hamster of the infected group showed inflammatory cell infiltration in the perimysium of the gastrocnemius muscle. Another one showed necrosis of some muscle fibers together with inflammatory cell infiltration which are signs of muscular inflammation. The results of this research correspond with previous similar studies, however, the pathogenesis of this study was quicker and the infection was more severe than in other studies. This may be due to the difference in serovar studied.