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The ability of a bacteria or virus to resist the effects of another microorganism is widely referred to as antibiotic resistance. A providential experiment in 1928 by Alexander Fleming led to the discovery of antibiotics. Antibiotics can be defined as naturally occurring substances produced by bacteria and work to kill other competing bacteria. Fleming’s finding was a landmark and led to large scale production of penicillin from the mold Penicillium notatum in the early ’40s. Most surprisingly, the resistance of antibiotic was experienced in the same year. This has so far contributed to 75% of acquired infections that are linked to antibiotic resistance worldwide (Anderson, p. 318). Generally, antibiotic resistance is genetically evolved via mutation in the pathogen genome (a phenomenon referred to as horizontal gene transfer) but it can also occur as a result of the application of an evolutionary strain on a population. This is seen in the microorganisms that mutate to allow their survival and later they pass the genes to their offspring. Consequently, this results in the likelihood of a fully resistant bacteria colony. The bacterium carries or transfers important information in persons by the plasmid method. The bacterium may carry one or several resistance genes, where the latter is known as the multi-resistant process. Another microorganism may also transport genes and this class encompasses antimicrobial resistance. In addition, the introduction of antibiotics, which is specifically a drug, can occur through transformation protocols. This is however useful in instilling effective genes into the microorganism. Recent studies have demonstrated that antibiotic resistance is contributed by how much antibiotic is consumed. For instance, the advancement of methicillin resistance is suggested to occur as a result of the overuse of second and third generation of cephalosporins (the broad-spectrum antibiotics). Other factors that cause this resistance includes; incorrect prescriptions and diagnosis, oral application of antibiotic in livestock among others (Mathew and Liamthong, p. 116). The bacteria cell is simply destroyed by an antibiotic and leads to the non-functionality of a critical process. An antibiotic can render the protein nonfunctional when it binds to its wall. This protein is then used in copying the DNA and making the walls of the cells more effective in the reproduction and growth of bacteria. The DNA of a bacterium may undergo a mutation that codes one or several proteins. The resulting protein is altered as the antibiotic is unable to bind to it and this leads to the survival of the bacteria by mutation. When antibiotic is present in individuals, the reproduction and survival of bacteria are highly enhanced (Purdom, p. 34). In most cases, antibiotics do not cause resistance but it creates an environment that is antibiotic-resistant friendly. Several microorganisms have shown resistance to a number of drugs. A drug-resistant infection occurs as a result of a patient contracting a resistant organism or once the antibiotic drug is introduced into the body. The patient becomes more serious with numerous complications which can lead to death. Antibiotics are key weaponry in the fighting of diseases caused by microorganisms. The penicillin drug first attaches to the walls of the bacteria and destroys it completely. This follows the destruction of the bacteria walls and eventual death. Resistant microbes thwart the binding of penicillin by producing enzymes that disintegrate the antibiotic. Further research demonstrates that ribosomes may also be attacked by erythromycin harboring them from manufacturing protein. The ribosomes of the resistant bacteria are distorted making the drug-wall binding process impossible. In addition, bacteria become resistant to various antibiotics through the ribosomal route. These antibiotics in the market today include tetracycline and streptomycin (Anderson, p. 321). There are three methods of how the gene can confer resistance as discussed in the following paragraphs. The first method is referred to as spontaneous DNA mutation. Here, the DNA in the bacteria undergoes mutation which has been linked to the resistance of most antibiotic drugs (Cesar and Murray, p. 443).
The second method is the microbial sex called transformation where a bacterium takes the DNA of another bacterium as shown in figure 2. An example of a disease linked to this transformation is penicillin resistant gonorrhea.
The third way is the most shocking resistance acquired to date. It involves a plasmid (a small circle of DNA) that darts from a different bacterium (shown in figure 3). One plasmid molecule slews number of resistant. In 1968, Shigella diarrhea claimed the lives of over 12,000 people in Guatemala. The disease was caused by the microbe that harbored the plasmid resistances.
Many scientists have established that antibiotic resistance is inevitable but considerable measures can be undertaken to slow the rate of infection. These have been suggested to improve infection control, to develop novel antibiotics and appropriate medication. In addition, patients often contribute to resistance when they take drugs for a very short time and stop once symptoms improve. This however helps the proliferation of the resistant microorganisms. The patient should be fully assisted when undergoing treatment. Finally, more research should focus on the ways of ‘narrowing the spectrum’ to target only a few bacteria types so that resistance can be restricted.
References
- Anderson, Kevin. “Bacterial resistance to antibiotics.” Creation Research Society Quarterly 41.4 (2005): 318–326.
- Cesar, A. and Murray, E. “Antibiotic-Resistant Bugs in the 21st Century – A Clinical Super-Challenge”. New England Journal of Medicine 360.5 (2009): 439-443.
- Mathew, C. and Liamthong, S. “Antibiotic resistance in bacteria associated wit food animals: a United States perspective of livestock production”. Foodborne Pathogical Disaster. 4.2 (2007): 115–33.
- Purdom, G. Is natural selection the same thing as evolution? In the New Answers Book. Arkansas: Master Books, Green Forest, 2006.
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