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Antibiotic resistant bacteria are bacteria that have developed, through the process of random mutation and natural selection, resistance to antibiotics normally used to control them. The problem is gradually but steadily worsening.
The best-known is the scourge of medical facilities, methicillin-resistant Staphylococcus aureus, usually referred to as "MRSA".
Human ignorance plays a large role in increasing the prevalence of antibiotic-resistant bacteria. Contributing factors include:
- Not taking antibiotics appropriately. For instance, not taking them for the prescribed amount of time or taking antibiotics when one is not suffering from a bacterial infection. Prescriptions can also be done for an inappropriate condition.
- Overuse of antibiotics.
- Using antibiotics in the production of animals raised for food to promote growth and resist diseases.
- Little diversity of antibiotics available.
These sorts of antibiotic misuse will kill some of the bacterial population, but leave the bacteria that are more resistant to that antibiotic. These bacteria are then free to multiply and pass along their resistant genes. Future mutations in this population may (and do) eventually produce bacteria that are not affected at all by the original antibiotic. When bacteria have reached a level where they are immune to multiple antibiotics, they are often termed "super-bugs" by the media and much hype is given to them.
Often, the best way to prevent antibiotic resistance is to combine different drugs in a course of treatment. The odds of a strain of bacteria randomly mutating an immunity to one drug is low, but plausible, considering the millions of cells in a single infection and the millions of infections that may occur over time. Using multiple drugs simultaneously would require that strain to have developed multiple resistances. The odds of such a thing happening are dramatically lower than the possibility of a strain developing resistance to a single drug, and a bug that can survive all these antibacterial treatments may become less effective against the immune system or develop traits otherwise detrimental to its survival in other ways. Alternatively, a less developed way of combating antibiotic resistant bacteria is to use bacteriophages. The idea is that the bacteriophages would evolve to handle any countermeasures the bacteria would have developed.
Bacteria can also be killed by less subtle means than antibiotics. Sterilizing areas with strong poisons such as alcohol, highly damaging substances such as bleach, open fire, or irradiation, will still work to destroy bacteria on surfaces. Although these methods are not suitable for treatment of an infection, they can reduce the number of infections. The reason that bacteria don't develop immunity to these things is similar to why they don't easily develop immunity to combined drug courses; the number of metabolic pathways that must be altered in a single mutated generation is much higher, and the odds of it happening are close to none, even with the vast number of bacteria in play. Developing a resistance to an antibiotic — typically, a strain of fungus — is like learning to outsmart a predator. Developing a "resistance" to bleach is like learning to breathe on the Moon.
Superbug: a misnomer?
When a bacterium evolves resistance to antibiotics, the new strain is typically weaker in some way, making the adjective "super" in "superbug" somewhat of a misnomer. The resistance is not "free"; most antibiotics target important cellular processes, and counteracting these comes with a cost. Take streptomycin resistance for instance. Streptomycin binds to ribosomes during protein synthesis, compromising the bacterium's ability to read the genetic code. Bacteria that become resistant to the drug have altered ribosomes that can get around this, but they're also often slower as a result, lowering rate of reproduction and inhibiting general cellular function. There are other examples: pseudomonads, bacteria in the genus Pseudomonas, that develop a resistance to fluoroquinolones are less mobile than ones that aren't, reducing their ability to escape predators, and building thicker cell walls or expelling antibiotics out of the cell comes with higher energy costs. Similar phenomena occur with organisms subject to control pressures such as weeds resisting herbicide or insects resisting pesticide.
So, if the bacteria are actually worse off with resistance, then how did antibiotic-resistant bacteria become so prevalent? Well, it's complicated. Sometimes, the bacteria develop other mutations that compensate for the weakness in some way, or there are other genes that don't necessarily affect resistance or particular aspects of the environment that help ameliorate the downsides.
Antibiotic resistant bacteria are also one of the saddest, but strongest examples showing the process of evolution, and why it should be taught properly. Despite the differences between how bacteria and animals evolve, the premise of natural selection is clearly shown to work in this example. Some people, however, don't accept this as evidence of evolution as the bacteria remain the same "kind", i.e., they haven't evolved into a horse. See the artificial distinction they like to make between macroevolution and microevolution.
One reason bacteria are able to genetically "respond" to human selective pressures so fast, and in a human observable period of time, is by virtue of their having many generations in a relatively small period of time (there are bacteria that can double their population roughly every 20 minutes given optimal conditions). This is also the case with viruses which are capable of millions of generations before the end of the week. The second reason, and one that throws a monkey wrench into our simplistic understanding of evolution, is horizontal gene transfer; bacteria are for the most part asexual, but they can still absorb foreign DNA into their own genome. So simply being in the presence of antibiotic resistant bacteria allows another species of bacteria to potentially acquire that resistance.
- Doonesbury strip on a creationist confronting antibiotic resistant tuberculosis
- CDC and WHO guidance on antibiotic resistance
- The humans are losing ground
- Ventola CL. The antibiotic resistance crisis: part 1: causes and threats. Pharmacy and Ther. 2015;40(4):277–283. PMC.
- Melnyk, A.H., Wong, A. and Kassen, R. (2015). The fitness costs of antibiotic resistance mutations. Evolutionary Applications, 8 ("Special Issue: Evolution and Drug Resistance"): 273-283.
- Springer, B., Y. G. Kidan, T. Prammananan, K. Ellrott, E. C. Böttger, and P. Sander 2001. Mechanisms of streptomycin resistance: selection of mutations in the 16S rRNA gene conferring resistance. Antimicrobial Agents and Chemotherapy 45:2877–2884.
- Stickland, H. G., P. W. Davenport, K. S. Lilley, J. L. Griffin, and M. Welch (2010). Mutation of nfxB causes global changes in the physiology and metabolism of Pseudomonas aeruginosa. Journal of Proteome Research 9:2957–2967.
- Todar, K. (n.d.). The Growth of Bacterial Populations (page 3). Todar's Online Textbook of Bacteriology
- Horizontally Transferred Genetic Elements and Their Role in Pathogenesis of Bacterial Disease