The Evolution of AntibioticResistant Bacteria










Since antibiotics, such as penicillin, became widely available in the 1940s, they have been called miracle drugs. They have been able to eliminate bacteria without significantly harming the other cells of the host. Now with each passing year, bacteria that are immune to antibiotics have become more and more common. This turn of events presents us with an alarming problem. Strains of bacteria that are resistant to all prescribed antibiotics are beginning to appear. As a result, diseases such as tuberculosis and penicillin-resistant gonorrhea are reemerging on a worldwide scale (1).
Resistance first appears in a population of bacteria through conditions that favor its selection. When an antibiotic attacks a group of bacteria, cells that are highly susceptible to the medicine will die. On the other hand, cells that have some resistance from the start or acquire it later may survive. At the same time, when antibiotics attack disease-causing bacteria, they also attack benign bacteria. This process eliminates drug-susceptible bacteria and favors bacteria that are resistant. Two things happen, populations of non-resistant and harmless bacteria are diminished, and because of the reduction of competition from these harmless and/or susceptible bacteria, resistant forms of disease-causing bacteria proliferate. As the resistant forms of the bacteria proliferate, there is more opportunity for genetic or chromosomal mutation (spontaneous DNA mutation (1)) or transformation, that comes about either through a form of microbial sex (1) or through the transference of plasmids, small circles of DNA (1), which allow bacteria to interchange genes with ease. Sometimes genes can also be transformed by viruses that can extract a gene from one bacterial cell and inject it into another (3). In this last situation, resistant genes become embedded in small units of DNA, called transpons, which can easily move into other DNA molecules. Making matters worse, many bacteria have specialized transpons called integrons, which act like flypaper when catching new genes (3).
These mutations, no matter what process that has led to their occurrence, block the action of antibiotics by interfering with their mechanism of action (1). Currently, antibiotics attack bacteria through one of two mechanisms. In both mechanisms the antibiotic enters the microbe and interferes with production of the components needed to form new bacterial cells. Some antibiotics act on the cell membrane, causing increased permeability and leakage of cell contents. Other antibiotics interfere with protein synthesis in cells. They block one or more of the steps involved in the transformation of nucleic acids into proteins.
Any mutation that would prevent the action of antibiotics, but not at the same time provide a selective advantage to the bacteria, would be one that interfered with the bacteria’s ability to reproduce. If this were to occur, then any selective advantage would be negated by the cell’s inability to take advantage of the diminished competition caused by the death of susceptible bacteria. This would be likely to occur in reaction to an antibiotic that interfered with protein synthesis, since it would also impact on the chain of reactions that occurs in the transformation of DNA to ribosomes and RNA and eventually the proteins necessary for the fission or reproductive process to occur.
If one were able to control all the variables, there is no reason to believe that certain bacteria would be more likely to mutate to resistant forms than others. It is normally not the type of organism that dictates its propensity towards mutation. This is normally dictated by the variables or changes in the bacteria’s immediate environment.
The advantages of using multiple antibiotics in combination are as follows: for broad coverage in a very sick patient who has an infection of unknown etiology, to prevent the emergence of resistance, and if the two or more drugs in combination achieve a greater effect than simply adding their effects together (4). In all cases, the use of multiple antibiotics does increase the risk of toxicity, in the individual who is the recipient of the therapy, and should be used tentatively and carefully.
It has been shown, that exact adherence to a prescribed drug regimen plays a huge role in the prevention of antibiotic-resistant bacteria (1 & 2). The sporadic use of antibiotics provides the optimum setting for resistant strains of bacteria (1) because it creates the ideal environment for the selection of these