The β-lactamases mediated degradation is the most common resistance mechanisms to β-lactam based drugs. The evolution of b-lactamase coding genes started long before the discovery and delivery of the first penicillins, presumably under the selective pressure of natural b-lactam compounds produced in different natural microbial ecosystems. However, recently - in an evolutionary time scale – the overuse of β-lactams has applied a strong selection, so favoring both evolution and spreading of resistance genes. Among the known b-lactamases, those able to inactivate carbapenems are some oxacillinases and, mainly, the Metallo-beta lactamases (MBLs) that comprise three “B” classes and the recently discovered New Dehli Metallo-β-lactamase (NDM-1). The majority of the metallo-β-lactamase is encoded by chromosomal genes and in mainly environmental bacterial species. It is very likely, therefore, that both the still unknown ancestral genes of MBL and the source of the mobile elements recently appeared in hospital Gram - negative isolates, could be found in the environmental microbiota. The studies in this field focused on B3 class with the discovery and characterization of the enzyme THIN-B of Janthinobacterium lividum, and the post-genomic cloning and characterization of the enzyme CAU-1, from Caulobacter crescentus. In 2011 a new B3 metallo-β-lactamase (POM-1) was detected and described in the newly defined species Pseudomonas otitidis, found from either environmental samples or from clinical specimens.