In this lecture, we are going to discuss vancomycin and its related antibiotic. Vancomycin is basically a glycopeptide antibiotic that actually inhibits the peptidoglycan synthesis. So basically, if we categorize the vancomycin, vancomycin is basically a glycopeptide antibiotic. So in the glycopeptide, you will see the vancomycin, vancomycin, and another antibiotic that is teicoplanin. So there are basically the two antibiotics that are actually glycopeptide in nature, okay? And there are also certain antibiotics that are lipoglycopeptide in nature. That includes dalbavancin, okay? Dalbavancin, oritavancin, and telavancin. These are basically the lipoglycopeptides. So we are going to discuss the mechanism of all of them because the mechanism of action of the glycopeptide and the lipoglycopeptide is similar. So that's why we are discussing.

the wenyin along with the tlin delba venin orav venin and the Tila venin. First of all, we will discuss the normal mechanism of the peptidoglycan synthesis. We will specifically discuss the S orus peptidoglycan synthesis stoc cus or yes pepo glycan. So basically, Pepto glycan has two most important components: glycan chain and the peptide linkage. So if you see here, this one n and the neag is basically the glycan chain, and in between the N neck chain, you will see the presence of the peptide linkage. Okay, so if you see the monomers of the Pepto glycan, so that's include the n n and atile and atile muramic acid and the nag and atile glucosamine. Okay, along with that, you will see at the Nam side, you will see the pentapeptide. You will see the attachment of the five amino acids that is actually called the pentapeptide. So in the amino acid, you

will see the L-alanine, D-glutamine, L-lysine, D-alanine, and the D-alanine. So, here are basically the five amino acids that are actually called the pentapeptide: L-alanine, D-glutamine, L-lysine, D-alanine, and D-alanine. So, here are basically the five units of the glycine (Gly). Okay, so it is basically the monomers. Okay, similarly, you will see the NAG (N-acetylglucosamine) and at the N side, you will again see the pentapeptide five amino acid segment similar to the previous one. Again, you will see the N-NAG and the five pentapeptide and along with that, you will see the presence of the glycine unit again. This is the unit. Okay, so basically two enzymes involved in the linkage of the glycine and peptide. Okay, so the most important enzyme that is actually involved in the linkage of the glycine here is the linkage and that linkage happens in the presence of the enzyme.

and that enzyme is actually called the transglycosyl enzyme, so G transglycosylase enzymes involved in the linkage of the n and the neag. That process is actually called the transglycosylation, okay? But in the linkage of the pentapeptide, you will see, first of all, breakage of the terminal deanine, so it is basically the last dine. Similarly, here is the dine. You will see the cleavage of the terminal dine at both sides, and as a result, you will see the release of the energy, and that energy is helpful in the linkage of the glycine side chain with the second D alanine, okay? And also, this process happens in the presence of the enzyme that is the trans pep days, okay? That's the most important thing in the linkage of the glycine with the second dine. Two things required: first is the transp enzyme, and second thing is the energy due to the cleavage of the Terminal D alanin at both sides. That is the normal process that happens.

in the synthesis of the peptidoglycan, how VY and its related drugs actually inhibit the peptidoglycan synthesis. So, similar process here is the monomer, monomers, and this is again the monomer, four monomers actually present in that case. First of all, you will see vancomycin binds to the D-alanine terminal. If I say here is the vancomycin, and the vancomycin will bind to the D. Here is the D-alanine, D-alanine, because at the last side, you will see the presence of the D-alanine. Okay, if you see the binding of the vancomycin with the D-alanine, then there is no cleavage of the D-alanine terminal cleavage, and ultimately, there will be the N-linkage of the glycine with the second D-alanine. And as a result, the activity of the transpeptidase will be inhibited when there is no binding site for the transpeptidase enzyme. So, that's why how vancomycin inhibits the.

