Resin salve made from Norway spruce (Picea abies) is traditionally used in folk medicine to heal skin ulcers and infected wounds. Its antimicrobial properties were studied against certain human bacteria important in infected skin wounds. The sensitivity of the resin against Gram-positive and Gram-negative bacteria was studied in vitro by methods that are routinely used in microbiology laboratories. The resin salve exhibited a bacteriostatic effect against all tested Gram-positive bacteria but only against Proteus vulgaris of the Gram-negative bacteria. Interestingly, the resin inhibited the growth of bacteria, including methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococcus (VRE), both on agar plates and in culture media. The study demonstrated antimicrobial activity of the resin salve and provided objective evidence of its antimicrobial properties. It gives some explanations why the traditional use of home-made resin salve from Norway spruce is experienced as being effective in the treatment of infected skin ulcers.
BackgroundArcanobacterium haemolyticum is an emerging bacterial pathogen, causing pharyngitis and more invasive infections. This organism expresses an unusual phospholipase D (PLD), which we propose promotes bacterial pathogenesis through its action on host cell membranes. The pld gene is found on a genomic region of reduced %G + C, suggesting recent horizontal acquisition.ResultsRecombinant PLD rearranged HeLa cell lipid rafts in a dose-dependent manner and this was inhibited by cholesterol sequestration. PLD also promoted host cell adhesion, as a pld mutant had a 60.3% reduction in its ability to adhere to HeLa cells as compared to the wild type. Conversely, the pld mutant appeared to invade HeLa cells approximately two-fold more efficiently as the wild type. This finding was attributable to a significant loss of host cell viability following secretion of PLD from intracellular bacteria. As determined by viability assay, only 15.6% and 82.3% of HeLa cells remained viable following invasion by the wild type or pld mutant, respectively, as compared to untreated HeLa cells. Transmission electron microscopy of HeLa cells inoculated with A. haemolyticum strains revealed that the pld mutant was contained within intracellular vacuoles, as compared to the wild type, which escaped the vacuole. Wild type-infected HeLa cells also displayed the hallmarks of necrosis. Similarly inoculated HeLa cells displayed no signs of apoptosis, as measured by induction of caspase 3/7, 8 or 9 activities.ConclusionsThese data indicate that PLD enhances bacterial adhesion and promotes host cell necrosis following invasion, and therefore, may be important in the disease pathogenesis of A. haemolyticum infections.
Patients with chronic underlying diseases are more likely to be infected with F. nucleatum than F. necrophorum. F. nucleatum bacteraemia may present as a febrile illness without severe symptoms. F. necrophorum caused sepsis mainly in previously healthy individuals. These infections may be accompanied with a jugular vein thrombosis characteristic of Lemierre's syndrome and septic shock. However, F. necrophorum infections present more frequently without any apparent venous thrombosis and may be accompanied by abscesses.
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