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Antimicrobial resistance.pptx

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Antimicrobial resistance.pptx

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This slide give you deep knowledge about antimicrobial resistance.
Antimicrobial resistance happens when germs like bacteria and fungi develop the ability to defeat the drugs designed to kill them. That means the germs are not killed and continue to grow. Resistant infections can be difficult, and sometimes impossible, to treat.

This slide give you deep knowledge about antimicrobial resistance.
Antimicrobial resistance happens when germs like bacteria and fungi develop the ability to defeat the drugs designed to kill them. That means the germs are not killed and continue to grow. Resistant infections can be difficult, and sometimes impossible, to treat.

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Antimicrobial resistance.pptx

  1. 1. Resistance Dr. Asif Anas Director Genomia Diagnostics Research Pvt. Ltd. New Delhi
  2. 2. Classification antibiotic resistance mechanisms 1. On the bases of gene 2. On the bases of action On the bases of gene i. Innate drug resistance mechanisms ii. Acquired drug resistance mechanisms a. By accruing mutation in gene b. By accepting drug resistance gene
  3. 3. On the bases of action i. Preventation of drug access to target a. Reduced permeability b. Increase the activity of efflux pump ii. Change in antibiotic target a. Modification (Protection) of drug target b. Mimicry of drug target iii. Direct modification of antibiotics a. Inactivation of antibiotics by transfer of chemical group b. By hydrolysis iv. Epigenetic drug tolerance
  4. 4. i. Presentation of drug access to target a. Reduced permeability • The outer membranes of Gram negative bacteria work as a permeable barrier in inhibit penetration of antibiotic. • Outer-membrane porin proteins were used by hydrophilic antibiotics to cross the outer membrane by diffusing. • In this case bacteria reduced their membrane permeability by changing their porins with more-selective channels. • These more selective channels are the result of mutation in gene encoding channel.
  5. 5. (Blair et al., 2015)
  6. 6. Increase the activity of efflux pump • Intrinsic resistance Gram-negative bacteria flush out antibiotic by bacterial efflux pumps that lead to bacteria escape from antibiotic. • In this case these efflux pumps overexpress their activity and confer high levels of resistance to previously useful antibiotics. • Overexpress efflux pumps can transport a large number of structurally dissimilar substrates and become multidrug resistance (MDR) efflux pumps. • There is large number of MDR efflux pumps already discovered and new MDR pumps is reporting continuously. • Ex. fuaABC in Stenotrophomonas maltophilia, mdeA in Streptococcus mutans, lmrS in S. aureus and kexD in K. pneumonia
  7. 7. ii. Change in antibiotic target a. Modification (Protection) of drug target • 23S rRNA ribosomal subunit of Gram-positive bacteria targeted by linezolid (the first oxazolidinone antibiotic). • The 23S rRNA ribosomal subunit have multiple allele, it bacteria acquire mutation in one of these copies and alter the antibiotic target, provide resistance from antibiotic than recombination between homologous allele take place which increase population of bacteria harboring mutant allele. • Without mutation into target gene bacteria can modify their target protein to provide resistance against antibiotic. • For example, the erythromycin ribosome methylase (erm) family of genes methylate 16S rRNA and alter the drug-binding site, thus preventing the binding of macrolides, lincosamines and streptogramins
  8. 8. (Blair et al., 2015)
  9. 9. Mimicry of drug target • This type of resistance mechanisms can be seen in fluoroquinolones. The fluoroquinolones are synthetic antibiotics, can restrict the growth of microorganisms by inhibit the transcription, DNA replication, and repair. • The mfpA gene in mycobacteria was first recognised showing low-level resistance to fluoroquinolones. • MfpA protein has maximum similarity to pentapeptide repeat proteins. The structure of mfpA protein of mycobacteria is nearly similar to the double helix DNA, and have cyclic pentapeptides coiled as right handed helix with same width as of DNA. • It is reported that DNA structure was mimicked by mfpA protein to deviate the fluoroquinolones.
  10. 10. iii. Direct modification of antibiotics By enzymatic hydrolysis • The hydrolysis of antibiotic by bacterial enzyme is a major resistance mechanism that has been prevalent since the use of first antibiotic penicillin which is a β-lactam antibiotic hydrolyzed by β-lactamase. • Till date, numbers of enzymes have been reported that can modify and degrade antibiotics of different classes, including β-lactams, phenicols, aminoglycosides and macrolides. • The enzyme β-lactamases exist in diverse range and can degrade dif- ferent antibiotics within the same class; for example penicillins, carbapenems, clavams, cephalosporins and monobactams.
  11. 11. (Blair et al., 2015)
  12. 12. Inactivation of antibiotics by transfer of chemical group • Bacterial enzyme added the chemical group on antibiotic and alters its original structure. Structurally changed antibiotic lose their activity due to hindrance with target. • There many antibiotic resistance enzyme which can transfer various chemical groups including acyl, nucleotidyl, phosphate and ribitoyl groups. • Aminoglycoside-modifying enzymes provide resistance to bacteria by adding hydroxyl and amide groups to aminoglycoside group of antibiotics. • Aminoglycoside-modifying enzymes are classified in three major groups: phosphotransferases, acetyltransferases and nucleotidyltransferases.
  13. 13. iv. Epigenetic drug tolerance • Epigenetic drug tolerance different kind of drug resistance tool, noticed in mycobacteria generally found latent or relapsed TB cases. • This type of drug resistance nullify the antibiotic activity when mycobacterial cell enter in dormant condition in case of latent or relapsed TB. • Mycobacterial cell slow down its growth in latent or relapsed TB cases by minimise their metabolic activity. So there is no or less requirement of metabolites or protein to the cell. • Thus, there is no lethal inhibition in dormant bacterium even when antibiotics targets their object. • Treatment of persister cells in case of latent infections is much challenging as than treatment of dividing cells in active tuberculosis.
  14. 14. Causes of Antimicrobial (Drug) Resistance 1. Inappropriate Use • Selection of resistant microorganisms is exacerbated by inappropriate use of antimicrobials. Sometimes healthcare providers will prescribe antimicrobials inappropriately, wishing to placate an insistent patient who has a viral infection or an as-yet undiagnosed condition. 2. Inadequate Diagnostics • More often, healthcare providers must use incomplete or imperfect information to diagnose an infection and thus prescribe an antimicrobial just-in-case or prescribe a broad-spectrum antimicrobial when a specific antibiotic might be better. These situations contribute to selective pressure and accelerate antimicrobial resistance.
  15. 15. 3. Hospital Use • Critically ill patients are more susceptible to infections and, thus, often require the aid of antimicrobials. The extensive use of antimicrobials and close contact among sick patients creates a fertile environment for the spread of antimicrobial-resistant germs. 4. Agricultural Use • Scientists also believe that the practice of adding antibiotics to agricultural feed promotes drug resistance. There is still much debate about whether drug-resistant microbes in animals pose a significant public health burden. 5. Gene Transfer • Microbes also may get genes from each other, including genes that make the microbe drug resistant. Bacteria that have drug-resistant DNA may transfer a copy of these genes to other bacteria. Non-resistant bacteria receive the new DNA and become resistant to drugs.

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