Initially, I carried on working with Mycobacterium tuberculosis, the major work being a long review article on the vaccine strain, BCG (Fenner, 1951). With a research assistant, Ronald Leach, I also continued laboratory studies of tubercle bacilli and began serious studies of the ‘Bairnsdale bacillus’. The first use of the name Mycobacterium ulcerans for this mycobacterium (since then the official name) appears as a footnote in my Inaugural Lecture, given in Canberra on 17 August ,1950, as a new professor in The Australian National University (Fenner, 1950). This organism is characterized by its low ceiling temperature, 34˚C (meaning that it will not grow, in culture or in vivo, at higher temperatures). It is now known to have a world wide distribution, and is particularly common in tropical Africa, where the disease is known as Buruli ulcer (Asiedu et al., 2000). It is a very interesting organism, not least because the severe skin ulceration is due to a soluble toxin, previously unknown among mycobacteria. Initially, with Leach, I showed that it was antigenically distinct from other mycobacteria. The feature which I investigated in detail, in parallel with my work on myxomatosis over the period 1952 to 1957, was the relation between its ceiling temperature and its pathogenicity (Fenner, 1956). This investigation was made more interesting by comparison with another mycobacterium which was also temperature-sensitive and also produced skin lesions in humans, named Mycobacterium balnei by two Swedish workers (Linell and Nordén, 1954). I had a long correspondence with Åke Nordén, before and after I had visited him at the University of Lund in 1953. In mice, both bacteria produced severe skin lesions when inoculated in the manner used in studies on ectromelia, i.e., in the footpad. M. balnei, which grew rapidly in culture, produced progressive lesions within 4 days which became very severe within 9 days. On the other hand, M. ulcerans, which grew as slowly as tubercle bacilli in culture, did not produce progressive lesions until the fourth week, and they became severe by 7 weeks. However, because of their low ceiling temperature, neither organism produced visceral lesions after intranasal, intraperitoneal or intravenous inoculation, but after a moderate interval in the case of M. balnei and long interval in the case of M. ulcerans, ulcerating lesions developed on the hairless peripheral parts of the body and on the scrotum. The low ceiling temperature is clearly the reason that in experimental animals, as well as in humans, the lesions are restricted to the skin. M. balnei is a saprophyte which is associated with water, sometimes water in swimming pools. M. ulcerans also appears to be associated with swamps; cases seem to be more common after disturbances to the water environment. According to his paper (Shepard, 1960), one interesting result of our work was that it led him to successfully exploit footpad inoculation as a way of growing leprosy bacilli in mice. Ron Leach did not come up to Canberra, and I was solely responsible for the later work, described in the 1956 reference.