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Co-production of ESBL and AmpC
ß-Lactamases in Clinical Isolates of A.
baumannii and A. lwoffii in a Tertiary Care
Hospital From Northern India
DC16-DC19
Correspondence
Dr. Pooja Singla,
Demonstrator, Department of Microbiology, PT. B.D. Sharma PGIMS Rohtak, India.
Phone: 9813078178, E-mail: pjsingla3@gmail.com
Background: Acinetobacter baumannii is an important cause of health care associated infections which are difficult to control and treat, because of widespread antimicrobial resistance which is possessed by this organism.
Aim: The aim of the present study was to know the prevalence of ESBLs and AmpC ß-lactamases in clinical isolates of Acinetobacter spp. which were cultured from various clinical specimens by using different phenotypic methods. Settings and Design: Study was conducted over a period of one year at the Microbiology Department of a tertiary care teaching hospital. A total of 100 consecutive, non-duplicate strains of Acinetobacter species which were isolated from various clinical samples were included.
Materials and Methods: All the isolates were identified by standard microbiological procedures and antimicrobial susceptibility testing was done by Kirby-Bauer disc diffusion technique. Isolates which showed reduced susceptibilities to third generation cephalosporins were tested for ESBL production by CLSI double disc synergy method and also by using sulbactam as an inhibitory agent. Isolates which showed reduced susceptibilities to cefoxitin were tested for AmpC detection by doing AmpC disc test. Statistical Analysis: SPSS, version 17 was used to calculate p-value. If the p-value was <0.05, it was considered to be significant.
Results: Out of 100 isolates, 82 were Acinetobacter baumannii and 18 were Acinetobacter lwoffii. ESBL were mentioned in 4% of the Acinetobacter isolates and in 77% of the isolates by using clavulanic acid and sulbactam as inhibitory agents respectively. AmpC ß-lactamase production was detected in 60% isolates of Acinetobacter spp. Co-production of both ESBL and AmpC enzymes were seen in 29% of the Acinetobacter strains.
Conclusion: Failure in detecting ß-lactamases contributes to their uncontrolled spread and therapeutic failures. Hence, these ß-lactamases should be detected routinely and they should be reported to clinicians in time, so that inappropriate use of antibiotics can be stopped in time.