Group A streptococci (GAS) depend on a hyaluronic acid (HA) capsule for evasion of phagocytosis and for binding to host cells. Paradoxically GAS also produces hyaluronidases (HYL), enzymes that cleave HA. It is commonly assumed that HYL acts on structurally identical HA in human tissue matrix to promote spread of the organism, however this assumption has not been tested formally. Preliminary data indicates that production of HYL has no apparent effect in spread of infection in murine model of skin infection. Data also indicates that HYL+ strains are able to survive on HA alone, suggesting a possible function of HYL may be to aid in survival in nutrient deprived conditions by consuming its own capsule. Genetic analysis of hylA gene in HYL+ and HYL- strains indicates a premature stop codon in HYL- strains, eluding to a possible elimination of this gene. The specific aims are 1) to determine if Streptococcus pyogenes hyaluronidase is a spreading factor in a murine model of skin and soft tissue infection. 2) to characterize a possible nutritional role for GAS hyaluronidase during growth and nutrient deprivation.3) to determine whether the hylA genes of Hyl- strains produce a product that is not enzymatically active but serves an alternative role.