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1 number 8 Done by Corrected by Doctor Dr Hamed Al-Zoubi 25 10/10/2017
2
3 Antibacterial therapy 2 د. حامد الزعبي Dr Hamed Al-Zoubi Antibacterial therapy Figure 2/ Antibiotics target
4 Inhibition of microbial protein synthesis Act at: Site of protein synthesis (ribosome) Tetracyclines (static), aminoglycosides (cidal), chloramphenicol (static) and macrolides (static), e.g erythromycin, clindamycin (static).
5 Aminoglycosides Aminoglycosides Gentamicin, amikacin G-ve aerobics and synergism with B lactams Mechanism: Bind to 30s subunit and Inhibit formation of ribosomal initiation complex Misreading of the mrna Side effects: ototoxicity and nephrotoxicity Drug level monitoring is required
6 Chloramphenicol Chloramphenicol Broad spectrum Mechanism: see Fig. Uses are limited because because of the occurrence of a rare but Some side effects; Aplastic anaemia!!!, grey baby syndrome!!!.
7 Macroilides Macrolides: Erythromycin, clarithromycins, azithromycin (good tissue penetration and a long terminal half-life) and telithromycins Used mainly as antistaphylococcal and antistreptococcal agents, though some have wider applications (broad spectrum) Clindamycins: G+ve,pseudomembranous colitis
8 Tetracycline Broad spectrum Inhibit binding of trna to ribosome leading to failure of peptide chain elongation G-ve, +ve, mycoplasma, rickettsia and malaria Tetracycline, doxycycline and tigecycline. Some side effects: Stain developing teeth, Discolor permanent teeth (yellow-gray brown), from infancy and childhood to eight years old and adulthood, Affect bone growth of the fetus, so should be avoided during pregnancy Fusidic acid has an unusual spectrum of activity that includes corynebacteria, nocardia and M. tuberculosis; But the antibiotic is usually regarded simply as an antistaphylococcal agent. Peptide elongation inhibition Penetrates well into bone Mupirocin: Topical anti MRSA
9 Linezolid is an oxazolidinone It is a narrow-spectrum anti-gram-positive agent Acts by preventing the formation of the ribosomal initiation complex. It is used exclusively against MRSA andother Gram-positive cocci resistant to older agents There is some evidence that it may be of use in drug-resistant tuberculosis. Inhibition of folate synthesis Sulphonamides and diaminopyrimidines as Trimethoprim Trim is less toxic Available as combination, Co-trimoxazole, or separately. G-ve and +ve aerobes
10 Inhibition of nucleic acid synthesis and function A. INHIBITORS OF RNA SYNTHESIS AND FUNCTION Rifampicin (bactericidal) a. Mode of action These antimicrobials bind to DNA-dependent RNA polymerase and inhibit initiation of mrna synthesis b. Spectrum of activity They are wide spectrum antibiotics but are used most commonly in the treatment of tuberculosis, leprosy and MRSA c. Combination therapy Since resistance is common, rifampicin is usually used in combination therapy and usually reserved for TB.
11 Inhibition of nucleic acid synthesis and function B. INHIBITORS OF DNA SYNTHESIS AND FUNCTION Quinolones - nalidixic acid (G-ve), ciprofloxacin (plus pseudpmonas and G +ve) and gemifloxacin (and some anaerobes) Bactericidal Mode of action These antimicrobials bind to the A subunit of DNA gyrase (topoisomerase) and prevent supercoiling of DNA, thereby inhibiting DNA synthesis. Absorbed well orally, good body distribution Children, pregnant and breast feeding!!! Inhibition of nucleic acid synthesis and function C. DNA STRAND BREAKAGE 5- Nitroimidazole e.g metronidazole Mechanism: At low redoox values they are reduced to a short intermediate form that damages the bacterial DNA So, the expected bacterial activity is against
12 Anti TB drugs Isoniazid and Ethionamide - chemically related - blocks mycolic acid synthesis Ethambutol - blocks arabinogalactan synthesis Rifampicin Resistance Resistance: meaning? Terms: Intrinsic or inherent: no target site or cell wall is impermeable to antibiotics as in gram negative bacteria (vancomycin is too big to cross the cell wall) Acquired resistance: Selection of resistant bacteria by antibiotics Common in areas of heavy antibiotic use e.g hospitals The resistance is initially emerged by genetic process then selected by antibiotics next figure
13 Cross resistance: Resistance to one member of a family will result in resistance or decreased susceptibility to other members within the same family e,.g fluroquinolones, Penicillins and Cephalosporins Multiresistance: Resistance to more than one antibacterial Usually acquired by separate mechanisms
14 Extra wrinkle here Doctors/nurse precribers are not the only culprits!!! > examples of R bugs due to agricultural overuse/misuse?? NB the food chain!! Genetics of resistance: 1. Intrinsic: No target 2. Acquired: A. Chromosomal mutations Single step mutation in the antibiotic target leading to decreased antibiotic efficacy (needs high concentration of antibiotic). Multistep mutations: Leading to complete resistance e.g: penicillin binding protein B. Transferable via Genetic transfer (plasmids and Tn)
15 Mechanism of resistance: FIGURE 1. Decreased accumulation: Decreased permeability secondary to porins mutations Increased efflux (pumping out the antibacterial using expressed efflux pump) 2. Modification of the target: Sequence mutation leading to target alteration: > Pneumocoocus resistance to penicillins > Quinilones Target bypass: Supplementary enzymes will do the same target function but without binding to the antibacterial agent e.g Meticillin resistant staph aureus MRSA Target hyperproduction: More drug is needed to inactivate the target
16 3. Inactivation of the antibacterial agent: β lactamase is an enzyme produced by the bacteria This enzyme will destroy the β- lactam ring (this is an essential ring in penicillins and cephalosporins) leading to inactivation of the antibacterial agent > Some types of bacteria produce a β- lactamase with a wide range of activity (ESBLs) Acetylating, adenylating and phosphorylating enzymes: Produced by bacteria (gram negative bacteria) and cause resistance to aminoglycosides and chloramphenicol Resistance
17 The End
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