Pseudomonas aeruginosa a gram negative bacteria, belong to family Pseudomonadaceae, ubiquitous in nature found in different habitats. It is differentiated from Enterobacteriace due their non-fermenter nature. Clinicaly it is consider main source of nosocomial infection throughout the world. It normally cannot cause infection in healthy individuals however immunocompromised or those that under surgeries or have some burns or lung infections are considered its common hosts. Beside its capabilities to cause infections it harbors various resistance mechnisims including, extended spectrum beta-lactamases, outer memberane proteins and efflux pumps etc. It produces different pigments and biofilm formation and expression of virulence factors which contribute in pathogencity of P. aeruginosa. In current study total of (n=3700) clinical samples were screened in which (n=102) isolates were characterized as P. aeruginosa on the basis of morphological and biochemical characterstics. Further confirmations were performed by using species-specific PCR and 16s rRNA sequencing. Samples were further analyzed for antibiotics susceptibilities and minimum inhibitory concentration determination using proper procdures. β-lactamases were confirmed using both phenotypic and molecular approaches. Further squecning of TEM, CTX and OXA were performed and later on analysed using bioinformatics approach. Virulence factors production including pigment production, biofilm formation and detection of virulence genes were scrrened in β-lactamases producing isolates. In current observations the persistence of P. aeruginosa was very common in pus specimens that were isolated from patients that have injuries or some surgeries. As current study revealed that MDR isolates are prevalent in our community which mount high risk for immunocompromised or patients under observations. Higher incidence were reported in male patients. It showed worst resistance (more than 90%) to beta-lactamases inhibitors, doxycycline, chloramphenicol and sulphamethoxazole/trimethoprim while less to imipenem, amikacin and cefoperazone/sulbactam. There were (16.6%) isolates that exhibits resistance to all groups of antibiotics which is very alarming. As carbapenems are the last hope for MDR so increasing resistance in P. aeruginosa make hindrance for future strategies of treatment. These MDR isolates also harbour TEM-116 having homology with TEM-1 but different by only two amino acids substitution. TEM-116 in P. aeruginosa was the first report from Pakistan. It has shown resistance to most of the antibiotics and showed (100%) resistance to sulphamethoxazole/trimethoprim, amoxycillin/clavulanic acid and doxycycline while one isolate was found that mount resistance against all antibiotics that were used in current study. Most of TEM-116 possessing isolates were found susceptible toward fluoroquinolones and aminoglycosides. In β-lactamases production large number of isolates bear metallo-β-lactamases (MBLs) followed by Extended-spectrum-β-lactamases (ESBLs) and AmpC which stipulate that increasing number of isolates possess β-lactamases. Phenotypically coproduction of β-lactamases were also observed in some isolates. Its molecular genotype TEM-116 was the most prevalent followed by CTX-M-15 and OXA-10 highlighting its spread in population. The incidence of CTX-M-15 were higher as compare to OXA-10. Higher number CTX-M-15 exhibit ESBL phenotype followed by MBL and AmpC while in some isolates there was coproduction of more than one phenotype. While some CTX carrying P. aeruginosa did not express any β-lactamase phenotype. In case of OXA-10 most of isolates express MBL phenotype. One isolate that bear TEM enzyme was resistant to all available antibiotics that were used in current study. These genotypes were first type reported in P. aeruginosa from Pakistani origin. These pathogens are capable to express other genotypes, should not be ignore as further planning should be done. Pathogenicity has strong correlation with antibiotic resistance and production of virulence factors. These isolates cherish virulence factors which make further difficulties for patients as well clinicians. Most of isolates were found produce pigments production and biofilm formation in the studied isolates. Along with biofilm formation most of the β-lactamases producer were found to release virulence factors including Exo-s, Tox-A, Las-B, Plc-H and both Opr-I and Opr-L. As virulence factors mainly contribute in the pathogenesis so whenever there is resistance strains which produce these toxins or some may involve in biofilm formation, the treatment of patients become difficult. As the contemporary study presents composite concept of drug resistance and β-lactamases in P. aeruginosa clinical isolates. CTX-M-15, OXA-10 and TEM-116 first time reported from Pakistan demonstrate the potential risk to be spread in the community. Also this was the first attempt to explore P. aeruginosa for their virulence factors contribution in clinical settings in Pakistan. To avoid its further spread proper diagnostic facilities, well trained staff and strict prescription of antibiotic policy should be adopted by clinicians. Also proper surveillance studies and updated data base should be maintained. MDR persistence in clinical samples strengthen the concept of its spread in other Enterobacteriaceae. CTX have insertional sequences which help in spread other Enterobacteriaceae. It need further screening to explore other mechanisms like PER, IMP VIM or NDM as have been reported in other parts of world.