This juxtaposition of significant mitigation of dermonecrosis with no detectable effect on bacterial burden in the early stages of cutaneous infection has been noted in other studies in this model [22], and suggests, as has been noted in the cutaneous and pneumonia mouse models, that AT binding to ADAM10 rapidly disrupts epithelial barriers in a manner that is independent of bacterial proliferation. The gene discussed is ADAM10; the disease is susceptibility to pneumonia measurement.