Penicillin kills bacteria by attaching to their cell walls. Then it destroys part of the wall. The cell wall breaks apart and bacteria dies. After four years, when drug companies started to mass produce penicillin, in , the first signs of penicillin-resistant bacteria started to show up. The first bacteria that fought penicillin was called Staphylococcus aureus. This bug is usually harmless In nine pages the resistance of antibiotics to bacteria is examined with the inclusion of discussions on overprescribing antibioti In an overview consisting of eight pages the resistance in bacteria to antibiotics and a landfill where this occurs are discussed In five pages the resistance to bacteria as a result of so called 'quick fixes' are discussed in terms of how eventually antibioti In five pages this paper discusses how antibiotics affects the growth of bacteria.
Five sources are cited in the bibliography New to eCheat Create an Account! Antibiotic Resistance in Bacteria Antibiotic Resistance in Bacteria For over 50 years, antibiotics have been the answer to many bacterial infections. Professionally written essays on this topic: Antibiotics and Bacterial Resistance In nine pages the resistance of antibiotics to bacteria is examined with the inclusion of discussions on overprescribing antibioti History, Etiology, and Treatment of Antibiotic Resistance could be used therapeutically both in the treatment of his own diseases and in those of the plants and animals he found important Clin Microbiol Rev 23 3: Clin Infect Dis 44 2: Systematic review, meta-analysis and economic modeling of molecular tests for antibiotic resistance in tuberculosis.
NIHR Journals library How to cope with the quest for new antibiotics. FEBS Lett Incidence and outcome of vancomycin-resistant enterococcal bacteremia following autologous peripheral blood stem cell transplantation. Bone Marrow Transplantation 25 2: Infection Control and Hospital epidemiology The complex evolution of antibiotic resistance in Mycobacterium tuberculosis.
International Journal of Infectious Diseases Antibiotic Resistance Threats in the United States. S Department of Health and Human Services.
The Elimination of Tuberculosis in the United States. J Med Microbiol 55 6: Evolution of Drug Resistance in Mycobacterium tuberculosis: Clinical and Molecular Perspective.
Antimicrob Agents Chemother 46 2: GMS Krankenhhyg Interdiszip 6 1: Infections, antibiotic treatment and mortality in patients admitted to ICUs in countries considered to have high levels of antibiotic resistance compared to those with low levels. BMC Infect Dis 22 Ambulatory multi-drug resistant tuberculosis treatment outcomes in a cohort of HIV-infected patients in a slum setting in Mumbai, India.
PLoS One 6 Guidelines for preventing the transmission of Mycobacterium tuberculosis in health-care settings, Health care associated invasive MRSA infections, The Journal of the American Medical Association, 6 , Ann N Y Acad Sci Strategies to Minimize Antibiotic Resistance. Factors impacting on the problem of antibiotic resistance. J Antimicrob Chemother 49 1: BMC Public Health Implications for Antibiotic Stewardship. Clin Infect Dis 49 8: Critical Care 12 4: Economic burden of healthcare-associated infections: Expert Rev Pharmacoecon Outcomes Res 9 5: Systematic review of economic analyses of health care-associated infections.
Am J Infect Control Multiple-antibiotic resistant pathogenic Bacteria. The New England Journal of Medicine Antimicrobial resistance in the Netherlands: Front Public Health 2 5. Part 1 Causes and Threats. The impact of hospital-acquired bloodstream infections. History of Antibiotic Resistance Resistance to single antibiotics became prominent in organisms that encountered the first commercially produced antibiotics.
In the case of streptomycin, introduced in for the treatment of tuberculosis mutant strains of Mycobacterium tuberculosis resistant to therapeutic concentrations of the antibiotic were found to arise during patient treatment Kang et al.
The resistance was due to plasmid, which carried different antibiotic resistance genes. The most prevalent Gram-negative pathogens, such as Escherichia coli, Salmonella enterica, and Klebsiella pneumonia cause a variety of diseases in humans and animals, and a strong correlation between antibiotic use in the treatment of these diseases and antibiotic resistance development has been observed over the past half-century. This is especially apparent with the -lactam class of antibiotics and their related inactivating enzymes, the -lactamases.
At this time, several groups and classes have been identified, comprising up to 1, resistance related -lactamases. In , NDM-1 New Delhi Metallobeta-lactamase-1 is an enzyme that makes bacteria to resist to a broad range of beta-lactam antibiotic. The infection caused by it is difficult to treat. It was first detected in K. Currently, the most notorious superbug is the Gram-positive organism Staphylococcus aureus.
