Prehospital cooling of severe burns: Experience of the Emergency Department at Edendale Hospital, KwaZulu-Natal, South Africa

Background. Early cooling with 10 - 20 minutes of cool running water up to 3 hours after a burn has a direct impact on the depth of the burn and therefore on the clinical outcome of the injury. An assessment of the early cooling of burns is essential to improve this aspect of burns management.Objectives. To assess the rates and adequacy of prehospital cooling received by patients with severe burns before presentation to the Emergency Department (ED) at Edendale Hospital, Pietermaritzburg, South Africa. Patients with inadequate prehospital cooling who presented to the ED within 3 hours were also identified.Methods. A retrospective review of the burns database for all the patients with severe burns admitted from the ED at Edendale Hospital from September 2012 to August 2013 was undertaken. Demographic details, characteristics and timing of the burns, and presentation were correlated with burn cooling.Results. Ninety patients were admitted with severe burns. None received sufficient cooling of their burns, 25.6% received cooling of inadequate duration, and 32.3% arrived at the ED within 3 hours after the burn with either inadequate or no cooling. The median time to presentation to the ED after the burn was 260 minutes.Conclusion. Appropriate cooling of severe burns presenting to Edendale Hospital is inadequate. Education of the community and prehospital healthcare workers about the importance of early appropriate cooling of severe burns is required. Many patients would benefit from cooling of their burns in the ED, and facilities should be provided for this vital function

Gymnemic acids inhibit hyphal growth and virulence in Candida albicans

Candida albicans is an opportunistic and polymorphic fungal pathogen that causes mucosal, disseminated and invasive infections in humans. Transition from the yeast form to the hyphal form is one of the key virulence factors in C. albicans contributing to macrophage evasion, tissue invasion and biofilm formation. Nontoxic small molecules that inhibit C. albicans yeast-to-hypha conversion and hyphal growth could represent a valuable source for understanding pathogenic fungal morphogenesis, identifying drug targets and serving as templates for the development of novel antifungal agents. Here, we have identified the triterpenoid saponin family of gymnemic acids (GAs) as inhibitor of C. albicans morphogenesis. GAs were isolated and purified from Gymnema sylvestre leaves, the Ayurvedic traditional medicinal plant used to treat diabetes. Purified GAs had no effect on the growth and viability of C. albicans yeast cells but inhibited its yeast-to-hypha conversion under several hypha-inducing conditions, including the presence of serum. Moreover, GAs promoted the conversion of C. albicans hyphae into yeast cells under hypha inducing conditions. They also inhibited conidial germination and hyphal growth of Aspergillus sp. Finally, GAs inhibited the formation of invasive hyphae from C. albicans-infected Caenorhabditis elegans worms and rescued them from killing by C. albicans. Hence, GAs could be useful for various antifungal applications due to their traditional use in herbal medicine

Evidence that Clostridium difficile TcdC Is a Membrane-Associated Protein

Clostridium difficile produces two toxins, A and B, which act together to cause pseudomembraneous colitis. The genes encoding these toxins, tcdA and tcdB, are part of the pathogenicity locus, which also includes tcdC, a putative negative regulator of the toxin genes. In this study, we demonstrate that TcdC is a membrane-associated protein in C. difficile

Bacteriophage-Mediated Toxin Gene Regulation in Clostridium difficile▿

Clostridium difficile has been identified as the most important single identifiable cause of nosocomial antibiotic-associated diarrhea and colitis. Virulent strains of C. difficile produce two large protein toxins, toxin A and toxin B, which are involved in pathogenesis. In this study, we examined the effect of lysogeny by ΦCD119 on C. difficile toxin production. Transcriptional analysis demonstrated a decrease in the expression of pathogenicity locus (PaLoc) genes tcdA, tcdB, tcdR, tcdE, and tcdC in ΦCD119 lysogens. During this study we found that repR, a putative repressor gene of ΦCD119, was expressed in C. difficile lysogens and that its product, RepR, could downregulate tcdA::gusA and tcdR::gusA reporter fusions in Escherichia coli. We cloned and purified a recombinant RepR containing a C-terminal six-His tag and documented its binding to the upstream regions of tcdR in C. difficile PaLoc and in repR upstream region in ΦCD119 by gel shift assays. DNA footprinting experiments revealed similarities between the RepR binding sites in tcdR and repR upstream regions. These findings suggest that presence of a CD119-like temperate phage can influence toxin gene regulation in this nosocomially important pathogen