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Are going to discuss cell wall synthesis inhibitors and cell membrane integrity them so antibiotics are broadly defined as chemical agents that kill or inhibit meaning they act against wide range of microorganisms or as narrow-spectrum antibiotics may be categorized as bactericidal meaning they kill bacteria antibiotic depends largely on clinical manifestation of the
Infection as well as results the kirby-bauer method is one of the most commonly performed tests that commonly performed to determine the lowest concentration of antibiotic that mic and the lowest concentration of antibiotic that kills at least 99.9% of bacteria known as the minimum bactericidal concentration or mbc now let’s on their mechanism of action antibiotics can be
Divided into five broad membrane integrity disruptors number three nucleic acid synthesis inhibitors detail starting with cell wall synthesis for the growth and survival of bacteria it gives the bacterial cell its shape osmotic pressure that results from high concentration of proteins within the of cell wall the first one is called gram-negative and it is composed of the
Second one is called gram-positive it is composed of many interconnected layers both cell wall types their rigid and protective qualities it consists of glycan chains of alternating n-acetylglucosamine nag for short and biosynthesis of peptidoglycan is mediated by transpeptidase enzymes also catalyze the final transpeptidation reaction that results in formation of alanine
On the other strand now in order for bacteria to grow and divide a new synthesis come into play most of antibiotics belonging to this which resembles substrates for penicillin-binding protein when is formed resulting in permanently blocked active site this makes the to death of bacteria due to osmotic instability or autolysis now the namely penicillins cephalosporins
Carbapenems and monobactams that belonged to this family keep in mind that this diagram is not meant to antibiotics that can easily kill all harmful bacteria right well not so fast selective pressures which led to emergence of different resistance antibiotics is bacterial synthesis of beta-lactamases beta-lactamases are beta-lactam ring and thus destroy antibacterial
Activity in an effort to fight lactamase inhibitors that irreversibly bind to and inhibit beta-lactamase enzymes the is currently the most successful strategy that we have to combat exceptions here which are carbapenems and monobactams unlike penicillins and because they have modified beta-lactam rings in their structures that provide them with significant resistance to
Beta-lactamases examples of beta-lactamase when it comes to side-effects all beta-lactam antibiotics are likely to patients may experience allergic reactions ranging from mild rashes to life-threatening anaphylaxis now beta-lactams are not the only antibiotics antibiotics that you may frequently encounter namely fosfomycin synthesis however they accomplish that through a
Different mechanisms in order take a closer look at the enzymatic steps involved in cell wall synthesis so enzyme enolpyruvate transferase abbreviated as mura mura catalyzes to form udp-n-acetyl-muramic acid to which then three amino d-alanine racemase that converts l-alanine into d-alanine and the second incorporated into the growing peptidoglycan precursor next with the
Known as bactoprenol this is followed along with five amino acid molecules now once this cell wall proteins catalyze the final step of polymerization of n-acetylmuramic acid via transpeptidation also at the very end the bactoprenol lipid carrier now let’s go back to our four antibiotics and let’s examine how they fosfomycin acts in the first cytoplasmic step of the cell wall
Synthesis by peptidoglycan precursor and eventually leads to bacterial cell death the synthesis because of its chemical resemblance to d-alanine cycloserine when both of these enzymes are inhibited previously formed d-alanine molecules cannot be joined together again the death of bacteria now let’s move on to our third antibiotic that is vancomycin so unlike fosfomycin and
Cycloserine vancomycin works in the late stages of transpeptidation and transglycosylation during peptidoglycan binding in turn prevents linking of long polymers of n-acetylmuramic acid and cross-linking between amino acid residues in the peptidoglycan chain bacterial cell death now let’s move on to our last antibiotic that is specifically bacitracin works by binding to
Bactoprenol after it inserts the thus making it unable to regenerate and perform its job in construction of the briefly discuss their side-effects so the first one fosfomycin cycloserine has been associated with neurologic and psychiatric the third one vancomycin when administered intravenously may cause syndrome in rare instances vancomycin may also cause nephrotoxicity
Lastly bacitracin when used topically rarely causes side-effects other than nausea vomiting allergic reactions and nephrotoxicity may occur so the cell wall synthesis in species of bacteria that both however there is one more type of bacterial cell that presents a mycobacteria are highly pathogenic organisms that are mycobacteria are notorious for their ability to resist
Most antibiotics one cell wall the mycobacterial cell wall is made up of five major components arabinogalactan surrounded by a thick layer of mycolic acid essential to the survival of mycobacteria couple of antibiotics has been target mycobacterial cell wall synthesis are well-known briefly discuss their primary mechanism of action so the first one isoniazid activated by
Bacterial catalase-peroxidase enzyme called katg once and thereby inhibits the enoyl-acyl carrier protein reductase abbreviated as inha now inha is a member of the type 2 fatty acid system which elongates long-chain fatty acids for the synthesis of mycolic acid inhibition of mycolic acid synthesis in turn leads results in bacterial cell death now let’s talk about our second
Drug that is inhibition of membrane associate enzyme called arabinosyl transferase embb arabinogalactan an essential component of the mycobacterial cell wall so as a allowing toxic substances to enter the cell now when it comes to major side while ethambutol optic neuritis that can lead to vision loss now before antibiotics that is cell membrane integrity disruptors target
Primarily the cell membrane of bacteria prominent members of this mechanism of action the first antibiotic daptomycin works by forming a complex aggregate within the membrane to form pore-like structures that allow ions potential and eventually cell death now in contrast to daptomycin which targets membrane of gram-negative bacteria specifically polymyxins initially bind
Turn allows polymyxins to enter in and disrupt the inner cytoplasmic membrane bacteria now when it comes to major side-effects daptomycin may cause skeletal muscle with that i wanted to thank you for watching i hope you enjoyed this video
Transcribed from video
Pharmacology – ANTIBIOTICS – CELL WALL & MEMBRANE INHIBITORS (MADE EASY) By Speed Pharmacology
