Among neonates, IE typically involves the tricuspid valve of structurally normal hearts and is associated with very high mortality rates.  It is likely that many of these episodes arise as a consequence of infected intra venous and right heart catheters as well as cardiac surgery. The vast majority of children with IE occurring after the neonatal period have identifiable structural cardiac abnormalities. Rheumatic heart disease is the major predisposition for IE in developing countries. Congenital heart abnormalities, particularly those involving the aortic valve; ventricular septal defects; tetralogy of Fallot; and other complex structural anomalies associated with cyanosis (TGA, single ventricle) are found in remaining cases. Of children with IE on congenital defects, 50 per cent develop infection after cardiac surgery; in these children, infection frequently involves prosthetic valves, valved conduits, or synthetic patches. Mitral valve prolapse generally in association with a regurgitant murmur has been recognized to predispose to IE in children.

Endocarditis among neonates is caused primarily by S.aureus, coagulase-negative staphylococci, and group B streptococci.  Occasionally infection is caused by  gram- negative bacilli and candida species. Among older children, streptococci, the predominant cause account for at least 40 per cent of cases, and S. aureus occurring as a nosocomial or community acquired  acute infection is the second most common cause of IE.

The clinical features and echocardiographic findings of IE in children are similar to those noted among adults with NVE or PVE, respectively. In contrast, IE among neonates is more cryptic; the clinical  picture is dominated  by  bacteremia, and classical signs of  IE  are  rare.