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      Staphylococcus aureusInfection of Human Gestational Membranes Induces Bacterial Biofilm Formation and Host Production of Cytokines

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          Abstract

          <p id="d15998298e178"> <i>Staphylococcus aureus,</i> a metabolically flexible gram-positive pathogen, causes infections in a variety of tissues. Recent evidence implicates <i>S. aureus</i> as an emerging cause of chorioamnionitis and premature rupture of membranes, which are associated with preterm birth and neonatal disease. We demonstrate here that <i>S. aureus</i> infects and forms biofilms on the choriodecidual surface of explanted human gestational membranes. Concomitantly, <i>S. aureus</i> elicits the production of proinflammatory cytokines, which could ultimately perturb maternal-fetal tolerance during pregnancy. Therefore, targeting the immunological response to <i>S. aureus</i> infection during pregnancy could attenuate disease among infected individuals, especially in the context of antibiotic resistance. </p>

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          Is Open Access

          Hiding in Plain Sight: Interplay between Staphylococcal Biofilms and Host Immunity

          Staphylococcus aureus and Staphylococcus epidermidis are notable for their propensity to form biofilms on implanted medical devices. Staphylococcal biofilm infections are typified by their recalcitrance to antibiotics and ability to circumvent host immune-mediated clearance, resulting in the establishment of chronic infections that are often recurrent in nature. Indeed, the immunomodulatory lifestyle of biofilms seemingly shapes the host immune response to ensure biofilm engraftment and persistence in an immune competent host. Here, we provide a brief review of the mechanisms whereby S. aureus and S. epidermidis biofilms manipulate host–pathogen interactions and discuss the concept of microenvironment maintenance in infectious outcomes, as well as speculate how these findings pertain to the challenges of staphylococcal vaccine development.
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            Characterization of a mixed MRSA/MRSE biofilm in an explanted total ankle arthroplasty.

            Bacterial biofilms have been observed in many prosthesis-related infections, and this mode of growth renders the infection both difficult to treat and especially difficult to detect and diagnose using standard culture methods. We (1) tested a novel coupled PCR-mass spectrometric (PCR-MS) assay (the Ibis T5000) on an ankle arthroplasty that was culture negative on preoperative aspiration and then (2) confirmed that the Ibis assay had in fact detected a viable multispecies biofilm by further micrographic and molecular examinations, including confocal microscopy using Live/Dead stain, bacterial FISH, and reverse-transcriptase-PCR (RT-PCR) assay for bacterial mRNA. The Ibis technology detected Staphylococcus aureus, Staphylococcus epidermidis, and the methicillin resistance gene mecA in soft tissues associated with the explanted hardware. Viable S. aureus were confirmed using RT-PCR, and viable cocci in the biofilm configuration were detected microscopically on both tissue and hardware. Species-specific bacterial FISH confirmed a polymicrobial biofilm containing S. aureus. A novel culture method recovered S. aureus and S. epidermidis (both methicillin resistant) from the tibial metal component. These observations suggest that molecular methods, particularly the new Ibis methodology, may be a useful adjunct to routine cultures in the detection of biofilm bacteria in prosthetic joint infection. © 2011 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved.
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              Alpha-Toxin Promotes Staphylococcus aureus Mucosal Biofilm Formation

              Staphylococcus aureus causes many diseases in humans, ranging from mild skin infections to serious, life-threatening, superantigen-mediated Toxic Shock Syndrome (TSS). S. aureus may be asymptomatically carried in the anterior nares or vagina or on the skin, serving as a reservoir for infection. Pulsed-field gel electrophoresis clonal type USA200 is the most widely disseminated colonizer and the leading cause of TSS. The cytolysin α-toxin (also known as α-hemolysin or Hla) is the major epithelial proinflammatory exotoxin produced by TSS S. aureus USA200 isolates. The current study aims to characterize the differences between TSS USA200 strains [high (hla +) and low (hla −) α-toxin producers] in their ability to disrupt vaginal mucosal tissue and to characterize the subsequent infection. Tissue viability post-infection and biofilm formation of TSS USA200 isolates CDC587 and MN8, which contain the α-toxin pseudogene (hla −), MNPE (hla +), and MNPE isogenic hla knockout (hlaKO), were observed via LIVE/DEAD® staining and confocal microscopy. All TSS strains grew to similar bacterial densities (1–5 × 108 CFU) on the mucosa and were proinflammatory over 3 days. However, MNPE formed biofilms with significant reductions in the mucosal viability whereas neither CDC587 (hla −), MN8 (hla −), nor MNPE hlaKO formed biofilms. The latter strains were also less cytotoxic than wild-type MNPE. The addition of exogenous, purified α-toxin to MNPE hlaKO restored the biofilm phenotype. We speculate that α-toxin affects S. aureus phenotypic growth on vaginal mucosa by promoting tissue disruption and biofilm formation. Further, α-toxin mutants (hla −) are not benign colonizers, but rather form a different type of infection, which we have termed high density pathogenic variants (HDPV).
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                Author and article information

                Journal
                Journal of Infectious Diseases
                J Infect Dis.
                Oxford University Press (OUP)
                0022-1899
                1537-6613
                July 19 2016
                : jiw300
                Article
                10.1093/infdis/jiw300
                5853272
                27436434
                5c262b7d-8d66-470b-a17f-475cd2cb65a7
                © 2016
                History

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