Abstract
Despite the well-known tendency of cellulitis due to beta-hemolytic streptococci to recur, little is known regarding the mechanisms of human immunity to this infection. We established cellulitis in mice by using a strain of group G streptococcus (1750) originally isolated from the bloodstream of a patient with acute cellulitis. This strain, which has been studied extensively in our laboratory, expresses M protein structurally and functionally analogous to that of group A streptococci, and we have cloned and sequenced the gene encoding this protein (emmMG1). Mice injected with 5 x 10(7) CFU of strain 1750 developed nonlethal necrotic skin and soft tissue infections that healed spontaneously after 14 to 16 days. After healing, the mice were repetitively reinoculated three times with the same challenge dose of 1750. Lesion size did not decrease in severity, size, or time to healing after repetitive challenge. The maximum lesion size and tissue concentration of microorganisms increased between the first and fourth challenges. Pretreatment of 1750 cells with opsonic antisera to MG1 diminished neither the maximum lesion size nor the time course of evolution of the lesions. Thus, in the mouse model used here, there was no evidence of acquired protective immunity to experimentally induced cellulitis.