Antibiotics and similar drugs, together called antimicrobial agents, have been used for the last 70 years to treat patients who have infectious diseases. Since the 1940s, these drugs have greatly reduced illness and death from infectious diseases. However, these drugs have been used so widely and for so long that the infectious organisms the antibiotics are designed to kill have adapted to them, making the drugs less effective.
Each year in the United States, at least 2 million people become infected with bacteria that are resistant to antibiotics and at least 23,000 people die each year as a direct result of these infections.
An increase in the frequency of antibiotic resistance in bacteria since the 1950s has been observed for all major classes of antibiotics used to treat a wide variety of respiratory illnesses, skin disorders, and sexually transmitted diseases.
Is this resistance the result of bacteria evolving new genes in response to the presence of antibiotic resistance genes beforehand?
There are several factors that involves in antibiotic resistance.
Brief look at an example penicillin resistance reveals the increase in the frequency of antibiotics resistance organism since the time when antibiotics use became common. Penicillin was discovered accidentally in 1929 by the British microbiologist, Alexander Fleming. In 1940s penicillin was available for medical use in world war 2 in soldiers.
In 1967 the first penicillin resistance streptococcus pneumonae was observed in Australia, and seven years later in the United States.
Since world war two many more antibiotics isolated from fungi (molds) and bacteria have been used to treat a wide range of human and animal infections.
One group of bacteria, the Streptomyces, produces most of the medically important antibiotics.Streptomyces release antibiotics into the soil in a sort of "biochemical warfare" scenario to eliminate competing organisms from their environment. These antibiotics are small molecules that attack different parts of an organism's cellular machinery. Streptomyces-produced quinolone and coumarin antibiotics, such as novobiocin, interfere with a protein called gyrase that assists in the normal separation of double-stranded DNA during replication of DNA or transcription of messenger RNA.Failure of DNA to properly separate during these processes results in a bacterium not being able to divide normally or produce functional proteins.
Ribosomes, the structures where protein synthesis is catalyzed, are the targets of many other Streptomyces antibiotics such as spectinomycin, tetracycline, and streptomycin. Spectinomycin and tetracycline prevent proteins from being assembled by the cell and streptomycin induces the assembly of the wrong amino acids into the translated protein Without proteins, which are necessary for normal cell function, the cell dies. The slight differences between human ribosomes which are not bound by these antibiotics and bacterial ribosomes make this type of antibiotic ideal for treating many illnesses.
Other antibiotics, such as penicillin, block the assembly of the bacterial cell wall causing it to weaken and burst. Penicillin is an effective antibiotic for human diseases because it interferes with a biological component in bacteria (cell wall) not found in human cells. The production of antibiotics by these organisms provides them with a competitive advantage over non-resistant bacteria in their environment. Just as large organisms such as plants and animals must compete for living space, food, and water, these microbes use antibiotics to eliminate competition with other microbes for these same resources.
However, not all bacteria are defenseless against the antibiotic producers. Many possess genes that encode proteins to neutralize the affects of antibiotics and prevent attacks on their cell machinery. Efflux pumps, located in the cell membrane, are one method of protection that many bacteria use against the influx of antibiotics.
Is it possible to transfer these resistance genes to other bacteria?
A unique bacterial characteristic that has not been demonstrated in plant and animal cells is the ability to transfer genes from one bacterium to another, a process called lateral gene transfer. Genes located on a circular strand of DNA called an R-plasmid may contain several antibiotic-resistant genes. Through a process called conjugation an antibiotic-resistant bacterium can transfer the antibiotic resistance genes from an R-plasmid to a non-resistant bacterium.
Antibiotic resistance in bacteria can also be achieved when mutations in a ribosome or protein change the site where an antibiotic binds. For example, four of the antibiotics mentioned earlier, tetracycline, streptomycin, kanamycin, and spectinomycin, bind to a specific region of a ribosome and interfere with protein synthesis. Mutations may prevent an antibiotic from binding to the ribosome (kanamycin)or allow the ribosome to function even while the antibiotic is bound (streptomycin and spectinomycin).Although it appears these mutations are beneficial and provide an advantage to the bacterium possessing them, they all come with a cost. Ribosomal mutations, while providing antibiotic resistance for the organism, slow the process of protein synthesis, slow growth rates, and reduce the ability of the affected bacterium to compete in an environment devoid of a specific antibiotic.Furthermore, a mutation that confers resistance to one antibiotic may make the bacterium more susceptible to other antibiotics.These deleterious effects are what would be expected from a creationist model for mutations. The mutation may confer a benefit in a particular environment, but the overall fitness of the population of one kind of bacterium is decreased as a result of a reduced function of one of the components in its biological pathway.The accumulation of mutations doesn't lead to a new kind of bacterium—it leads to extinction.