Whether it is the most serious superbug can be debated, since one wonders to what extent its bad reputation is due to its extensive press coverage. For example, Streptomyces has some genes responsible for resistance to its own antibiotic. Other examples include organisms that lack a transport system or a target for the antibiotics.
In other cases, the resistance can be due to increased efflux activity. Acquired resistance refers to bacteria that are usually sensitive to antibiotics, but are liable to develop resistance. Acquired resistance is often caused by mutations in chromosomal genes, or by the acquisition of mobile genetic elements, such as plasmids or transposons, which carry the antibiotic resistance genes Russell A.
Understanding the mechanisms of resistance has become a significant biochemical issue over the past several years and nowadays there is a large pool of information about how bacteria can develop drug resistance. Biochemical and genetic aspects of antibiotic resistance mechanisms in bacteria are shown in Figure: Which of these mechanisms prevails depends on the nature of the antibiotic, its target site, the bacterial species and whether it is mediated by a resistance plasmid or by a chromosomal mutation.
Biological strategies such as hydrolysis, group transfer and redox mechanism. A Hydrolysis Many antibiotics have hydrolytically susceptible chemical bonds e.
Some organisms produce such type of enzymes which can destroy antibiotic by targeting and cleaving these bonds. Beta-lactamase is the best example of hydrolytic enzyme that cleaves the beta-lactam ring of the penicillin and cephalosporin antibiotics. They are most commonly detected in Escherichia coli, Klebsiella pneumonia and Proteus mirabilis, but have also been found in other Enterobacteriaceae Bradford P.
B Group transfer The most diverse family of resistant enzymes is the group of transferases. By the chemical process such as adenylyl, phosphoryl or acetyl groups are added to the periphery of the antibiotic molecule and thus resistant enzymes inactivate the antibiotics Vetting M.
So, structure of antibiotics will be affected and it will lose its target site for binding. These covalent modification strategies all require a co-substrate for their activity consequently these processes are restricted to the cytoplasm. C Redox process The oxidation or reduction of antibiotics has been infrequently exploited by pathogenic bacteria. However, there are a few of examples of this strategy.
One is the oxidation of tetracycline antibiotics by the TetX enzyme. Streptomyces virginiae, producer of the type A streptogramin antibiotic virginiamycin M1, protects itself from its own antibiotic by reducing a critical ketone group to an alcohol at position However, it is possible for mutational changes to occur in the target that reduce susceptibility to inhibition. In some cases, the modification in target structure needed to produce resistance requires other changes in the cell to compensate for the altered characteristics of the target.
A Peptidoglycan structure alteration Peptidoglycan, the main component of the call wall of bacteria is the best site for antibiotic for inhibition. The antibiotic target the enzymes involving the peptidoglycan synthesis but bacteria will change the structure of that enzyme and it become resist.
The presence of mutations in the penicillin-binding domain of penicillin-binding proteins PBPs results in decreased affinity to b-lactam antibiotics. Alterations among PBPs result in ampicillin resistance among Enterococcus faecium, and penicillin resistance among Streptococcus pneumonia. Glycopeptides such as vancomycin inhibit cell wall of Gram-positive bacteria by binding C-terminal acyl-D-alanyl-D-alanine acyl-D-Ala-D-Ala -containing residues in peptidoglycan precursors.
B Protein synthesis interference Many antibiotics target the protein synthesis process to kill the bacteria. But for resistnce from antibiotic, they interfere in protein synthesis or transcription via RNA polymerase is achieved by the modification of specific target. Many groups of antibiotic like macrolide , streptogramin B block the protein synthesis by the binding with 50s ribosome subunit.
Resistance to this antibiotics, mainly Gram positive bacteria modify the 23s subunit of 50s ribosome. Mutations in 23S rRNA close to the sites of methylation have also been associated with resistance to the macrolide group of antibiotics in a range of organisms. In addition to multiple mutations in the 23S rRNA, alterations in the L4 and L22 proteins of the 50S subunit have been reported in macrolide-resistant S.
Resistance carried by the mutation the in some region of target enzyme and it altered the site. Antibiotic failed to inhibite that microorganism. Reduced outer membrane OM permeability results in reduced antibiotic uptake.
The reduced uptake and active efflux induce low level resistance in many clinically important bacteria. A Efflux pump Efflux pumps are the membrane bound proteins which throw out the undesired molecules from the cell. Efflux pumps affect all classes of antibiotics, especiallythe macrolides, tetracyclines, and fluoroquinolones because these antibiotics inhibit different aspects of protein and DNA biosynthesis and therefore must be intracellular to exert their effect.
