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Discovery of blaNDM-1 β-lactamase in plasmids of Escherichia coli and Pseudomonas aeruginosa and unresponsiveness of such infections to most antibiotics including imipenem and dorripenem shocked the whole drug industry in 2009 as well as discovery of mcr-1 gene in 2016 orchested such horror being colistin drug was useless now. We have checked such horror in Ganga River water which contains superbugs, resistant to most common antibiotics including methicillin, lomofloxacin, amikacin, imipenem, linozolid and vancomycin. Beta-lactamases (TEM, OXA, CTX-M, CMY, GIM, VIM, NDM, KPC), drug modifying acetyl/phospho/adenyl transferases and drugs efflux proteins (tetA/C, mexAB/CD/EF) are mostly diversified and mutated creating hundred to thousand isomers. Many MDR genes are accumulated now in large MDR conjugative plasmids and it is almost impossible to PCR identify all MDR genes in any clinical isolate for better prognosis and therapeutics. From in silico protein alignment studies, we concluded that blaNDM-1 gene might be originated from the rearrangement of other Metallo-β-lactamases genes present in same plasmids or multiple integrons. This conclusion supports our previous studies with Kolkata superbugs Escherichia coli KT-1_ MDR and Pseudomonas aeruginosa DB-2_ MDR which contain multiple small as well as large plasmids with many diverged MDR genes and transposons. Presence of ThiX gene (in pKOX_R1 plasmid) involved in Thiamine biosynthesis suggests the bacteria need vitamin synthesizing enzymes in plasmid if we continue high dose complex antibiotic intake. Thus many IS-elements and transposons are assembled in MDR plasmids for new MDR gene creation to save symbiotic relation between gut microbiota and human metabolosome.