ABSTRACT
The mechanisms conferring antibiotic resistance are varied and may result from the mutation of endogenous chromosomal genes, the acquisition of foreign intrinsically resistant genes, or combination of these events. Non-transferable resistance traits arise primarily through point mutations in the gene encoding the antibiotic target (e.g. rifampin, fluoroquinolones) or by deregulated expression of a regular cellular process (e.g. multiple antibiotic resistance efflux systems, inducible ß-lactamases). However, the activity of many anti-bacterial compounds cannot be circumvented by alteration of a pre-existing system and resistance genes must be imported. Given the critical role of gene exchange in bacterial evolution, it is self-evident that extensive inter-species and inter-genus gene transfer must have occurred during the golden age of antibiotics. Moreover, it is very likely that the potential reservoir for resistance gene recruitment by bacteria extends beyond the limit of the bacterial kingdom. Indeed, in a recent work (Brown et al., 1998) Brown and collaborators have provided strong support for an eucaryotic origin of the IletRNA synthetase gene which confers a high level of mupirocin resistance in S. aureus (Hodgson et al., 1994) and M. tuberculosis (Sassanfar et al., 1996).
