Polyhexamethylene guanidine hydrochloride (PHMGH), an antimicrobial biocide of the guanidine family, was tested for efficacy against quality-control strains of Staphylococcus aureus, Pseudomonas aeruginosa, Salmonella choleraesuis, meticillin-resistant S. aureus (MRSA) and Escherichia coli. Bactericidal activity against S. aureus, P. aeruginosa and Salmonella choleraesuis was determined using the official methods of analysis of the Association of Official Analytical Chemists, with modifications as recommended by the Canadian General Standards Board. For MRSA and E. coli, the MIC and minimal bactericidal concentration were determined using the broth dilution technique. The experiments were carried out at 20 6C under a range of conditions including varying PHMGH concentration (0.001-0.1 %), contact time (0.5-10 min) and water type (distilled, tap and hard water). The phenol coefficient values determined with S. aureus, Salmonella choleraesuis and P. aeruginosa were 7.5, 6.1 and 5, respectively. No matter what type of water was used to make the dilutions, PHMGH killed MRSA and E. coli at concentrations as low as 0.04 and 0.005 % (w/v), respectively, within 1.5 min. The mode of action of PHMGH was elucidated by transmission electron microscopy: the cell envelope was broken, resulting in cell content leakage into the medium. The ultimate aim of this study was to show that PHMGH can be used as an odourless, colourless, non-corrosive and harmless disinfectant for hospital and household facilities.

The balance between the products of l-arginine metabolism in macrophages regulates the outcome of Leishmania major infection. l-arginine can be oxidized by host inducible NO synthase to produce NO, which contributes to parasite killing. In contrast, l-arginine hydrolysis by host arginase blocks NO generation and provides polyamines, which can support parasite proliferation. Additionally, Leishmania encode their own arginase which has considerable potential to modulate infectivity and disease pathogenesis. In this study, we compared the infectivity and impact on host cellular immune response in vitro and in vivo of wild-type (WT) L. major with that of a parasite arginase null mutant (arg−) L. major. We found that arg− L. major are impaired in their macrophage infectivity in vitro independent of host inducible NO synthase activities. As with in vitro results, the proliferation of arg− L. major in animal infections was also significantly impaired in vivo, resulting in delayed onset of lesion development, attenuated pathology, and low parasite burden. Despite this attenuated pathology, the production of cytokines by cells from the draining lymph node of mice infected with WT and arg− L. major was similar at all times tested. Interestingly, in vitro and in vivo arginase levels were significantly lower in arg− than in WT-infected cases and were directly correlated with parasite numbers inside infected cells. These results suggest that Leishmania-encoded arginase enhances disease pathogenesis by augmenting host cellular arginase activities and that contrary to previous in vitro studies, the host cytokine response does not influence host arginase activity.