In 1972 we reported the first isolation of M. ulcerans in Germany and in 1973 we reviewed the epidemiology, clinical features and therapy of Buruli ulcer (6, 7). Initial isolation was done from swabs of the edge of the ulcer on Loewenstein-Jensen medium at 30-33 degrees C. Subcultures showed poor growth at 37 degrees C, and none at 22 degrees C or 42 degrees C or on Loewenstein-Jensen medium without glycerine. No acylamidase or lipolytic activity was detectable and the organisms were catalase positive, triphenyltetrazolium chloride reduction positive, nitrate reduction negative and nicotinic acid production positive (Table 2). Possibly our strain is a nicotinic acid positive variant, as is the strain described by RUNYON et al. (16). (The bacteriological characteristics are summarized in Table 2). Our strain was sensitive to dihydrostreptomycin, cycloserine, viomycin, rifampicin and a riminophenacin derivate (Lampren), but was resistent to isoniazid, para-aminosalicyclic acid, ethionamid and ethambutol (Table 3). White mice and rats but no guinea pigs are susceptible to infection with M. ulcerans. Injection into the foot pad is preferable to intraperitoneal or subcutaneous injection (Table 4). After such an injection of material from our patient, signs of disease appeared in the following order: 1. foot pad swelling; 2. redness and oedema of the whole leg; 3. ulceration of the dorsum of foot (fig. 1) with fluctuant, gross oedema of the subcutaneous tissue and loss of hair; 4. atrophy and contraction of the infected extremity with the development of further ulceration on the abdomen and tail. In the two months following an injection of a standard suspension of M. ulcerans the animals developed such gross oedema of the subcutaneous tissues of the abdomen that its progression could be followed by regular weighing (fig. 2). By the end of the two months, the total body weight was double that of control uninfected animals.