Adaptive Protein Evolution And Antibiotic Resistance

The development of antibiotics was an important advancement in 20th century medicine. Previously deadly infectious diseases are now routinely treated with antibiotics. Moreover, for modern-day medical procedures such as chemotherapy treatment to be successful, antibiotic use is necessary. For these reasons, the prospect of bacteria developing widespread resistance to antibiotics is a major concern as it would render many modern-day medical therapies unviable.

Many pathogenic bacteria species are becoming resistant to antibiotic. Explain how such adaptations can develop through the process of natural selection.

Many pathogenic bacteria species are becoming resistant to antibiotic. Explain how such adaptations can develop through the process of natural selection.

Antibiotic resistance has become a hot topic amongst scientists and healthcare professionals. It would be rare to observe in a clinical setting and not see some type of antibiotic resistant infection being treated. Scientists and medical doctors are scrambling trying to develop plans to discover new drugs or at least dampen the rate at which these organisms are developing resistance. Evolutionary biologists are claiming this type of resistance as proof of evolution, but is that a statement that is really supported by the evidence? It depends on which type of evolution is being talked about first. Macroevolution is the theory that one species can evolve into a totally different species. Microevolution is the change of genotypes and phenotypes

Like any other organism, bacterium are subject to evolutionary pressure. Antibiotic resistance in bacteria is rarely the result of a single mutation leading to full resistance, but rather the result of a series of mutations that incrementally increased antibiotic resistance. For example, in the case of fluoroquinolone resistance, resistance started with a mutation in the efflux pump, granting Streptococcus pneumoniae the ability to survive certain treatment regimens (13). This became an issue when people started to misuse their antibiotics. In this particular example, because patients did not follow their prescription regimens, they only killed the bacteria not resistant to fluoroquinolone. This selective pressure drove bacteria to further develop fluoroquinolone resistance, meaning that the initial infection remained untreated, and would now require a

Antibiotic resistance is and continues to be a global public health issue1.One of the main concerns stems from the ability for bacteria to obtain antibiotic resistance very easily as a result of chromosomal changes, or through plasmids and transposons which generate an exchange of genetic material2. Resistance can also result from single or multiple mutations1,3. To combat this rising force, scientists must research and analyse the many possibilities of mutations in a variety of genes and proteins in specific bacteria and ways to combat them.

Any mutation that would prevent the action of antibiotics, but not at the same time provide a selective advantage to the bacteria, would be one that interfered with the bacteria’s ability to reproduce. If this were to occur, then any selective advantage would be negated by the cell’s inability to take advantage of the diminished competition caused by the death of susceptible bacteria. This would be likely to occur in reaction to an antibiotic that interfered with protein synthesis, since it would also impact on the chain of reactions that occurs in the transformation

This paper describes the results of a laboratory experiment set up to study the adaptive evolution of E.coli, which has replicated in a novel environment.

Antibiotic resistant pathogens have evolved various mechanisms to evade antibiotic action. These include preventing the antibiotic from binding or entering it, modifying the binding site of the antibiotic or producing an enzyme that deactivates the antibiotic. Therefore it has become crucial to be able to design new antimicrobial substances that can overcome these existing antibiotic- resistant pathogens. [3]

Antibiotics was developed to combat bacteria by zero in on the bacteria’s structure. As time goes by bacteria can defeat antibiotics in their natural selection. Natural selection plays an important role in the progression of antibiotic resistance. Most of the bacteria dies when it is exposed to antibiotics they are sensitive to. Therefore, it creates more space and availability of nutrients for the surviving antibiotic-resistant bacteria. Subsequently,

Less than 50 years after penicillin was discovered, strains of bacteria were discovered to be resistant to antibiotics (Haddox, 2013). Over the years scientists have changed the structure of the antibiotics to avoid this resistance, every time the bacteria adapts to overcome the changes. Bacteria divides as fast as 20 minutes and have many different ways to adapt (Haddox, 2013). Bacteria pass their drug resistance between strains and species, causing antibiotics to be less effective to all bacteria (Haddox, 2013).

Discuss how recent advances in medicinal chemistry have addressed the challenges of bacterial resistance to natural antibiotics

This study concluded that resistance might become a global problem very quickly most likely due to a high volume of international travel among humans and animals. It is the job of the evolutionary biologists in conjunction with the medical community and profession to inform the public about bacterial resistance management. Some applications covered would be proper dosage requirements, combinational drug therapy and administering selective application of antibiotics with patients and animals. Learning about the evolutionary origins of disease as well as the basic processes of evolution may provide insight on how to treat current diseases such as Huntington's Chorea - which may help us better understand the genetic roots of disease.

In the second article Mcgarvey, Queitsch, and Fields are attempting to study and identify which genes and or proteins are accountable for generating antibiotic resistance in bacteria. The authors hypothesized that a screening of soil metagenomic DNA library in an Escherichia coli host for genes could project resistance to the following antibiotics: gentamicin, kanamycin, rifampin, trimethoprim, chloramphenicol, or tetracycline. The screen concluded that 41 genes were encoding novel protein variants of about eight families.

However with the advent of each new class of antibiotic used to treat bacterial infections, new β-lactamases emerged that caused resistance to that particular class of drug. It is assumed that the overuse of new antibiotics in the treatment of patients created a selective pressure eventually selecting for new variants of β-lactamase.