Is the prevention of infective endarteritis a valid reason for closure of the patent arterial duct?
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Clinical features of infective endocarditis developed in a two year old boy. He had successfully undergone anatomical correction of complete transposition of the great arteries during the neonatal period. At routine investigation one year later he showed evidence of important supravalvar pulmonary stenosis. He remained symptom free until endocarditis developed. Streptococcus pneumoniae was isolated from serial blood cultures. Despite prompt treatment with specific intravenous antibiotic treatment the patient died of overwhelming sepsis. At necropsy the stenosed portion of the left pulmonary artery was seen to be the site of infection.
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Experimental Marek's disease virus (MDV) infection in chickens was used to study the early pathogenesis of virus-induced atherosclerosis. Previous investigations using this model have reported the occurrence of atherosclerotic lesions after approximately 7 months postinfection. In this study, a total of 75 susceptible Cornell P-line chickens were inoculated intraperitoneally with the CU-2 strain of MDV at 3 days of age and subsequently perfused for histologic examination. At 2, 4, 8, 13, and 20 weeks postinoculation, the ascending aorta and the brachiocephalic and coronary arteries were evaluated for early changes. Expression of class II major histocompatibility complex (Ia) antigen by the vascular endothelium was demonstrated by indirect immunodetection as early as 2 weeks after virus inoculation. This change was followed by significant thickening of the intimal layer associated with mononuclear cell infiltration. All the arteries examined from the MDV-infected chickens were affected. Preliminary immunohistochemical staining showed the presence of CD3+ CD4+, and CD8+ cells among the infiltrating cells. The results suggest that an immunopathologic mechanism may be involved in the early pathogenesis of MDV-induced atherosclerosis in chickens.
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A 7-year-old, female spayed rottweiler was referred with a history of an acute onset of collapse attributable to cardiac tamponade. Thoracic radiographs revealed an enlarged cardiac silhouette compatible with pericardial effusion, sternal osteomyelitis, and an unusual mineralized lesion determined later to be within the aortic wall. The pericardial effusion was a septic exudate secondary to infection with Staphylococcus species and hemorrhage into the pericardium through a mineralized aortic lesion. The case demonstrates the importance of complete evaluation of thoracic radiographs in a patient with cardiac disease and the potential value of cytopathological evaluation of pericardial fluid.
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