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Year : 2008  |  Volume : 26  |  Issue : 1  |  Page : 89-90

Prevalence of inducible AmpC β-lactamase-producing Pseudomonas aeruginosa in a tertiary care hospital in northern India

Department of Microbiology, Institute of Medical Sciences (IMS), Banaras Hindu University (BHU), Varanasi - 221 005, India

Date of Submission30-Nov-2006
Date of Acceptance01-Aug-2007

Correspondence Address:
A Bhattacharjee
Department of Microbiology, Institute of Medical Sciences (IMS), Banaras Hindu University (BHU), Varanasi - 221 005
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0255-0857.38872

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How to cite this article:
Bhattacharjee A, Anupurba S, Gaur A, Sen M R. Prevalence of inducible AmpC β-lactamase-producing Pseudomonas aeruginosa in a tertiary care hospital in northern India. Indian J Med Microbiol 2008;26:89-90

How to cite this URL:
Bhattacharjee A, Anupurba S, Gaur A, Sen M R. Prevalence of inducible AmpC β-lactamase-producing Pseudomonas aeruginosa in a tertiary care hospital in northern India. Indian J Med Microbiol [serial online] 2008 [cited 2019 Oct 19];26:89-90. Available from:

Dear editor,

Inactivation of β -lactam antibiotics by enzyme is a major mechanism of resistance in gram-negative bacteria. Although a variety of β -lactamases has been described, class A and C are the most important. Pseudomonas aeruginosa , one of the most common pathogens responsible for hospital infection, is intrinsically resistant to many antibiotics. It also shows an increasing pattern of resistance towards β -lactam antibiotics, especially by production of class C chromosomal β -lactamases. [1] Hence, this study was designed to determine the prevalence rate of inducible AmpC β -lactamase-producing P. aeruginosa in a tertiary care hospital in North India as well as to detect in vitro susceptibility pattern of antipseudomonal antibiotics.

In a duration of six months (November 2005 to April 2006), 162 consecutive non-repetitive isolates of P. aeruginosa were obtained from SS hospital, Banaras Hindu University (BHU), Varanasi, India. The sources of isolates were pus (92), swab (33), urine (32) and blood (5). An in vitro susceptibility pattern to common antipseudomonal antibiotics was also determined according to CLSI guidelines [2] for all the strains. Screening of AmpC β -lactamase was performed by disc antagonism test. A 0.5 McFarland of test isolate was spread over Mueller-Hinton agar (Hi-Media, Mumbai, India) plate, and cefotaxime (30 μg) and cefoxitin (30 μg) (Hi-Media) discs were placed 20 mm apart from centre to centre. The isolates that showed blunting of cefotaxime zone of inhibition adjacent to cefoxitin discs were considered screen positive and were selected for confirmation of inducible AmpC β -lactamase production by the modified three-dimensional test described previously. [3] E. coli ATCC 25922 was used as negative control.

Among the test isolates, 36 (22%) were suspected to be AmpC b-lactamase producers, which were further confirmed by modified three-dimensional test. Among positives, 34 were isolated from hospitalized patients, and two were from out-patients who attended the clinic. Antibiotic susceptibility testing showed piperacillin/tazobactam, imipenem and cefoperazone/sulbactam to be the most effective [Table - 1].

β -Lactamase-producing bacteria can cause major therapeutic failure if they remain undetected. Although clinicians often treat infections based on the results of antibiotic susceptibility tests available, the number of infections caused by AmpC β -lactamase-producing organism, particularly P. aeruginosa , is on the rise and poses a threat to patients due to treatment failure. [4] This emphasizes the need for detection of isolates that produce this enzyme so as to avoid therapeutic failures and nosocomial outbreaks. It should also be mentioned that there is currently no clear consensus regarding guidelines for phenotypic screening or confirmatory tests for AmpC β -lactamase-producing organisms. [3] Although comparison between studies is difficult to do since the patient populations in these centers and methods of study differ, interestingly, we found a slightly high prevalence of AmpC β -lactamase-producing P. aeruginosa (22%) in our centre as compared to earlier studies in India. It was 17.3% in Kolkatta, [4] whereas in a study conducted in Aligarh, it showed 20%. [3]

The referral hospital had always shown a high prevalence of P. aeruginosa infection in the recent past. [5] In our study, all the 34 AmpC-producing isolates from the patients admitted at different wards of the hospital could be clonal dissemination of the same β-lactamase gene, although genetic analyses have not been performed. Antibiogram pattern of these isolates showed that there were cross-resistance between aminoglycosides and quinolones. Although carbapenems remain the first choice for the treatment of patients infected with ESBLs or AmpC β-lactamase, our study shows that β-lactam/β-lactamase inhibitor (sulbactam or tazobactam) combinations can also be a good option.

 ~ References Top

1.Shahid M, Malik A, Sheeba. Multidrug - resistant Pseudomonas aeruginosa strains harboring R - plasmids and AmpC β -lactamases isolated from hospitalized burn patients in a tertiary care hospital of North India. FEMS Microbiol Let 2003;223:147-51.  Back to cited text no. 1    
2.CLSI. Performance standards for antimicrobial disc susceptibility tests. CLSI: Wayne PA; 2005. p. M100-S15.  Back to cited text no. 2    
3.Shahid S, Malik A, Agrawal M, Singhal S. Phenotypic detection of extended spectrum and AmpC β -lactamases by a new spot inoculation method and modified three dimensional extract test: Comparison with the conventional three-dimensional extract test. J Antimicrob Chemother 2004;54:684-7.  Back to cited text no. 3    
4.Arora S, Bal M. AmpC β -lactamases producing bacterial isolates from Kolkatta hospital. Indian J Med Res 2005;122:224-33.  Back to cited text no. 4    
5.Anupurba S, Sen MR. Antimicrobial resistance profile of bacterial isolates from Intensive Care Unit: Changing trends. J Commun Dis 2005;37:58-65.  Back to cited text no. 5    


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