Jim Oliver began work in 1988 on Borrelia burgdoferi, the etiological agent of Lyme disease, and has been a leading figure in its study since that time. According to Jim, “The primary symptom of Lyme disease is a bulls-eye lesion on the skin that continues to expand.” This lesion is not just a localized hypersensitivity “reaction like you would see with the bite of a mosquito or a chigger. Clinically, this is the single-most diagnostic feature of infection with the spirochete that causes the disease.” I then asked if this is due to inflammation, or an indication of bacteria within the skin? Jim responded that he was not certain, but probably both are involved. “I say that because if I want to isolate spirochetes, a biopsy at the margin of the skin lesion would give me the best chance for success. The spreading of the lesion is referred to as erythema migrans.” This characteristic of the disease was initially described in Europe in the late nineteenth century. At the time, it was not associated with any other symptoms of the disease, or with an etiological agent. The disease in North America was first noted in Wisconsin in 1970. Subsequently, there was an outbreak of the disease in Old Lyme (hence Lyme disease) and surrounding counties in Connecticut in the mid 1970s. It seems that a group of children presented juvenile arthritic symptoms.