When a last resort life saving drug too don't work in patients because of development of drug resistance, patients life may get seriously affected, but now one of such a life saving drug too is designed to even work in such situation by not allowing virulent bacteria to develop antibiotic resistance.
Antibiotic vancomycine, is used as a last resort drug in critical situation in patients infected with gram positive bacteria and for individuals on dialysis, virulent strain of staphylococcus aureus which is resistant to drug methicillin (MRSA methicillin resistant s.a ) and to one who have not responded to methecill and all other antibiotics have failed to provide their antimicrobial activity because of development of antibiotic resistance by disease causing microorganisms.
It was observed that vancomycine too develop antibiotic resistance in some cases, resulting in life threatening situations.
The challenge is now answered by the scientists from The Scripps Research Institute have successfully developed a molecule which is a synthetic analog of vancomycin, which has antibiotic properties of vancomycin and do not develop resistance against vancomycine while providing its desired antimicrobial effect .
They have designed the molecule of vancomycin so that the molecule stays intact even in the event of mechanism of resistance is activated by disease causing bacteria with a small molecular change.
How it works:
Mechanism of action of Vancomycin and mechanism of development of resistance
Gram positive bacteria consist of a outer cell wall which is made up of peptidoglycan a complex of carbohydrate and protein which protects bacteria from chemical as well as from physical strain. Vancomycin owing to its structural properties is capable of forming a hydrogen bonding with peptidoglycan proteins , D-alanyl-D-alanine, aminoacids sequence in the process of cell wall synthesis, it forms hydrogen bonding with amide groups in vancomycin molecule resulting in to halting cell wall synthesis killing bacterial cell.
The bacterial resistance occurs as bactria now replace D-alanyl-D-alanine with D-alanyl-D-lactate or D-alanyl-D-serine because of mutation in genes.
Because of changes in amino acid sequence in mutant, the formation of hydrogen bonding of these amino acids in cell wall synthesis steps with vancomycin is hampered because of stearic hindrance(special arrangement in a molecule or clustering of molecules so as to hinder the activity around the active point).
Now the altered analog of Vancomycin molecule is developed by replacing amide with thioamide a one point change in molecule, replacing oxygen with sulfur now shows activity even in case bacteria produces resistance.
Professor Dale L. Boger is the senor author of the research he is from The Scripps Research Institute.
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