PATHOMORPHOLOGICAL FEATURES AND CLINICAL MANIFESTATIONS OF ACUTE RHEUMATIC FEVER

Acute rheumatic fever (rheumatism) is a systemic immune-mediated inflammatory disease that develops as a delayed complication of Group A β-hemolytic streptococcal infection. It remains a significant cause of acquired valvular heart disease in children and young adults, especially in developing countries. The pathogenesis is based on autoimmune mechanisms triggered by molecular mimicry between streptococcal antigens and host connective tissue components, leading to multisystem inflammatory involvement, predominantly affecting the heart. This study presents an analytical review of current data on the pathomorphological features and clinical manifestations of rheumatism, with particular emphasis on the correlation between structural tissue damage and clinical presentation. Classical pathological findings and contemporary diagnostic criteria were analyzed to establish clinicopathological relationships. Pathomorphological changes progress through several distinct stages, beginning with mucoid swelling and advancing to fibrinoid degeneration and fibrinoid necrosis of collagen fibers. The formation of Aschoff–Talalaev granulomas in the myocardium represents the pathognomonic lesion of the disease. Chronic inflammatory processes ultimately lead to fibrosis, sclerosis, and deformation of cardiac valves, most commonly affecting the mitral valve. Clinically, rheumatism typically develops 2–3 weeks after streptococcal pharyngitis and manifests with rheumatic carditis, migratory polyarthritis, Sydenham’s chorea, erythema marginatum, and subcutaneous nodules. Cardiac involvement is the most serious manifestation due to its potential to cause persistent valvular defects. In conclusion, rheumatism is characterized by immune-mediated connective tissue destruction with well-defined morphological stages that directly correlate with its clinical manifestations. Early diagnosis and timely treatment are essential to prevent irreversible cardiac complications and reduce the burden of rheumatic heart disease.