Abstract

Ever since that active and productive period during which Ehrlich discovered the arsenic-fastness of trypanosomes, the processes involved in the adaptation of microorganisms to various drugs and toxic substances have been studied from several angles. In addition to clarifying the biological significance of variability in microorganisms, it may reasonably be expected that research into the behavior of bacteria and protozoa under unfavorable environmental conditions will lead to a deeper insight into the changes that take place in the course of infection and immunity. Our conception of the phenomena of bacterial adaptation so far has been formed mainly from an accumulation of diverse observations on the morphology as well as on the cultural and serological characteristics of the adapted organisms. Scarcely any attempt has been made to explain the acquired resistance on the basis of a rational hypothesis (Pringsheim 1). This conception, however, has been considerably broadened in recent years by the contributions of Schnabel2 and his collaborators.3 The results obtained by these authors seem to indicate that contact with the same substance (a disinfectant or a chemotherapeutic agent) may induce under certain conditions, even in the same experiment, specific fastness as well as specific hypersensitiveness in various bacteria (pneumococcus, B. coli, V. cholerae). While it was found that bacteria grown in comparatively strong dilutions of a germicidal substance exhibited in the next passage a specifically increased tolerance for the same substance, those cultivated in weak dilutions of the same agent proved to be specifically hypersensitive under the same conditions. Between these two extremes there was generally found an inert zone which left the susceptibility of the bacteria unaltered for the next passage.

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