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Microbial producers of antibiotic substances which also possess the target molecule for the antibiotic attack are forced to develop self-protection mechanisms. For example, penicillin-producing Penicillium strains are fungi which do not have a bacterial, peptidoglycan-based cell wall. Therefore, they lack the peptidoglycanpolymerizing penicillin-binding proteins and consequently do not need any protection system. In contrast, Streptomycetaceae producing streptomycin or tetracycline share the target (the bacterial ribosome) with many other bacterial species and require particular precautions to avoid the toxic effects of the antibiotic that they are producing. In such cases, the most common mechanisms are either to keep the antibiotic inactive as long as it is inside the cells, e.g., by a modification that can easily be removed or reversed outside the cell, or to slightly alter the target molecule such that its function is not impaired, but that its affinity for the antibiotic is lost. Alternatively, and sometimes even additionally, cells have protein pumps which keep the intracellular concentrations of these potentially lethal products at low levels. Indeed, such protection mechanisms are supposed to represent the ancestors of resistance mechanisms, which developed independently from antibiotic production and spread out in bacterial communities. Currently, the dramatic increase in bacterial resistance among clinical isolates is viewed as the most serious threat to the concept of antibacterial chemotherapy. |
