Infective endocarditis (IE) is the disease that has high inhospital mortality. Heart valves dysfunction – both native and prosthetic – is the primary IE complication requiring a surgical intervention. The IE causes and its course have been discussed in this review. In particular, the role of concomitant infectious foci in the formation and development of IE have been considered, the mechanisms of mutual transition of subacute and acute clinical forms have been described. Modern diagnostic principles and methods based on the Duke criteria system have been mentioned, as well as the difficulties that follow the patient’s clinical status evaluation. The normobiotic microbiota participation, as well as the possibilities for their identification using blood culture and PCR technique, have been closely reviewed. According to modern researches and publications, there have been made the conclusion about the contribution of obligate anaerobic bacteria, fungi and viruses to the development of endocarditis. There have been described the hypothesis about the presumptive strategy for the cardiac dysfunction formation as a result of the IE causative agents cells metabolic activity based on a literature data analysis in the article: vegetation formed by Staphylococcus aureus can lead to the heart valve stenosis, and the influence of hyaluronidases, collagenases on a heart valve structure can lead to regurgitation. The pathogens cells ability to avoid the human immune system response is caused by the biofilms, fibrin vegetations formation and the enzymes production – cytotoxins (streptolysins, leukocidin, etc.). It has been suggested that the mediators of inflammation and leukocyte cells participate in the destruction of native and prosthetic tissues due to an IE pathogens inaccessibility for immunocompetent cells.