Molecular Characterisation and virulence Profiles of Group A Streptococci causing Human Infection in a South Indian community

Abstract

A highly sensitive molecular technique, emm typing was successfully standardized to identify a very high degree of heterogeneity among GAS isolates circulating and causing infections among south Indian rural school children. The findings of this study have shown a distinctly different epidemiology from those reported from western countries and Australia. However it is very similar to those reported from Africa, the indigenous population of Australia and Nepal. This study shows high diversity of genotypes among the GAS population that is encountered in different sites of the human body. Further, a comparison of emm types contained in the 26- valent hyper-variable region of M proteins with the types identified in this study shows that such a vaccine will not be effective in this population. It is also likely that the high heterogeneity of types encountered in this community will not permit the use of a multivalent M protein based vaccine. The distinction of throat and skin specific GAS becomes difficult due to the colonization of pharyngitis and impetigo associated types in the normal children combined with high heterogeneity and endemicity of GAS infections. Self transmission of skin isolates to throat plays a major role in the transmission of GAS in this community. There was no significant association between emm family pattern However, with 53 % of the 74 emm types belonging to pattern E, a high percentage of the GAS population in this community are generalists; i.e. they can infect throat or skin or both. The distribution of PAVF among GAS isolates from uncomplicated infections, colonizing strains as well as those causing invasive GAS disease did not show significance difference among them. However a relative lack of these factors were seen among these isolates probably indicating a lack of ability to express virulence factors that may be necessary for the development of disease complications. Therefore it is difficult to prove the precise role of these virulence genes in causing GAS disease.