Resistance Is Futile The Dile Essay Research

Resistance Is Futile: The Dile Essay, Research Paper

Resistance Is Futile: The Dilemma of Antibiotic-Resistance

Has man pinned the arm behind the back of Mother Nature. Have humans finally won this terrible pathogenic onslaught. Apparently not the Era of Epidemics has risen once again, and it looks as if humans are being bumped off the top of the food chain. Bacteria are mutating into antibiotic-resistant monsters. One of the main reasons why this is is because of the mass antibiotic misuse that increases the chance of bacterial DNA mutation. Bacteria, like all living things, must adapt to survive. DNA mutation is often a mechanism for adaptation. Our misunderstanding and ignorant use of this miracle drug diminishes the miracle and results in the outburst of anti-microbial invulnerability. What humans need is not another miracle drug, but knowledge on the prevention of antibiotic misuse.

First, what are antibiotics. Antibiotics are chemical agents created by certain organisms, such as fungi or molds, which are capable of destroying or inhibiting the growth of bacteria. They act by interfering with the nucleic acid synthesis, peptidoglycan synthesis, protein synthesis, or the membrane integrity within the bacterial cell.[2] The prokaryotic bacterial cell does not have a nucleus, however; its genes are composed mainly of two elements: chromosomes and plasmids. Plasmids are circular pieces of genetic material that replicate complementary to the chromosome, and are often the carrier of mutated genes that bestow resistance to antibiotics.[3]

Bacterial proliferation depends greatly on DNA and RNA synthesis. One of the enzymes involved in bacterial DNA replication is DNA gyrase. When DNA is being transcripted and replicated, the helix must be unzipped in order to be read, and it cannot bear any kinks or loops, lest it should be severely damaged or even broken by the tension of the twist and thus, cannot be read and transcripted. DNA gyrase relaxes the coiled strands and smoothes out the strand by breaking down the bond and releasing enzymes to relax the nick.[4] As we can see, DNA gyrase is essential to DNA replication. Some antimicrobial agents, such as Quinolone, inhibit bacterial DNA gyrase, rendering the chromosome unable to transcript and replicate.[1] Another target to attack is ribosomal RNA. Streptomycin, for example, prevents the initiation of protein synthesis, and causes the misreading of proteins being translated.[4] But when antibiotics are misused, a bacterium s genetic make-up will often mutate and cause the cell to become resistant to one or many types of antibiotics.

When an antibiotic is used inappropriately, the bacteria that do not die will be trained to withstand that chemical. Or, when a single mutant bacterium survives the bactericide, it will multiply rapidly into a colony. There are three ways bacteria spread in such a swift and effective manner. One way is by conjugation, a means by which bacteria mate and distribute their genetic material. Its process is similar to that in the passing of a computer virus or STDs. In conjugation, a fine filament of protein called a pilus reaches to another bacteria and pulls them together. The donor duplicates its plasmids and passes it to the recipient so that both now carry the same copy of DNA, and become donors of the new resistant strain as they continue to multiply and colonize.[8] Another alternative is transduction, which resembles a mosquito in the passing of a disease. Bacterial viruses called bacteriophages inject its DNA into a bacterium where it can both lyse and destroy the cell, or reside in the chromosome. If it resides, the phage DNA matures within the cell, possibly carrying pieces of the bacteria s mutant chromosome.[8] Finally, there is transformation, involving mutated antibiotic-resistance genes hidden in entities called transposons. A transposon is analogous to head lice; they are smaller pieces of mobile DNA sequences capable of transferring themselves from one piece of DNA chromosome to another recipient. These transposons may also be picked up by a bacteriophage, but unlike plasmids, transposons alone cannot replicate, and must be sustained within a plasmid or chromosome.[8]

Perhaps most ominous, some strains of Mycobacterium tuberculosis, have become resistant to a series of antibiotics.[11] So now just having enough money to buy antibiotics no longer guarantees a cure. Tuberculosis was once highly responsive to antibiotics. But this is no longer the case; the organism has become multi-resistant and more difficult to treat. Last-ditch antibiotics such as Vancomycin have also bred resistance, which is appearing more frequently in certain strains of enterococcus, a common gut bacterium. Enteroccocci usually do not cause life-threatening disease, but the gene for the resistance may spread to more deadly organisms like Staphylococcus aureus.[10] In 1992, 17 percent of the national cases of tuberculosis had erupted around New York City.[11] According to the World Health Organization, tuberculosis afflicts 7.5 million people, killing as many as 2.5 million people each year.[12] As the leading cause of death among infectious diseases, tuberculosis is particularly severe in AIDS patients, those who can’t afford medical care, and patients who disobey doctors.[10]

Hundreds of misinformed people believe that antibiotics are the cure-all pill, taking the anti