In Vitro Anti-Listerial Activities of Crude n-Hexane and Aqueous Extracts of Garcinia kola (heckel) Seeds

We assessed the anti-Listerial activities of crude n-hexane and aqueous extracts of Garcinia kola seeds against a panel of 42 Listeria isolates previously isolated from wastewater effluents in the Eastern Cape Province of South Africa and belonging to Listeria monocytogenes, Listeria grayi and Listeria ivanovii species. The n-hexane fraction was active against 45% of the test bacteria with zones of inhibition ranging between 8–17 mm, while the aqueous fraction was active against 29% with zones of inhibition ranging between 8–11 mm. The minimum inhibitory concentrations (MIC) were within the ranges of 0.079–0.625 mg/mL for the n-hexane extract and 10 to >10 mg/mL for the aqueous extract. The rate of kill experiment carried out for the n-hexane extract only, revealed complete elimination of the initial bacterial population for L. grayi (LAL 15) at 3× and 4× MIC after 90 and 60 min; L. monocytogenes (LAL 8) at 3× and 4× MIC after 60 and 15 min; L. ivanovii (LEL 18) at 3× and 4× MIC after 120 and 15 min; L. ivanovii (LEL 30) at 2, 3 and 4× MIC values after 105, 90 and 15 min exposure time respectively. The rate of kill activities were time- and concentration-dependant and the extract proved to be bactericidal as it achieved a more than 3log10 decrease in viable cell counts after 2 h exposure time for all of the four test organisms at 3× and 4× MIC values. The results therefore show the potential presence of anti-Listerial compounds in Garcinia kola seeds that can be exploited in effective anti-Listerial chemotherapy

Antimicrobial resistance (AMR) nanomachines: mechanisms for fluoroquinolone and glycopeptide recognition, efflux and/or deactivation

In this review, we discuss mechanisms of resistance identified in bacterial agents Staphylococcus aureus and the enterococci towards two priority classes of antibiotics—the fluoroquinolones and the glycopeptides. Members of both classes interact with a number of components in the cells of these bacteria, so the cellular targets are also considered. Fluoroquinolone resistance mechanisms include efflux pumps (MepA, NorA, NorB, NorC, MdeA, LmrS or SdrM in S. aureus and EfmA or EfrAB in the enterococci) for removal of fluoroquinolone from the intracellular environment of bacterial cells and/or protection of the gyrase and topoisomerase IV target sites in Enterococcus faecalis by Qnr-like proteins. Expression of efflux systems is regulated by GntR-like (S. aureus NorG), MarR-like (MgrA, MepR) regulators or a two-component signal transduction system (TCS) (S. aureus ArlSR). Resistance to the glycopeptide antibiotic teicoplanin occurs via efflux regulated by the TcaR regulator in S. aureus. Resistance to vancomycin occurs through modification of the D-Ala-D-Ala target in the cell wall peptidoglycan and removal of high affinity precursors, or by target protection via cell wall thickening. Of the six Van resistance types (VanA-E, VanG), the VanA resistance type is considered in this review, including its regulation by the VanSR TCS. We describe the recent application of biophysical approaches such as the hydrodynamic technique of analytical ultracentrifugation and circular dichroism spectroscopy to identify the possible molecular effector of the VanS receptor that activates expression of the Van resistance genes; both approaches demonstrated that vancomycin interacts with VanS, suggesting that vancomycin itself (or vancomycin with an accessory factor) may be an effector of vancomycin resistance. With 16 and 19 proteins or protein complexes involved in fluoroquinolone and glycopeptide resistances, respectively, and the complexities of bacterial sensing mechanisms that trigger and regulate a wide variety of possible resistance mechanisms, we propose that these antimicrobial resistance mechanisms might be considered complex ‘nanomachines’ that drive survival of bacterial cells in antibiotic environments

Postantibiotic and sub-MIC effects of benzylpenicillin against Streptococcus pneumoniae with different susceptibilities for penicillin

Background: The purpose of the study was to examine whether penicillin-susceptible and nonsusceptible strains of Streptococcus pneumoniae exhibited different pharmacodynamic responses to benzylpenicillin. Methods: The postantibiotic effects (PAEs) and the postantibiotic sub-MIC effects (PA SMEs) were investigated by optical density against strains of S. pneumoniae with different susceptibilities to benzylpenicillin. To validate the data, the PAE and PA SME of one susceptible and one resistant strain were also tested with the viable count method. The post-MIC effects (PMEs) were studied in an in vitro kinetic model, simulating human pharmacokinetics with a half-life of 1 h and a time above MIC of approximately 20% of 24 h. Results: There were no differences with respect to the PAEs, PA SMEs and PMEs of benzylpenicillin for the various strains of S. pneumoniae, irrespective of their susceptibility to penicillin. For both some of the susceptible and resistant strains investigated, longer PA SMEs at 0.2 and 0.3 x MIC were noted, indicating that these parameters might be more dependent on the type of strain rather than on the susceptibility status. Conclusion: No differences in the pharmacodynamic response after similar drug exposure were seen for S. pneumoniae strains with different penicillin susceptibility. Copyright (C) 2003 S. Karger AG, Basel