- Explain how overuse of antibiotics may be creating “superbugs”
The word antibiotic comes from the Greek anti meaning “against” and bios meaning “life.” An antibiotic is a chemical, produced either by microbes or synthetically, that is hostile to the growth of other organisms. Today’s news and media often address concerns about an antibiotic crisis. Are the antibiotics that easily treated bacterial infections in the past becoming obsolete? Are there new “superbugs”—bacteria that have evolved to become more resistant to our arsenal of antibiotics? Is this the beginning of the end of antibiotics? All these questions challenge the healthcare community.
One of the main causes of resistant bacteria is the abuse of antibiotics. The imprudent and excessive use of antibiotics has resulted in the natural selection of resistant forms of bacteria. The antibiotic kills most of the infecting bacteria, and therefore only the resistant forms remain. These resistant forms reproduce, resulting in an increase in the proportion of resistant forms over non-resistant ones. Another major misuse of antibiotics is in patients with colds or the flu, for which antibiotics are useless because these illnesses are caused by viruses, not bacteria. Another problem is the excessive use of antibiotics in livestock. The routine use of antibiotics in animal feed promotes bacterial resistance as well. In the United States, 70 percent of the antibiotics produced are fed to animals. These antibiotics are given to livestock in low doses, which maximize the probability of resistance developing, and these resistant bacteria are readily transferred to humans.
Antimicrobial resistance is not a new phenomenon. In nature, microbes are constantly evolving in order to overcome the antimicrobial compounds produced by other microorganisms. Human development of antimicrobial drugs and their widespread clinical use has simply provided another selective pressure that promotes further evolution. Several important factors can accelerate the evolution of drug resistance. These include the overuse and misuse of antimicrobials, inappropriate use of antimicrobials, subtherapeutic dosing, and patient noncompliance with the recommended course of treatment.
Exposure of a pathogen to an antimicrobial compound can select for chromosomal mutations conferring resistance, which can be transferred vertically to subsequent microbial generations and eventually become predominant in a microbial population that is repeatedly exposed to the antimicrobial. Alternatively, many genes responsible for drug resistance are found on plasmids or in transposons that can be transferred easily between microbes through horizontal gene transfer. Transposons also have the ability to move resistance genes between plasmids and chromosomes to further promote the spread of resistance.
How Resistance Happens
How Resistance Spreads
All animals carry bacteria in their intestines. Giving antibiotics will kill many bacteria, but resistant bacteria can survive and multiply.
- When food animals are slaughtered and processed, these resistant bacteria can contaminate the meat or other animal products.
- These bacteria can also get into the environment when an animal poops and may spread to produce that is irrigated with contaminated water.
There are several direct routes by which people can get antibiotic-resistant bacteria that develop in industrial food animal production:
- Improperly handling or consuming inadequately cooked contaminated meat.
- Contact with infected farm workers or meat processors, or perhaps their families, doctors and others with whom they interact.
- Drinking contaminated surface or ground water and eating contaminated crops.
- Contacting air that is vented from concentrated animal housing or is released during animal transport.
Due to increasing drug-resistance, physicians often have to recommend second- or third-choice drugs for treatment when the bacteria that cause infections are resistant to the drug of choice and this drug doesn’t work. But the alternative drugs might be less effective, more toxic, and more expensive. Preserving the effectiveness of antibiotics is vital to protecting human and animal health.
One of the Superbugs: MRSA
The imprudent use of antibiotics has paved the way for bacteria to expand populations of resistant forms. For example, Staphylococcus aureus, often called “staph,” is a common bacterium that can live in the human body and is usually easily treated with antibiotics. A very dangerous strain, however, methicillin-resistant Staphylococcus aureus (MRSA) has made the news over the past few years (Figure 1). This strain is resistant to many commonly used antibiotics, including methicillin, amoxicillin, penicillin, and oxacillin. MRSA can cause infections of the skin, but it can also infect the bloodstream, lungs, urinary tract, or sites of injury. While MRSA infections are common among people in healthcare facilities, they have also appeared in healthy people who haven’t been hospitalized but who live or work in tight populations (like military personnel and prisoners). Researchers have expressed concern about the way this latter source of MRSA targets a much younger population than those residing in care facilities. The Journal of the American Medical Association reported that, among MRSA-afflicted persons in healthcare facilities, the average age is 68, whereas people with “community-associated MRSA” (CA-MRSA) have an average age of 23.
In Summary: Antibiotic Resistance
The medical community is facing an antibiotic crisis. Some scientists believe that after years of being protected from bacterial infections by antibiotics, we may be returning to a time in which a simple bacterial infection could again devastate the human population. Researchers are developing new antibiotics, but it takes many years to of research and clinical trials, plus financial investments in the millions of dollars, to generate an effective and approved drug.
- Naimi, TS, LeDell, KH, Como-Sabetti, K, et al. Comparison of community- and health care-associated methicillin-resistant Staphylococcus aureus infection. JAMA 290 (2003): 2976–84, doi: 10.1001/jama.290.22.2976. ↵