The Effects Of Adaptation In Cell Diseases

Bacteria are not just all of a sudden becoming resistant to antibiotics they have always had a bit of resilence, as a human species we have always developed something it doesn’t work we will develop something stronger, that has been the downfall in this instance. Pencillan is a great example as it is one of the most highly used antibiotic and is derived and made from mold.

Certain E. Coli strains are also known to show resistance to bacteria killing antibiotics. This resistance is due to the plasmids, or small round DNA molecules, in the bacteria that carry the resistant genes. R Plasmids (resistance plasmids) are widely studied and bestow resistance to factors that inhibit growth of the organism. R plasmids code for proteins that can

Antibiotic resistance evolves in bacteria. Charles Darwin created the theory of evolution which focused on natural selection being the key factor of how things change. Natural selection is when organisms that are better suited to the environment are able to reproduce successfully. Evolution is descent with modification. Bacteria can become resistant to antibiotics by a mutation. The bacteria that did not die from the antibiotic inherited the gene from an ancestor that made it resistant. Since the other bacteria is dying faster than the resistant bacteria, the resistant bacteria are able to multiply

When antibiotic is used most of the bacteria die but a few bacteria with antibiotic resistance gene survive and reproduce and pass this advantage to their offsprings. This selective pressure exists naturally, however antibiotic misuse can be accused for fastening the spread of the antibiotic resistance gene [Refer to figure 2] (Learn Genetics 2015). Consequently, inappropriate antibiotic intake will lead to a greater chance of superbugs being developed. Antibiotic resistance can be defined as a new ability which a bacterium has developed to stay unattached in the presence of an antibiotic that was previously effective to destroy the bacterium (ABC science 2015). Four key mechanisms that has been identified for bacterial antibiotic resistance can be listed as: producing enzymes that inhibit the functionality of the drug, reducing the effectiveness of the drug by producing targets against which the antibiotic, reducing the permeability of the drug into the bacterium and active export of antibiotics using various pumps (Pogson 2012). All these mechanisms can be developed by any of the bacteria when the corresponding mutated gene of antibacterial resistance is received. The genes code for specific proteins, and variation in the gene leads to alteration of the shape of proteins. This leads to changing the functionality

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.

Under the circumstances where dosage of antibiotics is not necessary or not sufficient, even though normal bacteria will die, bacteria that possess genes for antibiotic resistance will likely survive, giving them the opportunity to reproduce, creating new bacteria with their traits of being resistant to antibiotics. This is because these types of bacteria have been naturally selected for antibiotic resistance so that they can survive under the conditions of antibiotics. As a result, bacteria can emerge to be drug resistant to antibiotics thanks to the process of natural

These mutations, no matter what process that has led to their occurrence, block the action of antibiotics by interfering with their mechanism of action (1). Currently, antibiotics attack bacteria through one of two mechanisms. In both mechanisms the antibiotic enters the microbe and interferes with production of the components needed to form new bacterial cells. Some antibiotics act on the cell membrane, causing increased permeability and leakage of cell contents. Other antibiotics interfere with protein synthesis in cells. They block one or more of the steps involved in the transformation of nucleic acids into proteins.

Antibiotics target specific structure or process of the cell. Such as, inhibition of cell wall synthesis, Inhibition of protein synthesis, Injury to plasma membrane, & Inhibition of nucleic acid synthesis. These drugs include, such as B lactam drugs that are bactericidal & kill bacteria by interfering with the synthesis of the cell wall, Polymyxin B drugs that injures the plasma membrane allowing the cell to burst. Tetracycline & Chloramphenicol that are bacteriostatic drugs, and inhibits protein synthesis. Fluoroquinolones & Rifamycin that are bactericidal drugs & interfere with the synthesis of nucleic acid. The pathogens can develop resistance against these drugs that are used to treat them. Resistance to antibiotics can be acquired by mutation

But for the sake of simplicity we will consider that resistance develops from one of two pathways: either built-in or acquired. Mutation is an example of built-in resistance development that typically comes about from errors of replication or incorrect repair of damaged DNA. These newly formed mutants make up a small portion of the overall population of a bacterial colony. However once treated with an antibiotic the major portion of the bacterial colony could be destroyed. Assuming the mutation made the bacteria resistant to the antibiotic; it would survive and have less competition for resources.

Bacterial Pathogens have been developing resistance to antibiotic treatment soon after these drugs were developed. Mutations in the genes of the bacteria allow it to survive despite being exposed to the medications designed to kill them. Through directional selection, the bell curve is shifted to a phenotype that is designed to survive in harsh conditions that would normally kill them.

Transformation is a procedure where cells take up foreign DNA from their environment. This can happen in either prokaryotic or eukaryotic cells. A circular self-replicating molecule of DNA known as a plasmid transfers genetic information between bacteria enabling the microbes to gain antibiotic resistance as well as the ability to adapt to a new environment. Bacteria also have the capability to acquire small pieces (at random) of DNA from their environment but this however is said to be inefficient because only a small fraction of cells will uptake DNA and become transformed. Expressions of genes on the plasmid will alter the genotype and phenotype of the cell. Under specific laboratory conditions a cell which is incubated with the plasmid DNA has the ability to absorb the plasmid into its own cytoplasm. Because these natural processes can potentially be modified by scientists, the transformation procedure can be used as a means of treating human diseases to increase the quality of life.

Resistance methods may also include inactivation of the antibiotic by an enzyme (acetyltransferase or phosphotransferase). There is also the possibility of mutations in the bacterial rRNA which interferes with the reception of the drug to the bacterial cell. Another mechanism of resistance includes an active efflux pump, which transfers chemicals such as antibiotics out of (bacterial) cells.It has been observed that “cells exhibited upregulation and downregulation of genes involved in protein biosynthesis, nutrient transport, gene regulation, stress and metabolism” in the presence of the

However, to completely understand the effects of antibiotic resistance, we need to understand the genetic component of how bacteria becomes resistant. An antibiotic can operate at different sites within the bacterial cell, some infect the cell wall or the membranes, making it

Bacteria are haploid organisms that lack the true nuclei of eukaryotic organisms. They contain one copy of each gene thus the genotype of bacteria can be deduced from phenotypes. Bacteria can reproduce asexually by means of binary fission and have the ability to transfer genes by several mechanisms: conjugation, transformation and transduction. Bacterial conjugation is a process that involves the transfer of genetic material between bacteria through a contact dependent process. The gene transfer is carried out from a donor cell that contains a conjugative plasmid to a recipient cell with no plasmid present. Plasmids are circular, double-stranded DNA molecules that can replicate independently of the host cell genome or can be integrated into the genome and replicate with it during cell division. Conjugative plasmids are present in both Gram-positive and Gram negative bacteria. The conjugative transfer of this bacterial plasmid encodes resistance of bacteria to antibiotics. Subsequently, conjugation and spread of antibiotic resistance represents a severe problem in anti-microbial treatment, particularly of immunosuppressed patients and in hospitals.

There are many mechanisms of MDR in Bacteria, but of particular interest is the role of efflux-mediated resistance. Efflux of antibiotics can occur naturally by bacteria, for example - those that produce their own antibacterial mechanism to fend off competition in the wild. It would also be necessary for a bacteria to be able to expel their own antibacterial products so not to kill themselves and in turn have antibacterial effects on competing bacteria.