Types Of Resistance : Mechanisms Of Antibiotic Resistance

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

The misuse and overdose of the antibiotics increase the resistance problem. It can cause these bacteria to

The two mechanism by which a bacterial cell can be resistant to antibiotics are mutation and gene transfer. Through mutation new alleles are introduced to populations during DNA replication, and through gene transfer, DNA is passed among bacterial species. 5. Do you think drug resistance is more likely to develop in a species of bacteria that can double its population every 20 minutes or a species that doubles its population every 24 hours? Explain your answer.

F. Describe three mechanisms by which microbes might become resistant to the action of an antimicrobial drug? Microbes may become resistant by producing enzymes that will detoxify or inactivate the antibiotic such as penicillinase and other beta-lactamases. Microbes may also alter the target site in the bacterium to reduce or block binding of the antibiotic in the process producing a slightly altered ribosomal subunit that still functions but to which the drug can't bind. Microbes may also prevent the transport of the antimicrobial agent into the bacterium thereby producing an

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

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.

Staphylococcal beta-lactamase used Penicillin binding proteins to prevent antibiotics from entering the cell wall, enzyme modification or inactivation, trapping the antibiotic, and pumping the antibiotic out of cells. Resistance to beta-lactams, methicillin, macrolides and others is due to these resistance mechanisms (Yazdankhah 2006). Resistance in Pseudomonas aeruginosa bacteria is caused by enzyme inactivation or modification, alteration of antibiotic, pumping out antibiotics or pore diffusion. These resistance mechanisms make (Yazdankhah

For a bacterium to become resistant a change in its DNA must occur. This can happen in more than one way. Bacterium may gain resistance through spontaneous mutation within the bacterium’s DNA. This occurs when a single amino acid that makes up a protein changes arrangement, the order of the peptide chain (made up of amino acids, joined together to make up proteins) then the purpose of the protein in the DNA changes. This causes the genetic makeup of the cell to alter. If the mutation is of benefit and gives the bacteria resistance, once all the other none resistant strains of bacteria are killed, the resistant bacteria multiplies and reproduces, creating a new strain of bacteria which is resistant to the antibiotic in hand. Once a resistance gene is obtained and inserted into the DNA, the bacterium can dominate other bacteria and

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.

When a bacterium, for example Escherichia coli, becomes multidrug resistant, multiple toxins and antibiotics have no effect on the bacteria. Right now, there are thousands of people suffering from the effects of this drug resistance because standard antibiotics become less and less effective against some infections. This is why research of the mechanisms in bacteria that cause antibiotic resistance is needed. There are four common mechanisms by which bacteria become drug resistant. One of these mechanisms involves the production of enzymes that modify antibiotics by inactivate them.

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

Once bacteria is exposed to an antibiotic, the sensitive bacteria are killed, but sometimes not all the bacteria are killed and those colonies that survive, are left to multiply. Bacteria can become resistant through many mechanisms, it depends on the bacteria. Some bacteria fight the drugs and push them out, others alter the attack site which makes the antibiotic unable to harm the bacteria in a way it did before. The attack site is altered when the bacteria has a stronger defense than the antibiotic has (Rice, 2006). If repeatedly exposed to antibiotics, this process allows selective pressure to occur which makes it more likely for the bacteria to mutate. Selective pressure is a process the bacteria take to become immune. Sometimes, however,

Inhibition of various targets in bacteria cells has long been a strategy for developing new antibiotics. Within a bacteria cell, there are nearly endless potential targets for inhibition that may interrupt cell metabolism, replication, synthesis of membrane components, etc. However, the rise of antibiotic resistance means researchers are continually searching for new targets or ways to make old targets viable again. For this reason, novel narrow-spectrum inhibitors are of great interest, especially since the more species-specific they are, the less potential there is for resistance to spread across bacterial species. However, there is also the hope for the discovery and development of new broad-spectrum inhibitors that could be used to side-step present antibiotic resistance while research on treatments that slow the acceleration of antibiotic resistance continue.

Modern-day advances have allowed scientists to develop methods to control pathogens. The more common methods include the use of antiseptics, antibiotics, and vaccines. By definition, antiseptics are chemicals used to kill pathogens. A few widespread antiseptics include soap, vinegar, and rubbing alcohol. Antiseptics are primarily used for the external destruction of pathogens, while antibiotics and vaccines target internal pathogens. Nevertheless, there are and can be difficulties concerning the use of antibiotics. “As antibiotic use has become more common, antibiotic-resistant bacteria have evolved.” This resistance due to evolution is called antibiotic resistance. It results in the antibiotics having no effect whatsoever on the bacteria, rendering the antibiotics useless. When antibiotic resistance occurs, scientists must resume their search to create a new medicine to can kill the mutant bacteria.

Antibiotics are selective agents that act on vital microbial functions without affecting host functions. They act in different ways, and the understanding of these ways is essential to understand mechanism of bacterial resistance. These agents are described either