Carbapenem resistance in Pseudomonas aeruginosa and Acinetobacter species at a large tertiary referral hospital in Lusaka, Zambia

Abstract Background Pseudomonas aeruginosa (P. aeruginosa) and Acinetobacter species and are among the leading causes of hospital-acquired infections (HAI). Treating patients with HAI caused by these pathogens is usually a challenge due to intrinsic and acquired resistance to the commonly used and affordable antibiotics, which has been heightened by the emergence of metallo-β lactamases thereby exhibiting resistance to carbapenems. Currently, carbapenem resistance represents an increasing problem in the health care settings globally but there is still a paucity of data on carbapenem resistance in our setting. Objective To detect carbapenem resistance and the susceptibility to other antimicrobial agents in P. aeruginosa and Acinetobacter species isolated from blood, sputum, skin and soft tissue specimens between March, 2018 and June, 2019 at the University Teaching Hospital (UTH), Lusaka, Zambia. Method This was a retrospective hospital based study, involving routine blood, sputum, skin and soft tissue samples submitted to the microbiology laboratory. Conventional microbiology methods were used to identify the organisms, while Kirby-Bauer disc diffusion method was used to determine the antimicrobial susceptibility profiles of the isolates. In order to detect carbapenemase production in P. aeruginosa isolates that were resistant to imipenem by disc diffusion, the isolates were subjected to the modified carbapenem inactivation method (mCIM) method. Results A total of 384 samples were analyzed, of which 84 P. aeruginosa and 11 Acinetobacter species were isolated. The P. aeruginosa isolates were susceptible to imipenem (94%), piperacillin-tazobactum (95.2%), amikacin (91%), ciprofloxacin (69%), gentamicin (63.1%) and ceftazidime (51.2%). The Acinetobacter species isolates were most susceptible to amikacin (90.9%), imipenem (82.9%) and piperacillin-tazobactum (82.8%), ciprofloxacin, tetracycline and cefepime all at 27.3% each but had the lowest susceptibility at 9.1% to both gentamicin and cefotaxime. Carbapenem resistance in P. aeruginosa was 5/84 (6%) and 2/11 (18.2%) in Acinetobacter species. Carbapenemase production was confirmed in all five P. aeruginosa isolates. Conclusion Carbapenem resistance was low in both organisms demonstrating that imipenem is still an effective treatment choice for invasive infections caused by these organisms in our setting. In order to reduce HAI and improve patient outcome, there is need to strengthen antimicrobial surveillance/stewardship and infection control at the UTH.