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      Antibiotic-tolerant Staphylococcus aureus Biofilm Persists on Arthroplasty Materials

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          Abstract

          The continued presence of biofilm may be one cause of the high risk of failure observed with irrigation and débridement with component retention in acute periprosthetic joint infection (PJI). There is a poor understanding of the role of biofilm antibiotic tolerance in PJI.

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          Staphylococcus aureus: new evidence for intracellular persistence.

          Christian Garzoni, William Kelley (2009)
          Many reports have documented that Staphylococcus aureus can invade host cells and persist intracellularly for various periods of time in cell culture models. However, it is not clear whether intracellular persistence of S. aureus also occurs in the course of infections in whole organisms. This is a subject of intense debate and is difficult to assess experimentally. Intracellular persistence would provide S. aureus with an ideal strategy to escape from professional phagocytes and extracellular antibiotics and would promote recrudescent infection. Here, we present a brief overview of the mounting evidence that S. aureus has the potential to internalize and survive within host cells.
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            Arrested protein synthesis increases persister-like cell formation.

            Natasha Wood, J. Valenta, Michael Benedik … (2013)
            Biofilms are associated with a wide variety of bacterial infections and pose a serious problem in clinical medicine due to their inherent resilience to antibiotic treatment. Within biofilms, persister cells comprise a small bacterial subpopulation that exhibits multidrug tolerance to antibiotics without undergoing genetic change. The low frequency of persister cell formation makes it difficult to isolate and study persisters, and bacterial persistence is often attributed to a quiescent metabolic state induced by toxins that are regulated through toxin-antitoxin systems. Here we mimic toxins via chemical pretreatments to induce high levels of persistence (10 to 100%) from an initial population of 0.01%. Pretreatment of Escherichia coli with (i) rifampin, which halts transcription, (ii) tetracycline, which halts translation, and (iii) carbonyl cyanide m-chlorophenylhydrazone, which halts ATP synthesis, all increased persistence dramatically. Using these compounds, we demonstrate that bacterial persistence results from halted protein synthesis and from environmental cues.
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              Multiple Toxin-Antitoxin Systems in Mycobacterium tuberculosis

              Ambre Sala, Patricia Bordes, Pierre Genevaux (2014)
              The hallmark of Mycobacterium tuberculosis is its ability to persist for a long-term in host granulomas, in a non-replicating and drug-tolerant state, and later awaken to cause disease. To date, the cellular factors and the molecular mechanisms that mediate entry into the persistence phase are poorly understood. Remarkably, M. tuberculosis possesses a very high number of toxin-antitoxin (TA) systems in its chromosome, 79 in total, regrouping both well-known (68) and novel (11) families, with some of them being strongly induced in drug-tolerant persisters. In agreement with the capacity of stress-responsive TA systems to generate persisters in other bacteria, it has been proposed that activation of TA systems in M. tuberculosis could contribute to its pathogenesis. Herein, we review the current knowledge on the multiple TA families present in this bacterium, their mechanism, and their potential role in physiology and virulence.
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                Author and article information

                Journal
                Title: Clinical Orthopaedics and Related Research®
                Abbreviated Title: Clin Orthop Relat Res
                Publisher: Springer Nature
                ISSN (Print): 0009-921X
                ISSN (Electronic): 1528-1132
                Publication date Created: July 2016
                Publication date (Print): February 2016
                Volume: 474
                Issue: 7
                Pages: 1649-1656
                Article
                DOI: 10.1007/s11999-016-4720-8
                PMC ID: 4887357
                PubMed ID: 26831479
                SO-VID: 65fd81f5-c300-4c10-9d6e-e3619553e501
                Copyright © © 2016
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