Abstract
Infections caused by Pseudomonas aeruginosa are tough to treat as the majority of these isolates exhibit varying degrees of beta-lactamase mediated resistance. These enzymes are capable of hydrolyzing broad spectrum cephalosporins and monobactams but inactive against cephamycins and imipenem. Resistance to broad-spectrum beta lactams, mediated by extended-spectrum beta lactamases (ESBLs), is an increasing problem worldwide. In addition, ESBL producing organism’s exhibit coresistance to several other classes of antibiotics resulting in limitation of therapeutic option. This resistance poses problems for testing and reporting. Increased prevalence of ESBLs among clinical isolates creates a great need for laboratory testing methods that will accurately identify their presence. Thus the present study was designed to investigate the prevalence of extended-spectrum beta lactamases (ESBLs) in clinical isolates of P. aeruginosa. A total of 150 clinical isolates of P. aeruginosa were isolated from various clinical samples were tested for antimicrobial susceptibility by Kirby-Baeur disk diffusion method. 75 isolates showing a zone diameter less than 18 mm to Cefoxitin (screen positive) were tested for the presence of extended spectrum beta-lactamase (ESBL) by disk approximation method using cefoxitin inducer and cefotaxime indicator method as per Clinical and Laboratory Standards Institute (CLSI) guidelines. Antibiogram of P. aeruginosa isolates revealed that, highest resistance was observed to gentamycin (73.67%), followed by ceftazidime (70.67%), amikacin (63.33%), ciprofloxacin (52.67%) in that order of frequencies. Maximum susceptibility was observed to carbenicillin (72%). Multiple drug resistance was common phenomenon observed, in more than 50% of strains. 78 (52%) isolates showed resistance to six or more antibiotics. 65.33% of P. aeruginosa strains showed extended spectrum beta-lactamase production in (70.73%) isolates from pus followed by urine (62.5%). The study emphasizes the high prevalence of multidrug resistant P. aeruginosa producing extended spectrum beta-lactamase using a simple disk approximation method. Thus proper antibiotic policy and measures to restrict the indiscriminative use of cephalosporins and carbapenems should be taken to minimize the emergence of this multiple beta-lactamase producing pathogens.
Highlights
Resistant bacteria are emerging world wide as a threat to the favourable outcome of common infections in community and hospital settings
Production of extended-spectrum beta lactamases (ESBLs) by P. aeruginosa has tremendous therapeutic consequences and poses a significant clinical challenge if it remains undetected, early identification of the infections due to these organisms is necessary as the appropriate treatment might reduce the spread of these resistant strains as well as reduce the mortality in hospitalized patients
Since there is no standard guideline for detection of most of these beta-lactamase enzymes in P. aeruginosa, the comparison between studies becomes difficult as the patient population in particular centres and the methods of study differ
Summary
Resistant bacteria are emerging world wide as a threat to the favourable outcome of common infections in community and hospital settings. Resistance to extended-spectrum cephalosporins is usually observed in members of the family Enterobacteriaceae, with extended-spectrum variants from class A beta-lactamases TEM-1, TEM-2, and SHV-1 [2] These plasmid mediated extended-spectrum enzymes were first reported in Klebsiella pneumoniae and later in almost all other Enterobacteriaceae. These variants differ from their parent enzymes by only a few amino acid positions [3] within their catalytic sites [3] but can hydrolyze broad-spectrum beta-lactam antibiotics such as penicillins and cephalosporins, including oxyimino beta lactams (cefotaxime, ceftazidime, and aztreonam). They do not hydrolyze cephamycins (cefoxitin) or carbapenems (imipenem or meropenem) [3]
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