Mutations in genes that code for particular proteins may result in antibiotic resistance. For example, if an antibiotic uses a particular protein in the cell membrane to enter the cell, a change in that protein (due to a mutation in the gene that codes for it) may prevent the antibiotic from entering the cell. Many genes that result in antibiotic resistance are found on DNA molecules that are easily transferred from one bacterium to another.
Antibiotic resistance in bacteria evolves by mutations in the bacterium's genes, by rearrangement of the bacterium's genes, or by acquisition of genes that result in antibiotic resistance from other bacteria. Regardless of the way a bacterium becomes resistant to a particular antibiotic, once this has happened, a vicious cycle begins. The resistant bacterium will survive treatment while most of the susceptible bacteria in the population die. After antibiotic treatment is completed, the few surviving susceptible bacteria and the resistant bacterium will reproduce, and the resistant bacterium will pass the gene that provides antibiotic resistance on to its progeny. If the infection recurs, there will now be a larger number of antibiotic-resistant bacteria in the population. Antibiotic treatment will be less successful or may fail completely. Across time, almost all of the bacteria of that type that people encounter will be resistant to the particular antibiotic, and new (and, in many cases, more expensive) antibiotics must be used to treat infections caused by that kind of bacteria.
Overuse of antibiotics has increased the numbers of antibiotic-resistant bacteria. The Centers for Disease Control and Prevention (CDC) estimates that half of the 100 million courses of antibiotics prescribed annually are unnecessary. This misuse means that bacteria will evolve resistance to common antibiotics sooner, and that doctors will have to use last-resort antibiotics such as vancomycin more and more. Therefore, to delay the development of antibiotic-resistant organisms, the CDC has developed a set of recommendations for appropriate use of antibiotics.
Nevertheless, following the CDC recommendations is challenging. One survey of pediatricians revealed that, during a one-month period, 96 percent of pediatricians polled had been pressured by patients to prescribe antibiotics, even when they were not needed. Another study found that, despite education about appropriate uses of the antibiotic vancomycin, 40-60 percent of vancomycin treatments did not follow the CDC recommendations.
Another challenge for preventing antibiotic resistance is that restrictions on the use of one antibiotic often lead to increases in the use of others. In one hospital, restrictions on the use of the antibiotic cephalosporin not only decreased the incidence of cephalosporin-resistant bacteria but also increased the use of another antibiotic (imipenem). Thus, the number of bacteria resistant to that antibiotic increased.
Several initiatives are under way to promote more careful uses of antibiotics. One hospital in Arkansas created a program to wipe out enterococcal bacteria that are resistant to vancomycin (called vancomycin-resistant enterococci, or VRE) by using strict containment protocols as well as extensive education of staff. For example, some effective precautions can be as simple as handwashing. Though some staff complained that the program was overly complicated and labor intensive, rates of VRE infection declined and the last case of VRE at that hospital was reported in May 1998.
Pharmaceutical companies spend an average $500 million and 12-15 years doing initial research to design a drug, developing large-scale production of it, conducting clinical trials of the drug's safety and effectiveness, and bringing the drug to market.
The term vancomycin-resistant Staphylococcus aureus, or VRSA, describes strains of Staphylococcus aureus (SA) bacteria that are resistant to doses of the antibiotic vancomycin at or above 32 micrograms per milliliter. Strains of SA that are killed by doses of vancomycin less than or equal to 4 micrograms per milliliter are considered susceptible to the antibiotic, whereas strains that require vancomycin doses of 8 to 16 micrograms per milliliter for killing are considered to have intermediate levels of resistance.
No strains of VRSA have yet appeared; however, since mid-1996, physicians in Japan, the United States, and Europe have described several cases of SA infections that required vancomycin doses of at least 8 micrograms per milliliter to cure the infection. Some medical workers have inaccurately called these strains of bacteria VRSA; however, they are actually SA with intermediate levels of vancomycin resistance.
Emerging vancomycin-resistant Staphylococcus aureus (VRSA) bacterial infections would likely have similar symptoms to Staphylococcus aureus (SA) infections, except that the infection would persist after vancomycin drug therapy. Doctors test for vancomycin resistance by taking samples of bacteria from an SA infection, culturing or growing them, and measuring their growth in media containing various levels of vancomycin. SA that are killed by vancomycin at a concentration of 4 micrograms per milliliter are considered susceptible, those that require 8 to 16 micrograms per milliliter for killing are considered to have intermediate resistance, and those that are resistant to vancomycin concentrations at or above 32 micrograms per milliliter are considered fully resistant to the drug. To date, the most resistant SA strains show intermediate rather than full resistance to vancomycin.
In bacteria, antibiotic resistance evolves by mutations in their genes, by rearrangement of their genes, or by acquiring genes that provide antibiotic resistance from other bacteria. The strains of Staphylococcus aureus (SA) bacteria that have intermediate resistance to vancomycin appear to be the result of mutations in their genes. However, scientists are concerned that SA might also acquire genes for full vancomycin resistance from other bacteria, specifically, vancomycin-resistant enterococci (VRE).
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