All living things are faced with selective forces. In the case of bacteria, human use of antibiotics is a major selective force. We presently have a whole arsenal of antibiotics to fight bacterial infections. But until the 1940s there were no antibiotics at all! Antiseptics such as alcohol and iodine were used well before antibiotics were discovered, but they were not effective against diseases like tuberculosis, pneumonia, and other internal or deep bacterial infections. In the pre-antibiotic days many women chose not to deliver their babies in hospitals because many babies and women died of bacterial infection. Hospitals were particularly unsanitary because doctors easily transmitted bacterial infections among their patients, in spite of all the precautions taken. In World War I, for example, more casualties were due to infections in wounds than to the wounds themselves because there were no antibiotics.
The discovery and subsequent production of penicillin in the 1930s and 1940s dramatically changed the prospect for patients with bacterial infections. Antibiotics became the magic bullet by which bacterial infections could be stopped in their tracks. The 1945 Nobel Prize for Medicine was awarded to Sir Alexander Flemming, Sir Howard Walter Florey, and Ernst Boris Chain for their life-saving work, the discovery and industrial production of the very first antibiotic: penicillin.
So, what has this got to do with selection? Antibiotics provide a tremendous selective force against bacteria, because the function of antibiotics is to kill bacteria. Only those bacteria that can somehow survive an onslaught of antibiotics pass on their genes to their progeny. This can only happen if some bacteria become resistant to an antibiotic. How is this possible? Bacteria have a variety of ways to thwart the action of antibiotics. First, an antibiotic cannot work if it cannot remain inside the bacterial cell. Some bacteria can actively pump out antibiotics and thus survive. Other bacteria can chemically break down the antibiotic so that it is no longer active. Finally, the target of the antibiotic, which is often a bacterial protein, can be modified (mutated) so that the antibiotic can no longer recognize it and poison it. With all these different ways—that is, mutations in different genes— to get around the killing effects of antibiotics, it is no surprise that resistant bacteria arose soon after their introduction.
Penicillin, for example, affects the protective cell wall of a group of bacteria. When cell-wall formation is blocked by the action of penicillin the bacteria burst and die. In the 1940s when penicillin was first introduced, 100 percent of staph infections were effectively treated with penicillin. Now, greater than 90 percent of staph bacteria are resistant to penicillin. A newer antibiotic called methicillin was introduced to counter the rise of penicillin resistance. In 1974, only 2 percent of staph infections were methicillin resistant, but, by 1997, 50 percent of the staph infections had become methicillin resistant. In 2000, over 30 percent of the most common bacteria that cause ear infections in children had developed resistance to penicillin. A similar trend has been found with almost every antibiotic produced to date. So there is an escalating arms race between the bacteria and us. We must continue to develop new antibiotics to keep ahead of the resistance that bacteria inevitably develop.
Why has so much antibiotic resistance appeared? To answer this question, we need to think about selection and survival of the fittest. As patients taking antibiotics, we are exerting selective pressure for antibiotic resistance among the bacteria that infect us. If we take a properly high dose of antibiotics for a sufficient amount of time, chances are excellent that the bacteria causing the problem are completely eliminated. Problems begin when we take an insufficient dose or an incomplete series. Under these circumstances, a few bacteria that survive better than the average, thanks to mutations, are not killed because of the lower dose or shorter time involved. They can now grow up and provide a large number of bacteria that can develop even higher resistance through mutation. These bacteria survive in our bodies and can also find their way into our environment through coughing, sneezing, and defecating. Now if we try to fight this bacterial infection with the same antibiotic, it is no longer as effective as before. The resistant bacteria also can infect other human victims. Then, if these individuals use the same antibiotic, all of the invading bacteria will be resistant to that antibiotic. Consequently, the antibiotic will no longer be effective for the population.
Overuse or inappropriate use of antibiotics also contributes to the rise of antibiotic resistance in bacteria. For example, using antibiotics for viral infections does nothing for the infection because viruses are not susceptible to antibiotics. Yet this course of action can promote antibiotic resistance of harmless bacteria that normally reside in our bodies. In and of itself, this does not seem particularly dangerous. However, these antibiotic-resistant harmless bacteria can transmit their genes to pathogenic bacteria as we see below, thereby rendering them resistant as well.
Finally, tremendous amounts of antibiotics are used in agriculture. Antibiotics are used to treat bacterial infections and promote growth in the beef and poultry industries. Antibiotics are also used for plant bacterial diseases. Thus, not surprisingly, bacteria resistant to widely used antibiotics have been found on farms. The particular problem with harmless bacteria or bacteria that are plant pathogens is the way that some bacteria have developed antibiotic resistance. Recall that many bacteria contain a minichromosome, or plasmid (chapter 5). These plasmids can be spontaneously transmitted to different bacterial species. Scientists have discovered a particular type of plasmid that they have named "multidrug-resistant plasmid." This plasmid has several different genes that confer resistance to a number of antibiotics. It can be transmitted from a harmless bacterium to a disease-causing one or from a bacterium that only infects fruit crops to one that is harmful to animals and people. This means its resistance to multiple antibiotics can be transferred to disease-causing bacteria. By all these different means, the rise of antibiotic resistance has reached epidemic proportions. If this situation is not dealt with effectively, we may soon be back to the pre-1940s days when we were without an effective weapon against bacterial infections.
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