Staphylococcal Toxic Epidermal Necrolysis (Ten): The Expanded Mouse Model**From the Division of Experimental Dermatology, I. Hautklinik (PME, PF, KW), the Institute of Pathology (GT), and the Hygiene Institute (HM) of the University of Vienna: and the Department of Dermatology. Harved Medical School, Boston, Massachusetts. (Reprint requests to: Dr. Elias, Departtment of Pathology, University of California School of Medicine, San Francisco, California 941143.)

Strains of phage Group 2 staphylococci and cell-free fractions isolated from the same strains induced toxic epidermal necrolysis (TEN) when injected into neonatal mice. Furthermore, adult mice developed TEN in both hairy and glabrous skin following intracutaneous (but not systemic) administration of cell-free fractions. While normal adult mice did not develop TEN after inoculation of cocci, generalized TEN could be produced in adult mice pretreated with systemically injected corticosteriods for 3 weeks. Mice which had survived injections of cell-free fractions as neonates remained susceptible to intracutaneously administered fractions in adulthood. Regardless of the age of the animal and the cause of TEN (cocci or cell-free filtrates), the pathogenesis appeared identical both hitologically and ultrastructurally, i.e., via intercellular cleavage without evidence of cell necrosis. These studies demonstrate that neither maturation nor hair development, as previously proposed, confer cutaneous resistance to TEN. Instead, an extracutaneous factor(s) probably confers resistance to the normal adult mouse. Since similar factors lead to naturally occurring and experimental staphylococcal TEN in adult humans and adult mice, the adult mouse may prove to be a valuable model for the study of factors resulting in staphylococcal TEN in adult human