Background: The emergence of AmpC beta-lactamase producing Enterobacter cloacae becomes a serious nosocomial menace due to wider resistance. The study aimed to know the existence of these superbugs in the hospital settings and to report the current trends in their antibiotic resistance. Methods: We chose a tertiary care pediatric hospital for this cross-sectional study and processed 27,000 clinical specimens for the isolation of E. cloacae using routine microbiological procedures. A total number of 96 E. cloacae isolates from various sources were screened for AmpC production with cefoxitin (30 mu g) and confirmed by inhibitor based technique. The antibacterial drug resistance studied against various groups of antibiotics in vitro. Results : Boronic acid inhibitor based method revealed 63 (65.6%) pathogens as AmpC beta-lactamase producing E. cloacae. Most of the infected patients with AmpC producing E. cloacae were neonates (34; 54.0%) and infants (11; 17.5%). The primary source of AmpC producing E. cloacae was blood (43; 68.3%), and they were frequently distributed in the neonatal nursery unit (33; 52.4%) and medical ward (13; 20.6%). All of these bugs showed a high level of resistance (100%) against the co-amoxiclav and cephalosporin group.The organisms exhibited less resistance to levofloxacin, imipenem and colistin sulphate as 23 (36.5%), 20 (31.7%) and 17 (27.0%), respectively. Conclusion: The consistent emerging threat of Amp C harbouring E. cloacae could disseminate AmpC genes in other genera of the bacteria which lead to the therapeutic failure and leave the doctors with limited treatment options of levofloxacin, imipenem and colistin sulphate.

Multi-drug resistant (MDR) bacteria and their biofilms are a concern in veterinary and human medicine. Protegrin-1 (PG-1), a potent antimicrobial peptide (AMP) with antimicrobial and immunomodulatory properties, is considered a potential alternative for conventional antibiotics. AMPs are less stable and lose activity in the presence of physiological fluids, such as serum. To improve stability of PG-1, a hybrid peptide, SynPG-1, was designed. The antimicrobial and antibiofilm properties of PG-1 and the PG-1 hybrid against MDR pathogens was analyzed, and activity after incubation with physiological fluids was compared. The effects of these peptides on the IPEC-J2 cell line was also investigated. While PG-1 maintained some activity in 25% serum for 2 h, SynPG-1 was able to retain activity in the same condition for up to 24 h, representing a 12-fold increase in stability. Both peptides had some antibiofilm activity againstEscherichia coliandSalmonella typhimurium. While both peptides prevented biofilm formation of methicillin-resistantStaphylococcus aureus(MRSA), neither could destroy MRSA's pre-formed biofilms. Both peptides maintained activity after incubation with trypsin and porcine gastric fluid, but not intestinal fluid, and stimulated IPEC-J2 cell migration. These findings suggest that SynPG-1 has much better serum stability while maintaining the same antimicrobial potency as PG-1.