transpeptidase. Along with that, when you see the inhibition of the transpeptidase, then you will also see the hindrance of the transglycosylation. So, that's the most important thing. Vancomycin inhibits two processes: transpeptidation (linkage of the peptide) and also inhibits the transglycosylation (linkage of the glycine subunits). So, this is how vancomycin and its related drugs inhibit the peptidoglycan synthesis. Okay, but certain bacteria develop resistance. Okay, that bacteria develop resistance by changing the terminal D-alanine. They change the D-alanine with the D-lactate. They change the D-alanine with the D-lactate. And as a result, you will see there is no binding of the vancomycin with the D-lactate at this terminal side. Here is the D-lactate. That is how different bacteria develop resistance against vancomycin. Okay, if we look at the spectrum of vancomycin, so basically it covers the gram-positive bacteria. Gram-positive bacteria that includes the

mara meth resistance SL cus Rus Mercy methene resistance stus epidermidis and and terus species and they can also use for the penicillin resistance streptococus numon that is streptococus and these are basically the stoc focus okay that's the most important thing and they can also use for the clust stre medium defile but important thing which you have to remember for the treatment of the Clum you will give the vancomycine in the oral form because vomisin is poly absorbed from the G tract so basically Clum present in the G tract so that's why if you give the Venoy through the AAL Ru then it will be helpful in the treatment of the CLA rium but not for the treatment of the other infections okay that is the important thing which you have to remember okay but with the passage of the time certain species of the Mera and the enti cus develop against the wenyine okay so that is that

will be the vomiting resistance status orus and the vomiting resistance and cus species. There are certain species that actually develop resistance against the vancomycin. If we discuss the dosage regimen of the vancomycin, so we will discuss it with the graph. We will take the time on the x-axis and the concentration of the drug on the y-axis. If we give the first dose of the vancomycin, then you will see the peak formation. Okay, here is the peak formation. That is actually the peak. Okay, and after that, you will see the decreased concentration of the vancomycin in the blood. Okay, so this is actually the first dose duration. Okay, after that, if you give the second dose, you will also see the increase in the concentration, and after that, you will see the TRU formation. TRU formation at that side, and again, you will see the peak formation. That second peak will be produced by taking the second dose. Here is the first dose, and here is the second dose. That's the

Most important thing, trough will decide the proper doors of the vancomycin. So, trough of the vancomycin should be 10 to 20 micrograms per ml. That is the trough concentration of the vancomycin. Okay, if you see here is the area under the curve, that is actually called the AUC, okay. And after that, you will also see the MIC, minimum inhibitory concentration, minimum concentration of the vancomycin to inhibit the different bacteria, okay. So, ratio of the area under the curve and the minimum inhibitory concentration will decide the optimal dose of the vancomycin. So, if you see the ratio, okay, so here is the ratio. In the ratio, you will see the area under the curve, our minimal inhibitory concentration. So, that should be 400 or greater than 400. So, it means that if the area under the curve is high, then the ratio will also be high. So, it means that area under the curve, large area under the curve will produce the large ratio.

and minimum inhibitory concentration. Low minimum inhibitory concentration means a large ratio, so that is the area under the curve in the direct relation, but the minimum inhibitory concentration will be in the reverse relation. So, actually, that ratio will decide the optimal dose of the vancomycin. Okay, if we discuss the adverse effects, so the most important adverse effect of the vancomycin is the red man syndrome. So, red man syndrome. So, in this syndrome, you will see the flushing of the skin due to the release of histamine from the basophils and the M cells due to the interaction of the vancomycin with these cells. So, it will result in the red man syndrome due to the vasodilation. Okay, next, you will see ototoxicity. Ototoxicity, hearing difficulty by taking the vancomycin, and also you will see nephrotoxicity. Nephrotoxicity is very much important. If the patient has renal failure, then the concentration of the vancomycin should be maintained accordingly because aminoglycosides are actually

executed through the kidney. Okay, next we will see the fever and the chill, fever and the chill in that case. And you can also see the last adverse effects of the vancomycin is the phlebitis, inflammation of the veins. So, this is all about the mechanism, classification, spectrum, and the adverse effects of the vancomycin and its related drugs. If you still have any questions, you may ask in the comment section. Thank you so much.

Vancomycin | Mechanisms | Spectrum | Dosage | Adverse Effects

Vancomycin | Mechanisms | Spectrum | Dosage | Adverse Effects

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