Detection of AmpC β-lactamase in Gram Negative Bacteria with their Predisposing Factors and Antimicrobial Susceptibility Pattern

Abstract

Introduction: The predominant mechanism for resistance to β-lactam antibiotics in gram-negative bacteria is the synthesis of the β-lactamase enzyme. Production of AmpC β-lactamase enzyme is a major mechanism of resistance in many Gram-negative bacteria. There are not many Indian data on the prevalence of AmpC β-lactamases in Gram-negative bacteria. AmpC β-lactamase was reported in many parts of the world like USA (85.5%), China (16.9%), Singapore (49.8%), Korea (29.6%), etc. and also some parts of India like New Delhi (20.7%), Chennai (37.5%), Aligarh (20%), Kolkata (17.3%), Bangalore (42.85%), Varanasi (22%), Pondicherry (47%), etc. However, no documented report is available in and around Mumbai. Materials and Methods: This is a study conducted in Lokmanya Tilak Municipal Medical College and General Hospital, Sion, Mumbai. The same is attributed to the population living in Sion and nearby localities. Two hundred non-duplicate isolates of Gram-negative bacteria recovered from different clinical specimens like wound swab, urine, Foley’s catheter tip, blood, sputum from patients admitted in the hospital were tested for AmpC β-lactamase production by Modified Double Disk approximation Method, AmpC Disk Test, Modified Three Dimensional Test. Results: Overall prevalence of AmpC β-lactamase by MDDM was 62%, AmpC β-lactamase by AmpC disk test was 40%, AmpC β-lactamase was 40%. All the isolates tested were resistant to cefoxitin. Multi-Drug Resistance (MDR) was seen in 15% (30/200) isolates. Maximum AmpC positive isolates were E. coli (36.25%), followed by K.pneumoniae (26.25%). No imipenem resistance was seen in AmpC producers. The patients with bacteria producing AmpC β-lactamase had multiple risk factors like Duration of hospital stay > 8days, urinary catheterization, central line insertion, previous antibiotic use, mechanical ventilation, etc. Patients with AmpC positive isolates who survived and responded to imipenem therapy was 93.75% and the mortality rate was 6.25%. Conclusion: The present study emphasizes the high prevalence (40%) of AmpC β-lactamases in Gram-negative bacteria. Early detection of these AmpC β-lactamase producing isolates in a routine laboratory would help avoid treatment failure. Inability to detect AmpC β-lactamase contributes to their uncontrolled spread and therapeutic failure. Hence their appearances in a hospital setting should be identified promptly, so that appropriate antibiotic usage and containment measures can be implemented. Antibiotic exposure may probably be the main risk factor for acquisition of AmpC β-lactamases. So, avoiding unnecessary antibiotic therapy may be the most important factor to prevent infections in patients with AmpC positive isolates. Therefore, strict antibiotic policies and measures to limit the indiscriminate use of cephalosporins and carbapenems in hospital environments should be undertaken to minimize the emergence and spread of AmpC β-lactamase producing bacteria.