A role for sigma factor B in the emergence of Staphylococcus aureus small-colony variants and elevated biofilm production resulting from an exposure to aminoglycosides

Mitchell, Gabriel; Brouillette, Éric; Séguin, David Lalonde; Asselin, Ann-Élise; Jacob, Christian L.; Malouin, François

doi:10.1016/j.micpath.2009.10.003

Cited by 61 publications

(89 citation statements)

References 56 publications

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“…The hypothesis that SCVs play a role in the development of chronic infections is well supported by in vitro experiments demonstrating that these variants have an increased ability to adhere to host tissue components (Mitchell et al, 2008;Vaudaux et al, 2002), to form biofilms (Mitchell et al, 2010a(Mitchell et al, , 2010bSingh et al, 2009Singh et al, , 2010 and to infect and persist within non-professional phagocytes (Mitchell et al, 2011b;Sendi & Proctor, 2009). These in vitro characteristics can be explained by the impact of the defective electron transport chain on the expression of virulence factors which seem to be mostly controlled by the activity of SigB rather than by the agr system in SCVs (Moisan et al, 2006;Senn et al, 2005).…”

Section: Pathogenesis Of P Aeruginosa In Cfmentioning

confidence: 95%

“…Scale bar is 50 μm. Biofilm formation was evaluated by crystal violet staining as previously decribed (Mitchell et al, 2010a(Mitchell et al, , 2010b.…”

Section: Pathogenesis Of P Aeruginosa In Cfmentioning

confidence: 99%

“…Conventional resistance mechanisms include the upregulation of bacterial efflux pumps and mutations of antibiotic target molecules . In addition, the formation of persister cells (Mulcahy et al, 2010) and of small-colony variants (Goerke & Wolz, 2010;Proctor et al, 2006;Schneider et al, 2008) as well as bacterial growth in biofilms Mitchell et al, 2010aMitchell et al, , 2010bWagner & Iglewski, 2008) are mechanisms that are well known for their involvement in difficult-to-treat infections (Galli et al, 2007;Stewart, 2002).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Outcome and Prevention of Pseudomonas aeruginosa-Staphylococcus aureus Interactions During Pulmonary Infections in Cystic Fibrosis

Mitchell¹,

Malouin²

2012

Cystic Fibrosis - Renewed Hopes Through Research

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Section: Pathogenesis Of P Aeruginosa In Cfmentioning

confidence: 95%

“…Scale bar is 50 μm. Biofilm formation was evaluated by crystal violet staining as previously decribed (Mitchell et al, 2010a(Mitchell et al, , 2010b.…”

Section: Pathogenesis Of P Aeruginosa In Cfmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Outcome and Prevention of Pseudomonas aeruginosa-Staphylococcus aureus Interactions During Pulmonary Infections in Cystic Fibrosis

Mitchell¹,

Malouin²

2012

Cystic Fibrosis - Renewed Hopes Through Research

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“…SCVs appear well adapted to the intracellular environment (Sendi & Proctor, 2009;Tuchscherr et al, 2010) and there are even some indications that SCVs could be induced by the intracellular milieu (Vesga et al, 1996). Further reported mechanisms leading to the formation of SCVs (in vitro and in vivo) include prolonged exposure to subinhibitory concentrations of antibiotics (Massey et al, 2001;Mitchell et al, 2010a;von Eiff et al, 1997a) or to exoproducts from other bacteria, e.g. Pseudomonas aerugenosa (Mitchell et al, 2010b).…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, there is growing evidence that the formation of SCVs could also be due to regulatory mechanisms, involving global regulators (e.g. sigB, sarA and agr), Clp ATPases Mitchell et al, 2008Mitchell et al, , 2010a or nonprotein-coding RNAs as regulatory molecules (Abu-Qatouseh et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Staphylococcus aureus phenotype switching: an effective bacterial strategy to escape host immune response and establish a chronic infection

2011

SciVee

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Staphylococcus aureus is a frequent cause for serious, chronic and therapyrefractive infections in spite of susceptibility to antibiotics in vitro. In chronic infections, altered bacterial phenotypes, such as small colony variants (SCVs), have been found. Yet, it is largely unclear whether the ability to interconvert from the wild-type to the SCV phenotype is only a rare clinical and/or just laboratory phenomenon or is essential to sustain an infection. Here, we performed different long-term in vitro and in vivo infection models with S. aureus and we show that viable bacteria can persist within host cells and/or tissues for several weeks. Persistence induced bacterial phenotypic diversity, including SCV phenotypes, accompanied by changes in virulence factor expression and auxotrophism. However, the recovered SCV phenotypes were highly dynamic and rapidly reverted to the fully virulent wild-type form when leaving the intracellular location and infecting new cells. Our findings demonstrate that bacterial phenotype switching is an integral part of the infection process that enables the bacteria to hide inside host cells, which can be a reservoir for chronic and therapy-refractive infections.

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Detection and quantification of Staphylococcus in chronic rhinosinusitis

Mackenzie

Baker

Douglas

et al. 2019

Int Forum Allergy Rhinol

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Background:The sinonasal microbiota has been implicated in chronic rhinosinusitis (CRS) pathogenesis, particularly related to the presence of Staphylococcus aureus. Staphylococcus epidermidis is also prevalent within the sinonasal microbiota and may inhibit S. aureus colonization. We investigated polymerase chain reaction (PCR) primer pairs for measuring absolute abundances of S. aureus and S. epidermidis, then compared bacterial community composition and absolute abundances of these species between CRS patients and controls. Methods: Six candidateStaphylococcus species-specific primer pairs were tested in silico and in vitro against pure bacterial isolates. Quantitative PCR (qPCR) for absolute quantification of S. aureus, S. epidermidis, and overall bacterial load were assessed in 40 CRS (CRS without nasal polyposis [CRSsNP] = 22, CRS with nasal polyposis [CR-SwNP] = 18) patients and 14 controls. Amplicon sequencing of the V3-V4 hypervariable regions of the 16S ribosomal RNA (rRNA) bacterial gene were conducted to investigate community composition. Results: Primer pairs targeting the gmk gene of S. aureus and nrd gene from S. epidermidis were the most specific and sensitive primers. S. aureus (CRSsNP = 81.8%occurrence, CRSwNP = 83%, control = 92.9%) and S. epidermidis (CRSsNP = 95.5%, CRSwNP = 100%, control = 92.9%) were very prevalent, as indicated by qPCR results. Both CRSsNP and CRSwNP had significantly (p < 0.05) higher bacterial load when compared with controls (p < 0.05 for both). No significant correlation was observed between S. aureus and S. epidermidis abundances (p > 0.05). Conclusion: Bacterial community sequencing detectedStaphylococcus-assigned sequences in nearly all patients; however, it could not differentiate between S. aureus and S. epidermidis. Here, we present primer pairs that can distinguish between these species. We report a very high prevalence of S. aureus in both CRS patients and controls. C 2019 ARS-AAOA, LLC.

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A role for sigma factor B in the emergence of Staphylococcus aureus small-colony variants and elevated biofilm production resulting from an exposure to aminoglycosides

Cited by 61 publications

References 56 publications

Outcome and Prevention of Pseudomonas aeruginosa-Staphylococcus aureus Interactions During Pulmonary Infections in Cystic Fibrosis

Outcome and Prevention of Pseudomonas aeruginosa-Staphylococcus aureus Interactions During Pulmonary Infections in Cystic Fibrosis

Staphylococcus aureus phenotype switching: an effective bacterial strategy to escape host immune response and establish a chronic infection

Detection and quantification of Staphylococcus in chronic rhinosinusitis

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