13.10: Bacteria’s resistance to drugs can evolve quickly.

Penicillin was the first antibiotic to be manufactured and used widely against illness-inducing bacteria. It came into use during the Second World War and caused a revolution in the care of the wounded. But antibiotic-resistant infections soon appeared, and the number of resistant bacteria has increased rapidly ever since (FIGURE 13-14). Now, 70 years after the first use of antibiotics, many bacteria are resistant to many, or even to most, antibiotics. In the United States, more people now die of Staphylococcus aureus infections that are resistant to many different antibiotics (MRSA infections) than die of HIV/AIDS. A few years ago, antibiotic-resistant staph infections were acquired only in hospitals, but now these infections have spread to the community at large.

Microbes live everywhere they can, and compete for the best places to attach themselves and for the richest sources of food to eat. This competition takes many forms: rapid growth to crowd competitors out of a living space, superior ability to take in nutrients and thus to starve competitors, and—this is the key to both the benefits of antibiotics and the problem of antibiotic resistance—production of chemicals that kill other microbes, or at least stop them from growing. Antibiotics are produced by microbes to help them compete with other microbes, and most of the antibiotics we use today are derived from microbes.

Bacteria and other microbes have developed a variety of ways to resist antibiotics. For example, some bacteria pump an antibiotic out of their cells as fast as it enters, so it never reaches a lethal concentration inside the bacterial cell. Other bacteria have proteins that bind to the antibiotic molecule and block its lethal effect. Still others carry that approach a step further—they have enzymes that break down the antibiotic molecules, which are then used as fuel to help the bacteria grow faster! Antibiotic resistance within a population of bacteria can spread quickly, because many of the genes that code for resistance are on plasmids. This means that a bacterium carrying a resistance gene can transmit the gene to other bacteria by conjugation; there’s no need to wait for natural selection over multiple generations.

When an antibiotic is taken as prescribed—that is, at the times specified on the label and until all the pills have been consumed—the population of target bacteria is greatly reduced. All of the target bacteria that remain are resistant to the antibiotic, but there are not very many of them. The growth of these resistant bacteria will be held in check by competition with other types of bacteria. But, if you stop taking the antibiotic before you have finished all of the prescription, many of the target bacterial cells will remain alive, including the ones that are most resistant to the antibiotic. These resistant cells will be the founders of a new population of bacteria in your body, so the next time you take that drug it will be ineffective. Even worse, taking antibiotics when they are not needed—to treat a viral infection, for example—selects for resistant bacteria without providing any benefit. Antibiotics have no effect on viruses.

The use of antibiotics in agriculture is another reason for the spread of antibiotic resistance. Low concentrations of antibiotics are routinely added to the feed for cattle, hogs, chickens, and turkeys. This can be beneficial in the short term, promoting growth and minimizing disease in the crowded conditions of commercial meat and milk production (FIGURE 13-15). But in the long run it can have disastrous consequences, as the practice can lead to selection for bacteria resistant to the antibiotics.

The antibiotics can also pass through the food chain to humans. Data gathered by the Union of Concerned Scientists indicate that agriculture in the United States uses about 25 million pounds of antibiotics each year—about eight times more than is used for all human medicine!