I have often reflected, in an idle moment, on how Hamlet’s father could have been killed by the juice of hebona poured into his outer ear, while napping in the orchard after lunch (Hamlet, Act 1, scene 5, line 62) [1], but never pursued the problem, as I wished to get on with the rest of the play. In much the same way, when I worked with Borrelia in the laboratory, I wondered who Borrel was and how his name became attached to the genus. Amedee Borrel was born in 1867, in the small town of Cazouls-les-Beziers in Herault, France. He qualified at the age of 25 years as a doctor from the nearby Montpellier University. His doctoral thesis was on epithelioma. The thesis attracted the attention of Metchnikoff, who, in 1892, appointed Borrel to the research staff of the Pasteur Institute in Paris, with the particular responsibility of assisting Roux with the microbiology course. Borrel eventually assumed full responsibility for the course, and therefore was in charge of cultivating and maintaining the collection of microbes in the Pasteur Institute library. In his early years at the Institute, Borrel published articles with the disciples of Pasteur. With Calmette and Yersin (1895) [1], he showed that experimental immunization with heat-treated plague bacillus protected against plague. It was this finding that provided the basis for Haffekine’s plague vaccine. With Roux (1898) [2], he investigated the possibility of serotherapy (antibody) protection in experimental cerebral tetanus. And with Nocard (1898) [3], he achieved the successful in vitro cultivation of mycoplasma. It is during this period (1893) [4,5] that Borrel wrote about the spread of tubercle bacilli in parenterally infected rabbits, describing the resulting histological structure of the developing tubercles in the lungs and kidneys of these animals. He had already described, as an undergraduate (1890) [6], the giant cells of leprosy, drawing parallels with tuberculosis. Borrel was thought of as a cytopathologist, and, as such, was asked to ‘debunk’ a current idea of a coccidian-causing cancer, which he did decisively, with detailed microscopic examinations (1901) [7]. This strengthened Borrel’s interest in cancer pathogenesis, and the remainder of his life was devoted to finding a cause for epitheliomata and comparing them to the pox infections (epitheliosis) of mice and sheep. He developed a very personal theory that a carcinogenic virus was present within a new tropho-pigmentary germ layer under the skin that he had discovered, between the ectoderm and mesoderm. He suggested that the branches of this new layer could transfer the virus from the inner layers to the outer surface, where the virus would then cause a cancer. He further suggested that the transfer, and subsequently the cancer, were provoked by helminth, or sometimes by protozoan, infections. In the last years of his life, Borrel devised a ‘supercolouring’ method of cell staining, which, he averred, allowed the virus to appear as microscopic ‘grains’. He published this painstaking work in nearly 50 single-author papers. His findings have never been confirmed, and have been ignored by other workers, in his lifetime and since. The only lasting result of all this effort was the invention of the coverslip, which he used to take imprints from cell cultures in order to transfer them onto microscopic slides. In 1919, Borrel was promoted to the Chair of Bacteriology at Strasbourg, where, in 1923 he organized an exhibition to celebrate the centenary of the birth of Pasteur, who had been a professor of chemistry there some 80 years earlier. Borrel retired shortly afterwards, and returned as an emeritus scientist to the Pasteur Institute in Paris, where, until his death in 1936, he continued to work on the causes of cancer. Borrel’s training in microscopy was a parttime affair, undertaken while studying medicine, and compares unfavourably with that of his great contemporary