Introduction to Section II: Gastrointestinal Microbiota and their Role in the Metabolism of Endogenous and Exogenous Substances

Abstract

I joined the laboratory of Professor P. De Somer in 1952 when I was still a medical student. In 1952 Professor De Somer was especially interested in the, then unexplained, extremely high toxicity of penicillin for guinea pigs and hamsters. A. single dose of a few thousand units of penicillin killed 80 to 90% of the animals within 2–4 days. Usually, 10–20% of the guinea pigs survived and proved to be resistant to high and repeated doses of penicillin. The same toxic effects were seen after oral administration of bacitracin, a non-absorbed antibiotic. Tetracyclines also were highly toxic. Animals resistant to administration of penicillin, could be killed by a single dose of tetracycline, and vice versa. We postulated that antibiotics, by eliminating the so-called “normal” or indigeneous microflora (microbiota) caused a fatal enterocolitis by microorganisms not susceptible to the antibiotic. This, or at least very similar, types of enterocolitis have been noted after antibiotic therapy in man. In the 1950’s and 1960’s this enterocolitis was due to an overgrowth of staphylococci; in more recent years it can be ascribed to Clostridium difficile (after lincomycin therapy).