Download Running Head: EVOLUTION OF RESISTANT

Evolution 1
Running Head: EVOLUTION OF RESISTANT
Evolution of Resistant Bacteria and Viruses
Nancy Portillo
Jibran Rana
Matt Kletti
Peter Chen
December 10, 2007
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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)
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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
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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
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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.
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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.
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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.