Objective: Several mechanisms account for carbapenem resistance in Pseudomonas (P) aeruginosa which is an emerging problem at a tertiary care hospital (TCH) in Jamaica. The observed pattern of carbapenem resistance that results from efflux mechanisms is unique because it is specific to meropenem (MEM). An investigation of efflux as a mechanism of carbapenem resistance was needed as the information obtained could inform therapeutic and infection control strategies. Methods: At the Microbiology Laboratory of a TCH in Jamaica, from May 2009 to March 2011, of 105 multidrug-resistant Gram-negative bacilli isolated from clinical specimens submitted for routine identification and susceptibility testing, all the MEM-resistant P aeruginosa isolates (a total of 10) were selected. They were tested for efflux using the efflux inhibitor phenylalanine-arginine-β-naphthylamide (PAβN) in a method described by Giske et al in 2008. Results: This study detected evidence of MEM efflux in 80% of MEM-resistant P aeruginosa implicated in nosocomial infections at this TCH in Jamaica, using the PAβN inhibition assay. Meropenem-efflux-positive isolates belonged to two unrelated chromosomal lineages. Conclusion: These results underscored the need for improved surveillance and control to prevent this mechanism from emerging in further P aeruginosa strains.

Objective: The global problem of resistance to carbapenem antibiotics, through the production of carbapenemases by clinically significant bacteria, continues to increase while options for antibiotic therapy remain limited. It is important to determine the mechanism of carbapenem resistance in the multidrug resistant (MDR) Acinetobacter spp. isolated at a tertiary care hospital, Jamaica (TCHJ) because of the implications for therapy which is the goal of this study. Methodology: 82 MDR Acinetobacter spp collected at a TCHJ were identified as potential carbapenemase producers during routine susceptibility testing for a one year period from May 2009 to April 2010. These isolates were subjected to phenotypic and genotypic tests for carbapenemase detection using the modified Hodge test and PCR respectively. Multiplex PCR for OXA-23,-24,-51,-58 was performed and PFGE was used to determine if carbapenemase-positive isolates were related. Results: PCR for OXA-carbapenemases found 13 blaOXA-24, two blaOXA-23 and one blaOXA-58, establishing a prevalence of 19.5%. PFGE results showed that Acinetobacter spp sharing phenotypic and genotypic similarites were clonally related. Conclusions: Carbapenemase production was found to be a cause of antibiotic resistance in MDR Acinetobacter spp. isolates at a TCHJ. These isolates were thought to have been derived from an outbreak or endemic strain whose presence is likely to significantly impact patient management and antibiotic policy.