Figure 3
Figure 3. Diverse spectrum of cardiovascular lesions in pathogenic SIVagm infection of PTMs. Thrombotic microangiopathy (TMA) characterized by numerous thrombi in capillaries and small arteries was detected in multiple organs. (A) Kidney (H&E staining). (B) Immunohistochemistry for fibrinogen (brown). (C) Lung (H&E staining). (D) Brain (H&E staining). (E) Glomerulopathy characterized by either focal and segmental glomerulosclerosis or collapse and fibrosis of the entire glomerular tuft was observed in SIVagm-infected PTMs (H&E staining). (F) Arteritis, characterized by significantly thickened wall (double arrow) and lumen occlusion (arrow) was detected in the kidney (H&E staining). (G) Heart hypertrophy characterized by enlarged myocytes with irregular nuclei (arrow) was observed (H&E staiing). (H) Fibrosis of the heart characterized by increased diffuse deposition of collagen replacing drop-out or lysed myocytes (blue), or (I) focal large area of fibrosis replacing areas of infarction was detected using Gomori 1-step trichrome staining (nuclei-black, muscle-red, collagen-blue). (J) Myocarditis characterized by severe infiltration with mononuclear cells (arrows; Gomori staining) and (K) extensive myocyte cytolysis (arrows; Gomori staining) was also diagnosed. (L) Incipient lesion of atherosclerosis (fatty streaks) were found in the aorta of SIVagm-infectd PTMs, characterized by accumulation of foamy macrophages (inset) in the tunica intima, under the aortic endothelium (H&E staining). Slides were visualized with a Carl Zeiss Axio Imager M1 microscope using the following objectives: 10×/0.3 DICI Plan Neofluar, 20×/0.8 DICII Plan Apochromat, and 40×/0.75 DICII Plan Neofluar. Micrographs were taken with a Carl Zeiss AxioCam MRc5. Images were acquired and analyzed using Carl Zeiss Axio Vision SE64 Release 4.8.2. The original magnification of all the pictures was 400×. Images were cropped with Adobe Photoshop CS6.

Diverse spectrum of cardiovascular lesions in pathogenic SIVagm infection of PTMs. Thrombotic microangiopathy (TMA) characterized by numerous thrombi in capillaries and small arteries was detected in multiple organs. (A) Kidney (H&E staining). (B) Immunohistochemistry for fibrinogen (brown). (C) Lung (H&E staining). (D) Brain (H&E staining). (E) Glomerulopathy characterized by either focal and segmental glomerulosclerosis or collapse and fibrosis of the entire glomerular tuft was observed in SIVagm-infected PTMs (H&E staining). (F) Arteritis, characterized by significantly thickened wall (double arrow) and lumen occlusion (arrow) was detected in the kidney (H&E staining). (G) Heart hypertrophy characterized by enlarged myocytes with irregular nuclei (arrow) was observed (H&E staiing). (H) Fibrosis of the heart characterized by increased diffuse deposition of collagen replacing drop-out or lysed myocytes (blue), or (I) focal large area of fibrosis replacing areas of infarction was detected using Gomori 1-step trichrome staining (nuclei-black, muscle-red, collagen-blue). (J) Myocarditis characterized by severe infiltration with mononuclear cells (arrows; Gomori staining) and (K) extensive myocyte cytolysis (arrows; Gomori staining) was also diagnosed. (L) Incipient lesion of atherosclerosis (fatty streaks) were found in the aorta of SIVagm-infectd PTMs, characterized by accumulation of foamy macrophages (inset) in the tunica intima, under the aortic endothelium (H&E staining). Slides were visualized with a Carl Zeiss Axio Imager M1 microscope using the following objectives: 10×/0.3 DICI Plan Neofluar, 20×/0.8 DICII Plan Apochromat, and 40×/0.75 DICII Plan Neofluar. Micrographs were taken with a Carl Zeiss AxioCam MRc5. Images were acquired and analyzed using Carl Zeiss Axio Vision SE64 Release 4.8.2. The original magnification of all the pictures was 400×. Images were cropped with Adobe Photoshop CS6.

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