Antimicrobial resistance and genetic diversity in ceftazidime non-susceptible bacterial pathogens from ready-to-eat street foods in three Taiwanese cities.

Bacterial contamination of ready-to-eat (RTE) street foods is a major concern worldwide. Dissemination of antibiotic resistant pathogens from food is an emerging public-health threat. To investigate the prevalence of antibiotic resistance genes and ceftazidime resistance-associated efflux pumps in foodborne pathogens, 270 RTE street foods samples were collected in three densely populated Taiwanese cities. Among 70 ceftazidime non-susceptible isolates, 21 Stenotrophomonas maltophilia, 12 Pseudomonas spp., 22 Acinetobacter spp., and 15 Enterobacteriaceae isolates were identified. Phylogenetic analyses revealed high levels of genetic diversity between all of the different strains. Multi-drug resistance was observed in 86.4% (19/22) of Acinetobacter spp., 100% (12/12) of Pseudomonas spp., 71.4% (15/21) of S. maltophilia, and 93.3% (14/15) of Enterobacteriaceae. Of 70 ceftazidime non-susceptible isolates, 13 contained ESBLs or plasmid-mediated ampC genes and 23 contained ceftazidime resistance-associated efflux pumps, with Acinetobacter spp. identified as predominant isolate (69.6%; 16/23). AdeIJK pump RNA expression in Acinetobacter isolates was 1.9- to 2-fold higher in active efflux strains. Nine clinically resistant genes were detected: catIII and cmlA (chloramphenicol); aacC1, aacC2, aacC3, and aacC4 (gentamicin); tet(A), tet(C), and tet(D) (tetracycline). The scope and abundance of multidrug-resistant bacteria described in this report underscores the need for ongoing and/or expanded RTE monitoring and control measures.

5-Episinuleptolide Decreases the Expression of the Extracellular Matrix in Early Biofilm Formation of Multi-Drug Resistant Acinetobacter baumannii.

Nosocomial infections and increasing multi-drug resistance caused by Acinetobacter baumannii have been recognized as emerging problems worldwide. Moreover, A. baumannii is able to colonize various abiotic materials and medical devices, making it difficult to eradicate and leading to ventilator-associated pneumonia, and bacteremia. Development of novel molecules that inhibit bacterial biofilm formation may be an alternative prophylactic option for the treatment of biofilm-associated A. baumannii infections. Marine environments, which are unlike their terrestrial counterparts, harbor an abundant biodiversity of marine organisms that produce novel bioactive natural products with pharmaceutical potential. In this study, we identified 5-episinuleptolide, which was isolated from Sinularia leptoclados, as an inhibitor of biofilm formation in ATCC 19606 and three multi-drug resistant A. baumannii strains. In addition, the anti-biofilm activities of 5-episinuleptolide were observed for Gram-negative bacteria but not for Gram-positive bacteria, indicating that the inhibition mechanism of 5-episinuleptolide is effective against only Gram-negative bacteria. The mechanism of biofilm inhibition was demonstrated to correlate to decreased gene expression from the pgaABCD locus, which encodes the extracellular polysaccharide poly-ß-(1,6)-N-acetylglucosamine (PNAG). Scanning electron microscopy (SEM) indicated that extracellular matrix of the biofilm was dramatically decreased by treatment with 5-episinuleptolide. Our study showed potentially synergistic activity of combination therapy with 5-episinuleptolide and levofloxacin against biofilm formation and biofilm cells. These data indicate that inhibition of biofilm formation via 5-episinuleptolide may represent another prophylactic option for solving the persistent problem of biofilm-associated A. baumannii infections.