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Acinetobacter baumanii has emerged as an important opportunistic pathogen within the hospital environment, being able to colonize and produce infections in ventilator associated pneumonia, secondary meningitis, urinary tract, septicaemia and other conditions in intensive care unit (ICU) patients. It is also causing infections in other immunocompromised patients, including burns patients. Antimicrobial treatment of such severe infections is complicated by a wide spread multidrug resistance pattern. One of the most striking features of A.baumanii is its extraordinary ability to develop resistance against major antibiotic classes by various mechanisms. A. baumanii resistance is mediated by the presence of mechanisms such as various enzymes, penicillin binding protein alterations and reduced penetration across the outer membrane. In isolates of A. baumanii, sometimes there can be co-expression of multiple mechanisms in the same isolate, resulting in total resistance with the exception of colistin and tigecycline. Beta-lactam resistance appears to be primarily caused by β-lactamase production, including the extended spectrum β-lactamases, AmpC beta-lactamases, metallo-βlactamases and oxacillinases. Other modalities of beta-lactam resistance are antibiotic target site alterations, efflux pumps and finally porin channel deletion, which also appears to contribute to β-lactam resistance. Because of the multiple antibiotic resistance exhibited by A.baumanii, serious infections caused by this organism are difficult to treat. In A.baumanii, phenotypic tests can be used to detect resistance to various β-lactam group drugs via ESBLs, AmpC, and MBL, but for others it is necessary to resort to molecular mechanisms. Phenotypic testing may also be misleading, especially when both ESBL and Amp C β-lactamases co-exist and mask each other, which results in misreporting and failure in clinical treatment of patients. For this reason, different inhibitors have been used to improvise the phenotypic tests for B-lactamase detection. In patients suffering from burns infected with these drug resistant pathogens, their detection and that of their resistance patterns becomes a priority in order to avoid further complications, as well as to commence appropriate antibiotics. In our study, we considered the detection of all three of these β-lactamases in A. baumanii, which were Annals of Burns and Fire Disasters Pending Publication