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Evolution 1 Running Head: EVOLUTION OF RESISTANT Evolution of Resistant Bacteria and Viruses Nancy Portillo Jibran Rana Matt Kletti Peter Chen December 10, 2007 Evolution 2 Evolution of Resistant Bacteria and Viruses Physicians and clinicians face an ongoing challenge: to keep up with increasingly stubborn, resistant bacteria that cause significant infections. In addition, the resistant virus’s strains also pose a problem to many physicians. The more exposure bacteria have to our available antibiotics, the higher their chances of evolution into a resistant form. Over the past 10 years, the number of resistant bacteria has proliferated at an alarming rate. There are several technologies that currently help scientists’ research methods of predicting, diagnosing, designing, and researching methods to slow down this evolution of resistance. The increased prevalence of antibiotic resistance is an outcome of evolution, as Darwin’s theory implies, “Survival of the Fittest.” For example, when a person takes an antibiotic, the drug kills the defenseless bacteria, leaving behind those that can resist. The more resistant bacteria then multiply; increasing their numbers and becoming predominate. As mentioned by Lewis (1995) “A patient can develop a drug-resistant infection either by contracting a resistant bug or by having a resistant microbe emerge in the body once antibiotic treatment begins” (para. 8). Antibiotic resistance results from gene action. In addition, bacteria acquire gene resistant in three ways. First, in spontaneous DNA mutation, bacterial DNA may mutate spontaneously. The second form antibiotic resistance occurs in a form of microbial sex called transformation. Transformation occurs when one bacteria takes up DNA from another bacteria. Lastly, the most frightening according to Lewis, is resistance acquired from a small circle of DNA called a plasmid. A single plasmid can provide a lot of different resistances to antibiotics. (para. 12) Evolution 3 In addition to the new microarray chip which locates resistant bacteria genes, there are studies being done to stop or inactivate the resistant bacteria from reproducing. Bacteria reproduce during conjugation, which is when two bacteria collide their membranes together. After each opens a hole in their membrane, one spurts a single strand of DNA to the other. Many highly-drug resistant bacteria rely on an enzyme, DNA relaxase, to obtain and pass on their resistance genes. This enzyme starts and stops the movement of DNA between bacteria, “Relaxases is the gatekeeper of the resistance process” (University of North Carolina, 2007, para. 6). Researchers found that DNA relaxase uses two phosphate rich DNA strands at the same time. They then suspected that a phosphate ion could plug this dual DNA binding site. They then found that biophosphonates were the right size to decoy. According to the University of North Carolina, “There are several bisphosphonates on the market: clodronate and etidronate” (para. 8). Exactly how biophosphonates destroy bacteria is unknown, but the drug is effective. Scientist can now block the mechanism of bacteria that may become resistant, by blocking the enzyme that is used to replicate them. The disadvantage is that a person has to be monitored because the scientists do not the correct dosage at this time. Scientists are conducting many studies in order to find a solution for bacteria that are becoming resistant to antibiotics. In September of 2007, the Veterinary Laboratories Agency in Surrey, developed microchips capable of quickly and cheaply identifying dangerous and drug resistant bacteria. Doctors and veterinarians will be able to test clinical samples from their patients for the presence of the genes for antibiotic resistance in bacteria, within twenty-four hours. Dr. Anjum from the UKS Veterinary Laboratories, states that they “have developed a test chip which can accurately identify 56 virulence Evolution 4 genes in E. Coli and 54 antimicrobial resistant genes covering all the known families of gram-negative bacteria” (para. 2). The advantage to this new technology is that is will be able to give doctors quicker results. In addition, it will provide for routine surveillance of such genes and how they are spread in the environment, food samples, or farm and wild animals. The disadvantage of this microarray chip is that it is very selective in the bacteria that it uses. As mentioned by Dr. Anjur “The most common antibiotic resistance gene was identified in 90% of E. coli and 56% of Salmonella bacteria” (2007, para. 5). In addition to resistant bacteria, there is also the possibility of resistant viruses. Nowadays, doctors are being challenged with resistant viruses due to the excess use of drugs, and lack of proper dosing. Even the common cold viruses are getting harder to treat. Pretty soon most of the viruses that infect humans would be hard to treat and could become deadly. According to Interest (2007), resistance means that virus is multiplying rapidly despite the drug taken to kill or stop the progress of it. Mutations in the virus cause resistance. Even though it might seem that the virus is outsmarting the drug, it is merely by accident that mutations occur. For example, an antiretroviral drug (ARV) will not control a virus that is resistant to it; rather, it can "escape" from the drug. If a person keeps taking the drug, the resistant virus will multiply the fastest. This is called "selective pressure." If a person stops taking medications, there is no selective pressure. The wild type virus will multiply the fastest. Although tests may not detect any drug resistance, it might however, return if people re-start the same drugs. (Interest, 2007) A virus usually becomes resistant when it is not completely controlled by the drugs someone is taking. The more the virus multiplies, the more mutations occur and the more resistant it becomes. According to Interest (2007), there are three types of Evolution 5 resistance which are: clinical resistance, genotypic resistance, and phenotypic resistance. Clinical resistance is when the virus multiplies rapidly in your body despite the drugs, phenotypic resistance is when the virus multiplies in a test tube when the drug is added, and genotypic resistance is when the genetic code of the virus has mutations that are linked to drug resistance. There are also several tests which accompany these resistance types to test if they are resistant or not. In phenotypic testing a sample virus is grown in the laboratory which is accompanied by a drug. The rate of the virus is compared to the rate of the wild type virus. If the sample grows more than normal, it is resistant to the medication. In genotypic testing the genetic code of the sample virus is compared to the wild type. Mutations are described by a combination of letters and numbers. The virtual phenotype test is really a method of interpreting genotypic test results. First, genotypic testing is done on the sample. Phenotypic test results for other virus samples with a similar genotypic pattern are taken from a database. These matched samples tell you how the virus is likely to behave. Sometimes a mutant version of a virus may be resistant to multiple drugs; therefore a cross-resistance testing may be necessary. (Interest, 2007) According to Vella & Palmisano (2005), high level of viral replication and turnover and the lack of a proofreading mechanism of HIV reverse transcriptase lead to the spontaneous generation of a large number of genetically distinct viral quasi species coexisting in the same person. In an individual, resistance is not all-or-nothing process but, rather, a gradual one that evolves through the accumulation of multiple mutations. This then provides variable levels of reduced susceptibility because of their different effects on the replication capacity of the virus. Evolution 6 Overall, the evolution of resistant bacteria and viruses may be inevitable. There are many mutations that may be spontaneously or genetically transferred. Hence, being able to get rid of these resistant bacteria may take many years, if possible. Through advancements in science and technology we will be able to control the replication and mutation of bacteria and viruses in the future. Evolution 7 References Anjum, M. (September, 2007). Quick microchip test for dangerous antibiotic resistant bacteria. Retrieved December 9, 2007, from Science Daily. Interest. (2007). HIV Resistance Testing: AIDS.ORG. Retrieved December 10, 2007, from http://www.aids.org/factSheets/126-HIV-Resistance-Testing.html Lewis, R. (1995). The rise of antibiotic-resistant infections. Retrieved December 8, 2007, from http://www.fda.gov/fdac/features/795_antibio.html University of North Carolina at Chapel Hill (2007, July 12). New way to target and kill. Retrieved December 9, 2007, from http://www.sciencedaily.com/releases/2007/07/070709171636.htm Vella, S & Palmisano,L. (2005). The global status of resistance to antiretroviral drugs. Clinical Infectious Diseases, 41(1), p239-246. Retrieved December 10, 2007, from Academic Search Premier database.