I have found no reference to kerion celsi reaction in tinia capitis cases due to Microsporum audouini treated with griseofulvin, and this may be with good reason. The pathogenesis of kerion is likely a reaction in the infected tissue to elaboration of altered protein by altered or destroyed fungus organisms or to combination of drug and altered protein (hapten). The tissue cells, thus damaged by the allergic reaction, are then additionally assaulted by the skin bacterial flora, especially staphylococci. Blank and Roth, in their memorable paper presented before the American Academy of Dermatology meeting in December, 1958, reported that the beneficial effect of the systemically administered griseofulvin is accomplished as follows. The drug is incorporated into the newly formed horn of hair, skin, and nails, and in an incompletely understood way prevents utilization of this horn by the fungi, thus stopping the invasive process. There is no killing effect and