Only the Dsg1 protein is broken up, say the scientists, and not other closely related proteins. The consequent breakdown in skin cell adhesion gives Staphylococcus a way to proliferate and cause more damage. The researchers suspected Dsg1 was the toxin's target because it is also the target of autoantibody attacks in pemphigus follaceus, a blistering skin disorder with similar cellular characteristics. The work was carried out in cell culture, mouse skin, and with recombinant Dsg1, and the results emphasize the importance of the protein's functioning to healthy, protective skin. The major therapy for the infection will continue to be antibiotics, say the researchers, even though agents that fight protein breakup might help prevent the spread of the bacterium.
Bullous impetigo is a common infection among children aged two to six.
The findings also extend to its more generalized form, staphylococcal scalded-skin syndrome. It was also supported by Grants for Research on Specific Diseases from the Ministry of Health and Welfare of Japan. This information is provided for educational purposes only. Please read the disclaimer .