Prevalence, Genotyping of Escherichia coli and Pseudomonas aeruginosa Clinical Isolates for Oxacillinase Resistance and Mapping Susceptibility Behaviour

Abstract

In the present study, multi-drug resistant isolates of Escherichia coli and Pseudomonas aeruginosa were obtained from different clinical specimens and were subjected to molecular typing to detect the genes encoding oxacillinases in these isolates. Subsequently, antibacterial activity of drugs was tested against selected clinical isolates. Two hundred forty six isolates including 98 of E. coli and 148 of P. aeruginosa were collected from clinical specimens of different centers across India. Out of 246, 123 isolates showed weak synergy for ceftazidime or cefepime and imipenem or clavulanate and were considered as oxacillinase producers. Polymerase chain reaction (PCR) was performed to identify the variants of oxacillinases genes. Our results show a great diversity of occurance of oxacillinase (OXA) genes among clinical isolates. OXA-48 and OXA-10 were more prevalent in both E. coli (32.6% OXA-48; 16.3% OXA-10) and P. aeruginosa (OXA-48 32.4%; 27.0%) as evident by PCR. The incidence of other OXA genes in E. coli and P. aeruginosa varied from 4.0 to 12.1%. Of the tested drugs, cefepime plus sulbactam was found to be the most efficacious antibacterial agents with 81.6 to 89.2% susceptibility. Cefepime plus tazobactam was second most active antibacterial agent with 46.9 to 56.7% susceptibility. Surprisingly, imipenem plus cilastatin showed susceptibility to less than 45% isolates.From the above results, it is evident that cefepime plus sulbactam has enhanced in vitro antibacterial activity compared to cefepime alone imipenem plus cilastatin and cefepime plus tazobactam combination in oxacillinases. One significant finding of this study was that cefepime was found to be effective only against the isolates caring OXA-1 and OXA-2 but was found to be resistant to OXA-10, OXA-23, OXA-24, OXA-48, OXA-51 and OXA-58 genes; whereas cefepime in combination with sulbactam was found to be effective against most of these OXA genes in comparison to tazobactam combination.

In vitro activity of cefoperazone and cefoperazone-sulbactam against carbapenem-resistant <em>Acinetobacter baumannii</em> and <em>Pseudomonas aeruginosa</em>

“…In this study, the concentration of sulbactam was higher than the conventional concentration, and this concentration may increase the affinity of sulbactam for class D β-lactamases and therefore the activity against these carbapenem-resistant A. baumannii isolates. Thus, we found that after adding a relatively high concentration of sulbactam with cefoperazone, the in vitro activity against carbapenem-resistant A. baumannii could be enhanced 15. However, further studies are warranted to elucidate the role of cefoperazone and sulbactam in the treatment of infection and assess β-lactamase gene expression.…”

Antimicrobial Drug Resistance in Escherichia coli from Humans, and Identification of Carbapenemase-Producing E. coli in the City of Zabol, Iran

“…The study of Chaudhary and Payasi (19) showed a great diversity of occurrence of oxacillinase (OXA) genes among clinical isolates. OXA-48 and OXA-10 were more prevalent in both E. coli (32.6% OXA-48; 16.3% OXA-10) and P. aeruginosa (OXA-48 32.4%; 27.0%) as evident by PCR.…”

The emergence of plasmid-encoded oxacillinase and carbapenemase among uropathogenic Escherichia coli (UPEC) isolated from hospitalized patients in the North of Iran

“…The attributed mechanisms to Enterobacteriaceae for resistance to carbapenems include the following: (i) efflux pumps, (ii) acquisition of β-lactamases encoding genes, such as carbapenemase; and (iii) modification of porins in the outer membrane and penicillin-binding proteins [ 4 ]. According to Ambler's molecular classification, beta-lactamases are grouped into four distinct classes, A (ESBLs), B (MBLs), C (AmpC), and D (OXA-types), based on their amino acid sequence [ 5 ]. The class D β-lactamases (oxacillinases) are a global crisis and significant concern due to being encoded by transmissible genes.…”