Antibiotic Resistance in Bacteria: Origins and Emergence
Most clinically useful antibiotics exhibit their selective toxicity by specifically blocking one or another type of bacterial macromolecular synthesis (e.g.protein, nucleic acid or cell wall synthesis) — acting on targets that are not present or accessible in animal/human cells. Since the 1940s, when drugs such as penicillin, streptomycin, and chloramphenicol were introduced widely as “miraculous” agents for treating bacterial infections, the emergence of strains resistant to these and subsequently-developed drugs has represented a continuing clinical challenge. The eventual appearance of strains simultaneously resistant to multiple antibiotics significantly worsened the problem. The latter was found to involve different resistance genes linked to each other on segments of DNA able to move efficiently from one bacterial cell to another by phenomena known as horizontal gene transfer (HGT).
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The immune system is prone to the same grave misfortunes as any defense system handling weapons: collateral damage that comes with the destruction of the enemy on one’s own territory and friendly fire due to mistaken identity. Whereas the collateral damage is the price we pay for clearance of infections, autoimmunity is a pathological process. Nevertheless, the effector mechanisms involved in both processes are the same. Whether environment can be a cause, a trigger or an amplifier of an autoimmune disease are questions that are being intensively investigated.
