The last decade has witnessed a remarkable change in the epidemiology of group A streptococcal infections. There has been a marked increase globally in the reporting of invasive infections caused by Streptococcus pyogenes, Lancefield group A streptococci. Many of these cases were deep-seated infections associated with shock and multi-organ failure and are defined as streptococcal toxic shock syndrome. In addition, reports of streptococcal sequelae, in particular, acute rheumatic fever, have re-emerged and remain a serious health threat in developed countries. It appears that these infections are related to the type distributions of the organism among the general population, with the re-emergence of more 'virulent' strains, such as the M1 serotype which in earlier decades was primarily seen in cases of either superficial disease or scarlet fever. Population-based surveillance studies have clearly indicated the importance and relevance of type identification for epidemiological purposes. There have also been suggestions that certain extracellular products and toxins play a major role in the so-called 'increased virulence' of the organism; these include cell surface molecules such as the M protein, opacity factor, the hyaluronic acid capsule, C5a peptidase and streptococcal inhibitor of complement (SIC), in addition to secreted proteins, pyrogenic exotoxins, cysteine proteinase, streptolysins O and S, hyaluronidase, streptokinase and other enzymes. All these factors, and events during the last decade, strongly emphasize the need for a better understanding of the epidemiology, pathogenesis, treatment and prevention of group A streptococcal infections.