Inhibition Of Various Targets On Bacteria Cells Essay

The antibiotics will have different zones of inhibition on different bacteria. Also, a range of concentrations of the nutrients in the bacteria will change the bacterial growth.

There is a huge need for antibacterial drugs as infectious diseases are the second leading cause of death worldwide and the third leading cause of death in developed countries (Projan, 2003). Over the past 60-70 years, most antibiotics have been discovered by screening of soil samples for natural products that kill bacteria, including known pathogens, first on culture plates and then in animal infections (Walsh, 2000). There are three proven targets for the main antibacterial drugs, bacterial cell all biosynthesis, bacterial protein synthesis, and bacterial DNA replication 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.

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.

Tyrothricin, one of the first antibiotics discovered after penicillin, treated many wounds and helped fight diseases in the body (“Antibiotic” 1). Scientists tested the efficiency of Tyrothricin on open wounds. After twelve days, the Tyrothricin that had been administered to one of the wounds had miraculous results in comparison to the injury without the ointment (Williams 1). Tyrothricin has benefitted many people with flesh wounds particularly soldiers at war. Their accessibility to the drug had increased their bodies productivity in healing the laceration. Moreover, Actinomycete is another example of Penicillin blooming the beginning of all antibiotics. Actinomycete, when tested its capability of eliminating marine alga Phaeocystis globosa, proved to be highly efficient in that after 7 days, marine alga Phaeocystis globosa decreased its toxicity by 60% (Zhang 1). Actinomycetes contribution to society includes drugs like Bestain. When combined with Aminopeptidase, Bestain resists and reduces the size of liver cancer stem cells and also xenograft tumors (Sun 1). Derived from Penicillin, Actinomycetes is the benefactor and savior to the once ravenous diseases that once spread among people by producing many different antibiotics. Eventually, antibiotics created by cephalosporins commenced into society with drugs such as Cefixime, Cephalexin, and Cefuroxime which suppress infections like skin,

In this age of antibiotic resistance, there is an emergence for new line of therapies against pathogenic bacteria. Antibiotics are semi-synthetic or synthetic compounds that target specific bacterial molecules and cause suppression or killing of the pathogen. The bacteria in-turn has developed resistance against many of the available antibiotics causing a more severe and often fatal infections. There exist viruses that eat up/lyse the bacteria called as bacteriophages (baterio: bacteria and phage: to devour). They can kill the bacteria without causing any kind of harm or side-effects to the patient as seen in case of antibiotics and hence are also known as the silent killers of bacteria. The reason why these phages can only infect the bacteria is because the bacterial cell surfaces contain specific structures for the phage to attach which are absent on the human cells. These are called PAMPS i.e Pathogen Associated Molecular Patterns which include Lipopolysaccharide (LPS), Flagella, Pili etc.

they are two procedure by which the antibiotic attacks the bacterial cells. one is by interfering which the bacterial ability to repair the damage DNA. by stopping the bacterial ability to make what it needs to grow new cells to make what it needs to grow. the other one is by weakening the bacterial's cells wall until it burst

It has been thirty years since the last antibiotic was discovered in 1987. This is huge problem when tackling antibiotic resistance. Continually developing new drugs for a new strain of antibiotic resistance is not what will solve the problem in the long run, this comes from preventing the bacteria from mutating and becoming resistant so rapidly. However, in the short term, for the bacteria that are now resistant to the antibiotics we already have, we need a new type of antibiotic that kill be effective in killing these bacteria.

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.

Antibiotics are commonly used to treat bacterial infections in both humans and animals however the overuse and inappropriate prescription of antibiotics has caused a worldwide concern in antibiotic resistance (FDA, 2015). Antibiotic resistance is when bacteria is able to evolve in such a way enabling the bacteria to survive in the conditions it is in, consequently causing antibiotics being ineffective to the patient (CDC, 2013). Due to this issue implementations and actions have been taken to aid in the reduction of antibiotic resistance.

Several antibiotics known to man have been already discovered since the 1940’s, in which most of it are obtained from natural sources (Chaeychomsri et al., 2010). Synthesizing large amounts of antibiotics nowadays have given way to the bacteria, as well as viruses to develop immunity to a certain antibiotic strain, thus poses a threat of bacterial resistance, as these bacterial and viral species tend to become resistant to several antibacterial agents as a result of chromosomal and genetic mutation and adaptation to the agent (Neu, 1992). Due to this setback, many scientists have also initiated solutions that could be derived from natural sources, which led to the exploration and research on several animals,

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]

Resistance via modification of the anti-microbial compounds: Bacterial pathogens have evolved strategies to chemically modify the antibiotics via the production of enzymes that adds specific moieties to the compounds, inhibiting their therapeutic effects (Jose at al., 2015). These enzymes exert their action through the process acetylation, phosphorylation and or adenylation to sterically hinder the compound so it is no longer able to bind its target. Due to these biochemical reactions, the drug is unable to bind its target sites and thus results in increased resistance and higher MICs among bacterial populations (Wilson, 2014;

Treatment of infectious diseases becomes more difficult in the past few decades. This is especially true for infections caused by the human pathogen P. aeruginosa. This pathogen has the ability to rapidly develop the low antibiotic susceptibility to multiple classes of antibiotics. Some important regulatory factors, such as two-component systems, quorum sensing systems, and the type III secretion systems (T3SS), have been considered as attractive targets to reduce bacterial virulence [33]. The T3SS has been thought a novel target for antibacterial drugs because this virulence factor is required for the full bacterial pathogenesis but does not influence the growth of the parasite. In this study, we presented the effective T3SS inhibitors, TS187 and its analogs, which may have potential in drug development against antibiotic-resistant Pseudomonas. We demonstrate that compounds TS187 and its analogs abolished T3SS expression and effectors secretion. Our data further indicate that TS187 inhibits T3SS gene expression through two distinct mechanisms. First, as reported previously, expression of T3SS-related genes is activated by ExsA, an AraC-type DNA binding protein that recognize a consensus sequence located upstream of the transcriptional start site of T3SS genes [8]. Interestingly, the strains engineered to constitutively express of the exsA-FLAG fusions with different exsA upstream regions with or without TS187 showed different EsxA protein levels (Fig. 2). These

Using antibiotics to treat infectious diseases as a result of bacteria has added 20 years to our lifespan, but the rapid emergence of antibiotic resistance is hindering their effectiveness. Cutting-edge antibiotics are required, but they have not been developed in the last 25 years (WHO, 2016). One class of antibiotics are beta-lactams, which are sub-divided into four different groups of antimicrobial agents, as shown in Figure 1.