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Explain How Penicillin Stops Bacteria Without Harming Human Cells

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Prior to World War II, having a bacterial infection would most likely lead to death. Drugs were needed to combat bacterial infections, especially during the war. After Alexander Fleming accidental discovered penicillin in 1928 penicillin dramatically decreased the number of deaths and amputations caused by bacterial infection. Dorothy Crowfoot Hodgkins solved its structure. Penicillin is an effective drug to combat bacterial infections because it targets bacteria-specific proteins and has no effect on human proteins.

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Sometimes in life, you make an amazing discovery while trying to do something completely different. In 1928, the Scottish bacteriologist, Alexander Fleming, was going through some old bacterial plates, to clean up his lab a bit, when he discovered this moldy plate. He was about to toss it into the trash can when he noticed something unusual. Around the colony of mold, the bacteria, Staphylococcus aureus, weren't growing as well. That's funny… how could that happen? It turns out that the mold was conducting chemical warfare! It was releasing a compound that could kill bacteria in an attempt to have more space to grow and more nutrients to itself

When a microorganism produces a substance that can kill other microorganisms, it is called antibiosis. You can compare this word to 'symbiosis,' which is when organisms live together in a way that is often mutually beneficial. The word 'antibiotic' comes from this 'antibiosis.' The antibiotic-producing mold was identified as a member of the genus Penicillium, and its antibacterial compound was eventually isolated and named penicillin. In the early 1940s, Howard Florey and Ernst Chain carried out the first clinical trials of penicillin, just in time for the drug to be used on wounded soldiers in the final stages of World War II. From that time forward, antibiotics have made a huge impact on human history and drastically reduced the infectious disease burden in the world. By now, you're probably super curious about how penicillin actually works. It turns out that penicillin interferes with the synthesis of peptidoglycan in bacterial cell walls. Remember that peptidoglycan is a complex molecule made of sugars and polypeptides that forms a tough, strong lattice that surrounds bacterial cells. Peptidoglycan is a major component of most bacterial cell walls. The rigid peptidoglycan layer helps bacteria stay intact in the face of osmotic pressure, which is when water tends to flow into or out of a cell to balance out the concentration of solutes on either side of a membrane.

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As stated in the first major WHO report on AMR, appropriate global data on AMR is missing. Collecting data globally to monitor AMR is necessary to establish the link between antibiotic use and resistance across different countries and to design intervention strategies to target AMR on a global scale. However, there are challenges in the methods used for global collection of data. AMR is constantly evolving, and so it is clear that resistance data collected from several countries provides us with only a snapshot of a highly dynamic situation. Better systems to monitor AMR have to be designed to take into account people exposed to antimicrobials, the density of the human population, as well as the effect of individual antibiotic classes on specific bacteria. Recently, the U.K. Government commissioned a Review on Antimicrobial Resistance. This has highlighted one crucial point: the AMR epidemic that we are facing now is a global problem, which involves not just the medical and scientific communities, but also society as a whole (Lowy FD., 2003). The authors examined the financial burden of AMR as well as the human cost, and outlined the steps the global community should take to target AMR and new approaches for antimicrobial therapies. A ten-point plan proposed in this report aims to present key strategies that have to be implemented to address the problem of AMR. At the heart of the plan lies a call for international cooperation, which is essential to stop inappropriate antibiotic administration, to increase surveillance, and to develop new therapies. Significant progress has been made by creating several global funds including the Global Innovation Fund that combines the action of several governments with existing funding bodies.An example to show the successful impact of vaccines on AMR is the introduction of pneumococcal conjugate vaccine (PCV). The vaccine was introduced in the U.S. in children during 2001 and led to a striking decrease in pneumococcal diseases, including antibiotic resistant infections. Penicillin-resistant cases dropped by 81 percent, and a general downturn of resistant pneumococcal infections was observed among older children as well as adults who did not receive the vaccine (Rammelkamp T., 1942). This demonstrated herd immunity, leading to an estimated 50 percent reduction of the total number of penicillin resistant cases.

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Briefly, in 2014, the World Health Organization reported that antibiotic resistance is a worldwide threat to public health. In areas around the world, disease-causing bacteria are already resistant to all initial forms of antibiotic and are quickly developing resistance mechanisms to treatments of last resort. Some antibiotic-resistant bacteria are highly contagious and can quickly spread throughout a family or community, creating a serious public health risk. As bacteria continue to gain resistance to some of the strongest antibiotics available, pharmaceutical development of new antibiotic agents is in decline

This is due to several reasons, including low profitability due to short treatment cycles, lack of new therapeutic targets or strategies for killing bacterial cells, and low tolerability in the medical community for side effects.

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Rammelkamp T. Resistance of Staphylococcus aureus to the action of penicillin. Exp Biol Med. 1942;51:386–389.

Lowy FD. Antimicrobial resistance: the example of Staphylococcus aureus. J Clin Invest. 2003;111(9):1265–1273.

Hartman B, Tomasz A. Altered penicillin-binding proteins in methicillin-resistant strains of Staphylococcus aureus. Antimicrob Agents Chemother. 1981;19(5):726–735.

Matsuhashi M, Song MD, Ishino F. et al. Molecular cloning of the gene of a penicillin-binding protein supposed to cause high resistance to beta-lactam antibiotics in Staphylococcus aureus. J Bacteriol. 1986;167(3):975–980.

Katayama Y, Ito T, Hiramatsu K. A new class of genetic element, staphylococcus cassette chromosome mec, encodes methicillin resistance in Staphylococcus aureus. Antimicrob Agents Chemother. 2000

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