Although some are drug-specific, many efflux systems are multidrug transporters that are capable of expelling a wide spectrum of structurally unrelated drugs, thus contributg significantly to bacterial multidrug resistance MDR. Inducible multidrug efflux pumps are responsible for the intrinsic antibiotic resistance of many organisms, and mutation of the regulatory elements that control the production of efflux pumps can lead to an increase in antibiotic resistance Nikaido H.
For example, the MexAB-OprM efflux pump in Pseudomonas aeruginosa is normally positively regulated by the presence of drugs, but mutations in its regulator mexR lead to the overexpression of MexAB-OprM, which confers increased resistance to antibiotics such as beta-lactams. Recently, a large tandem of the E.
Single component pumps transport their substrates across the cytoplasmic membrane Webber et al. Multicomponent pumps, found in Gram-negative organisms, function in association with a periplasmic membrane fusion protein MFP component and an outer membrane protein OMP component, and efflux substrates across the entire cell envelope.
B Outer membrane OM permeability changes Gram negative bacteria possess a outer membrane consisting of an outer layer contains lipopolysaccharide and inner layer contain phospholipid. So, the entry of antibiotic is slow down due to this outer membrane and transport across the OM is achieved by porin proteins that form water-filled channels.
Drug molecules can penetrate the OM employing one of the following modes: The mode of entry employed by a drug molecule largely depends on its chemical composition Tenover, F.
For example, hydrophilic compounds either enter the periplasm through porins. Antibiotics such as beta-lactams, chloramphenicol and fluoroquinolones enter the Gram-negative outer membrane via porins. As such, changes in porin copy number, size or selectivity will alter the rate of diffusion of these antibiotics. The mutation in the lipopolysaccharides, resist the entry of antibiotics.
Resistance can be either intrinsic property or acquired. Acquired bacterial antibiotic resistance can result from a mutation of cellular genes, the acquisition of foreign resistance genes or a combination of these two mechanisms. Thus, there are two main ways of acquiring antibiotic resistance: Through mutation in different chromosomal loci and 2.
A Spontaneous mutations In the replication error or in DNA repair mechanism this mutation can occur in actively diving cells. They are called growth dependent mutations and present an important mode of generating antibiotic resistance. By nucleotide point mutation, the resistance occurs and it able to produces resistant phenotype. Each pathway requires the gene expression and these variety of gene involve in antibiotic resistance for protection of bacterial cell.
There are a substantial number of biochemical mechanisms of antibiotic resistance that are based on mutational events, like the mutations of the sequences of genes encoding the target of certain antibiotics. The uptake system of antibiotic and efflux system can be modified by the mutation in regulatory system or in promoter region.
The over expression of the efflux system may confer the multiple drug resistance. Many Gram-negative microorganisms produce chromosomal beta-lactamases at low levels and mutations producing up-regulation of their expression may lead to resistance to most cephalosporins. In this particular environment resistance is achieved through chromosomal mutations that are able to produce resistance to all antibiotics used in clinical practice, without any acquisition of exogenous DNA.
B Hypermutators Low spontaneous mutation rates are maintained by the activity of many molecular mechanisms that protect and repair DNA, as well as by the mechanisms that assure high-fidelity of DNA replication. However, bacteria with hypermutable strains among natural and laboratory populations have been found.
Hypermutators have been found in populations of E.
Keywords: antibiotic resistance essay, antibiotic resistance mechanism A challenge for modern medicine Antibiotic resistance is a serious matter which .
A. General problem of antibiotic resistance to medicine. 1. Statistics. Antibiotics are chemical substances utilize to prevent and treat infections caused by microorganisms, .
The phenomenon of antibiotic resistance, only now in the world spotlight, has been present since the beginning of time. The increase in antibiotic resistance can be attributed to sociological, ecological, and genetic factors. These include overuse, random mutation, horizontal gene transfer, and selective pressure/5(11). Antibiotics use to be the talk of the medical world just fifty years go, now the talk is about trying to find a better antibiotic than the ones they came up with less than a five decades ago. Antibiotic Resistance has taking the world by storm.
Jul 30, · (WHO), antibiotic resistance is one of the world’s greatest health threats to date (Haddox, ). In the article, The Health Threat of Antibiotic Resistance, Gail Haddox () discusses the danger antibiotic resistance poses in today’s society and strategies to prevent the expansion of antibiotic resistance. Essay on Micro-Organisms and Antibiotic Resistance. suffering is the antibiotic resistance between microorganisms. Antibiotics are medicines used to kill or slow down the growth of bacteria that causes infectious diseases (Department of Health, ).