We are aware of the fact that Vancomycin 1.0—has been used since 1958 to combat dangerous infections like methicillin-resistant Staphylococcus aureus. But due to the increase in the population of resistant bacteria the efficiency Vancomycin 1.0 has reduced and the need for a more potent versions of the drug. Thus, Vancomycin 2.0 was engineered.
Now, version 3.0 has a unique three way approach to kill bacteria that gave doctors a powerful new armament against drug-resistant bacteria and help researchers engineer more durable antibiotics.
Scott Miller, a chemist at Yale University said that it was pretty special and it was really the conclusion of a decades-long effort.
Mechanism of action of Vancomycin:
Vancomycin recognizes and binds to the two D-ala residues on the end of the peptide chains. However, in resistant bacteria, the last D-ala residue has been replaced by a D-lactate, so vancomycin cannot bind. In resistant bacteria, cross-links are successfully formed. However, in the non resistant bacteria, the vancomycin bound to the peptide chains prevents them from interacting properly with the cell wall cross-linking enzyme. In the resistant bacteria, stable cross-links are formed and cell wall synthesis is not halted.
According to the U.S. Centers for Disease Control and
Prevention, about 23,000 Americans die from 17 antibiotic-resistant infections each year.To rectify the D-lac problem, researchers led by Dale Boger, a chemist at the Scripps Research Institute in San Diego, California, began formulating new versions of vancomycin that attach to peptides ending in D-ala and D-lac. They succeeded in 2011 which became version 2.0 of the drug. Meanwhile, other groups developed new ways of killing bacteria with vancomycin: One type of modification found a new way to halt cell wall construction, whereas another caused the outer wall membrane to leak, leading to cell death.
