Antibiotics—medicine’s “magic bullets”—save tens of thousands of lives annually in the United States. But these magic bullets are losing their power. The problem is the ability of bacteria to resist the effects of an antibiotic—that is, to become antibiotic resistant. Antibiotic resistance occurs when bacteria undergo a genetic change that reduces or eliminates the effectiveness of drugs or other agents designed to cure or prevent infection. Resistant bacterial infections have inevitably followed the widespread use of every new antibiotic introduced.

The more we use antibiotics, the more widespread bacterial resistance to these drugs becomes. Every time a person takes an antibiotic, sensitive bacteria are killed while resistant germs are left to grow and multiply—a classic case of natural selection. Too frequent and improper uses of antibiotics are the main causes of today’s increase in drug-resistant bacteria.

 

Another source of antibiotic resistance originates with the way we raise livestock, fish, and orchard crops. About 80 percent of all of the antibiotics produced in the United States are added to animal feeds—not to fend off disease but to boost growth. While many of these drugs are not specifically used to treat people, these non-therapeutic uses of antibiotics are a perfect way to cultivate resistant organisms, including Campylobacter and Salmonella, bacteria that can sicken people who eat meat and poultry products.

 

The Toll of Resistance

Antibiotic resistance, also referred to as antimicrobial resistance, has been called one of the world’s most pressing public health problems. Almost every type of bacteria has become less responsive to the antibiotic treatment designed to combat it. And antibiotic resistance affects everyone’s health in a way that no single disease does. It is a particularly serious problem for patients whose immune system is compromised, such as people with human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS), patients in critical care units, cancer patients, and transplant recipients. Resistant pathogens lead to higher health care costs because they often require more expensive drugs with more adverse side effects and extended hospital stays.

 

But healthy people are also at risk. A child with an ear infection who in the early 1990s would have been instantly cured by penicillin may now need two, three, or four courses of different drugs. A new mother may contract a drug-resistant urinary tract infection that keeps her in the hospital an extra day or more.

 

The United States and the European Union are both taking steps to combat the problem of antibiotic resistance. The National Strategy for Combating Antibiotic-Resistant Bacteria identifies priorities and coordinates efforts to prevent, detect, and control outbreaks of resistant pathogens recognized by the Centers for Disease Control and Prevention (CDC) as urgent or serious threats. These include carbapenem-resistant Enterobacteriaceae (CRE), methicillin-resistant Staphylococcus aureus (MRSA), ceftriaxone-resistant Neisseria gonorrhoeae, and Clostridium difficile, which is naturally resistant to many drugs used to treat other infections and can cause disease after antibiotics are given. This national effort is also working to ensure continued availability of effective therapies for the treatment of bacterial infections and to detect and control newly resistant bacteria that emerge in humans or animals. The European Centre for Disease Prevention and Control (ECDC) has similar concerns and is working to improve awareness and surveillance throughout Europe. The World Health Organization (WHO) also has developed an action plan on how to slow antimicrobial resistance worldwide. The plan stresses the importance of limiting antibiotic use and encouraging industry to develop new antibiotics.

 

How Bacteria Become Drug Resistant

Bacteria are able to resist drugs through one of several mechanisms. Some develop the ability to inactivate or destroy the antibiotic before it can do harm. Others can rapidly pump the antibiotic out of bacterial cells. Still others can change the place in the cell that antibiotics target so that the drugs are ineffective. The more these resistant organisms spread, the more they add to the pool of resistance genes in all bacteria, raising the odds that these genes will jump to more and more disease-causing microbes.

 

The story of staph bacteria and antibiotics illustrates the perils of drug resistance. Scottish bacteriologist Alexander Fleming discovered the first antibiotic, penicillin, in 1928, an achievement for which he was co-awarded a Nobel Prize in 1945. By the early 1940s, the drug was used in patients. But penicillin-resistant staph bacteria emerged as early as 1942. Today, virtually all Staphylococcus aureus are penicillin resistant.

 

Staph bacteria are commonly carried on the skin or in the nose of healthy people. MRSA—methicillin-resistant Staphylococcus aureus—is a type of staph that is resistant to antibiotics called beta-lactams. In the past the majority of MRSA infections occurred among patients in hospitals or other health care settings. But drug-resistant staph is also showing up in healthy people who have not been staying in a hospital. If common staph bacteria were to become resistant to all readily available antibiotics, the practice of medicine would change dramatically. Any surgery or invasive procedure could bring life-threatening complications. As was the case in the pre-antibiotic era, even the most minor cuts in the skin could prove fatal.

 

Though this discussion focuses on the evolving resistance of bacteria to antibiotics, the issue of antimicrobial resistance is actually much broader. The resistance of viruses such as human immunodeficiency virus (HIV) and influenza to antivirals and of protozoan parasites to antimalarial drugs is a huge problem around the globe. Microbes have the capacity to develop resistance, whether they are bacteria, viruses, or protozoa.

 

How to Protect Yourself

To avoid encouraging antibiotic-resistant strains of infections to develop: