Open AccessMolecular characterisation of multidrug-resistant Pseudomonas aeruginosa from a private hospital in Durban, South Africa
Author(s) -
Cosmos B. Adjei,
Usha Govinden,
K Moodley,
Sabiha Y. Essack
Publication year - 2018
Publication title -
southern african journal of infectious diseases
Language(s) - English
Resource type - Journals
eISSN - 2313-1810
pISSN - 2312-0053
DOI - 10.4102/sajid.v33i2.19
Subject(s) - ticarcillin , microbiology and biotechnology , piperacillin , ceftazidime , imipenem , biology , amikacin , aztreonam , pseudomonas aeruginosa , tazobactam , multiple drug resistance , ciprofloxacin , drug resistance , antibiotics , antibiotic resistance , bacteria , genetics
Background: Multi-drug resistant Pseudomonas aeruginosa pose a clinical challenge globally. This study delineated the molecular mechanisms of resistance to β-lactam antibiotics in multidrug-resistant P. aeruginosa isolated from a single private hospital in Durban, South Africa and ascertained clonality with regard to the isolates carrying β-lactamase genes.Methods: Seventeen P. aeruginosa isolates recovered from sputum, urine, catheter tips, pus swabs, nasal swabs and endotracheal aspirates underwent MIC determination, and phenotypic screening using the Double Disk Synergy Test (DDST) and Modified Hodge Test (MHT) to identify putative extended-spectrum β-lactamases (ESBLs), metallo-β-lactamases and other carbapenemases. Selected β-lactamase encoding genes were genotypically confirmed by PCR and sequencing. REP-PCR was conducted to determine the clonal relatedness of the 11 isolates carrying β-lactamase genes. Results: Sixteen isolates (94%) were resistant to aztreonam and piperacillin, 15 isolates (88%) were resistant to imipenem and ticarcillin, 14 (82%) were resistant to meropenem, and 13 isolates (76%) were resistant to ceftazidime and piperacillin/tazobactam. Resistance to ciprofloxacin and amikacin were 82% and 29% respectively. Of the 17 isolates tested, GES-2, VIM-2 and OXA-21 were present in 10 (59%) four (24%) and one (6%) of the isolates respectively. Three of the isolates harboured both GES-2 and VIM-2 and one isolate harboured OXA-21 and VIM-2. REP-PCR revealed seven clusters with clusters A and F having two (18%) and four (36%) isolates respectively, while the remaining five isolates were unrelated.Conclusion: GES-2 and VIM-2 enzymes were predominantly responsible for carbapenemase resistance. Clones A and F intimated patient-to-patient spread within the ICU and surgical ICU. This apparent dissemination as well as the multi-drug resistance observed points to sub-optimal infection prevention and control and dwindling antibiotic treatment options for P. aeruginosa respectively in this institution.