At start, M. tuberculosis bacteria are ingested by phagocytic cells in the alveoli. These phagocytic cells include macrophages, neutrophils, monocyte-derived macrophages and dendritic cells. They recognize the pathogen and undergo phagocytosis in attempt to destroy the invading organisms. The clash between the phagocytic cells and the pathogen begins with the recognition of the invading organisms by receptors such as the C-type lectin receptors (CLRs), the scavenger receptors (SRs) and the complement receptors (CRs). The CLRs are essential for attaching and inducing the mycobacteria.
One of the greatest achievements in the 20th century was the invention and mass production of antibiotics. Antibiotics or antimicrobials are chemical drugs that are used to treat a variety of different infectious bacterial diseases by destroying or slowing the growth of the bacteria. Antibiotics are toxic to the target cell but do not harm the host. They are designed to attack various kinds of parasites, fungus, and bacteria. Contrary to popular belief antibiotics do not work against viruses like those that cause the common cold.
But when it gets past the power of WBCs, antibiotics are prescribed to prevent permanent damage to the body, permanent internal damage, sepsis or even death. The first antibiotic was Penicillin and this is a big component of modern day antibiotic medications such as ampicillin, amoxicillin and benzylpenicillin. Antibiotic resistance is when an antibiotic has lost its ability to effectively control or kill bacterial growth due to the bacterial organism changing its genetic makeup. In other words, the bacteria become resistant and continue to multiply despite the presence of therapeutic levels of an antibiotic. When a disease becomes antibiotic resistant, it is often considered incurable, and can pose a serious public health threat as a consequence.
Introduction: Antibiotics have the ability to kill or hinder the growth of bacteria. Antibiotics contain compounds that are naturally produced by organisms to combat diseases caused by microbes. Discovery of penicillin by Sir Alexander Fleming became the first stepping stone of many new antibiotics of today’s modern medicine. Antibiotics typically invade the very components that make up bacteria, such as cell walls and metabolic pathways (Sato et al., 2014). However, frequent mutations of bacteria cause today’s strains to become more resistant.
The Resistance Against The Resistance Antibiotic resistance is when certain antibiotics lose their ability to render harmful pathogens inactive. When bacteria become resistant to antibiotics they will continue to grow and multiply without the antibiotics having any effect on them. Bacteria that are resistant to antibiotics are called superbugs because they are very hard to be destroyed within the body. Antibiotic resistance can be caused by many things. The most common way in which bacterium build up a defence to antibiotics is by mutation.
This article discusses how antibiotics work. It is important to understand how antibiotics work so we can better understand how to control antibiotic resistance. Each antibiotic works differently, but they all do the same thing in the end and that is to stop the bacteria from living and growing. This can be done by stopping the cell wall of the bacteria from forming properly which will lead to the cell filling with water and dying due to the membrane rupturing. Another way antibiotics work is by preventing the synthesis of protein.
Ampicillin is a derivative of penicillin that inhibits bacterial growth by interfering with the synthesis of bacterial cell walls. Since E. coli is gram negative, and ampicillin kills the gram-negative bacteria by synthesizing with the cell wall, E. coli should perish under no transformation. However, the ampicillin resistance gene is the enzyme Beta-lactamase, which is secreted by transformed cells into the surrounding medium where it destroys ampicillin (Dörr, 2010). In order to resist ampicillins, E.coli utilizes pGLO plasmid to protect the cell from ampicillin’s invasion. There are four components to... ... middle of paper ... ...n ampicillin resistance, and able to decompose ampicillin, while untransformed gene would perish because of ampicillin damaging the bacteria’s cell wall.
Alternative therapies are safer: fewer, if any, chemicals are involved in them. Radiation, for example, is a mainstream cancer “fighter,” yet it is poisonous, so is it not insanity to treat a weakened patient with it? Whether a treatment is popular with mainstream medicine practitioners or not should not matter. What is best for the patient’s wellbeing should be the deciding factor. And if ingesting inexpensive plants or taking a vial of venom is the answer, then the pharmaceutical companies should not interfere, as more than money is at stake in the battle against disease.
When people refer to pathogens, they are talking about bacteria that cause disease. The toxins actually excreted... ... middle of paper ... ...on of an antibody for immediate effects to cure serious diseases. A vaccine is a way to acquire artificial active immunity. It is usually dead pathogens or weakened pathogens. This dosage would not get you ill be just enough for you body to have reactions and make their own antibodies.
Methods ... ... middle of paper ... ... the common bacterium Escherichia coli.” – too much triclosan Triclosan interferes with an enzyme crucial to the growth of bacteria. But it also trips a genetic master switch called the multiple antibiotic resistance (mar) operon. This activates a pump in the bacterial cell wall that expels a host of unwanted chemicals.” – Groceries trip triclosan switch Triclosan is an antimicrobial agent that is widely used in a variety of consumer products and acts by inhibiting one of the highly conserved enzymes (enoyl-ACP reductase, or FabI) of bacterial fatty-acid biosynthesis. But several key pathogenic bacteria do not possess FabI, and here we describe a unique triclosan-resistant flavoprotein, FabK, that can also catalyse this reaction in Streptococcus pneumoniae. Our finding has implications for the development of FabI-specific inhibitors as antibacterial agents.