Detection of the icaADBC gene cluster and biofilm formation in Staphylococcus epidermidis isolates from catheter-related urinary tract infections

Cho, Seung-Hak; Naber, Kurt G.; Hacker, Jörg; Ziebuhr, Wilma

doi:10.1016/s0924-8579(02)00101-2

Cited by 72 publications

(52 citation statements)

References 18 publications

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“…In pathogenic bacteria, adaptation to an altered environment often includes activating transcription of virulence genes; hence, synthesis of many virulence determinants is regulated by environmental/nutritional signals (e.g., nitrogen, iron, and calcium) (47). Because PIA is the most important virulence determinant of S. epidermidis (2,7,38,56,57,84), it is not surprising that PIA synthesis is regulated by environmental and nutritional signals (13,16,18,22,53).…”

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confidence: 99%

Tricarboxylic Acid Cycle-Dependent Regulation of Staphylococcus epidermidis Polysaccharide Intercellular Adhesin Synthesis

et al. 2008

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Staphylococcus epidermidis is a major nosocomial pathogen primarily infecting immunocompromised individuals or those with implanted biomaterials (e.g., catheters). Biomaterial-associated infections often involve the formation of a biofilm on the surface of the medical device. In S. epidermidis, polysaccharide intercellular adhesin (PIA) is an important mediator of biofilm formation and pathogenesis. Synthesis of PIA is regulated by at least three DNA binding proteins (IcaR, SarA, and B ) and several environmental and nutritional conditions. Previously, we observed the environmental conditions that increased PIA synthesis decreased tricarboxylic acid (TCA) cycle activity. In this study, S. epidermidis TCA cycle mutants were constructed, and the function of central metabolism in PIA biosynthesis was examined. TCA cycle inactivation altered the metabolic status of S. epidermidis, resulting in a massive derepression of PIA biosynthetic genes and a redirection of carbon from growth into PIA biosynthesis. These data demonstrate that the bacterial metabolic status is a critical regulatory determinant of PIA synthesis. In addition, these data lead us to propose that the TCA cycle acts as a signal transduction pathway to translate external environmental cues into intracellular metabolic signals that modulate the activity of transcriptional regulators.

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confidence: 99%

Tricarboxylic Acid Cycle-Dependent Regulation of Staphylococcus epidermidis Polysaccharide Intercellular Adhesin Synthesis

et al. 2008

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“…In animal models, PIA-negative mutants were significantly less likely to cause catheter-associated infections than their PIA-positive isogenic counterparts (27). Epidemiological studies have clearly shown that the majority of commensal Staphylococcus epidermidis isolates lack the ica operon, whereas clinical strains obtained from device-associated infections harbor the genetic information for biofilm formation in addition to certain insertion sequences (IS256) and genes that mediate methicillin and aminoglycoside resistance (1,9,10,17,36). Currently, the genetic origin of the ica genes in S. epidermidis is not known, and it is also uncertain how biofilm-forming isolates establish and disseminate within the hospital environment.…”

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Clonal Analysis of Staphylococcus epidermidis Isolates Carrying or Lacking Biofilm-Mediating Genes by Multilocus Sequence Typing

et al. 2005

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Staphylococcus epidermidis is part of the normal microflora of the human skin but is also a leading cause of device-associated infections in critically ill patients. Commensal and clinical S. epidermidis isolates differ in their ability to form biofilms on medical devices; the synthesis of biofilms is mediated by the icaADBC operon. Currently, the epidemiological relatedness between ica-positive and -negative isolates is not known; neither is it known whether the ica genes can spread to biofilm-negative strains through horizontal gene transfer. In this study, multilocus sequence typing (MLST) was employed for the clonal analysis of 118 S. epidermidis icapositive and -negative strains. MLST revealed that the majority of ica-positive and -negative strains were closely related and formed a single clonal complex. Within this complex one sequence type (ST27) was identified which contained exclusively ica-positive isolates and represented the majority of clinical strains tested. ST27 and related ica-positive clones carried different SCCmec cassettes (conferring methicillin resistance) and the insertion sequence IS256. The findings suggest that the S. epidermidis infections analyzed in this report are mainly caused by a single clone (ST27) which occurs preferentially in hospitals and differs from clones in the community. It is hypothesized that the successful establishment of ST27 within nosocomial environments has been facilitated by the presence of genes encoding biofilm and resistance traits.Staphylococcus epidermidis is a bacterium that constitutes a major component of the normal skin and mucosal microfloras of humans. It is a leading cause of hospital-acquired infections, mostly associated with the use of medical devices in seriously ill or immunocompromised patients. Staphylococcus epidermidis pathogenesis relies on the ability of the bacteria to form thick multilayered biofilms on a wide variety of polymer and metal surfaces (12). In general, biofilms consist of bacteria embedded into a polysaccharide matrix which protects bacteria against hostile environments, including antibiotics and the action of the host immune system, and therefore are an important factor in the development of chronic and recurrent infections (13,30). Although the production of staphylococcal biofilm is dependent upon multiple regulatory proteins, an essential factor is the presence and expression of the four-gene icaADBC operon (15). The operon encodes enzymes necessary for production of polysaccharide intercellular adhesin (PIA), which is required for biofilm formation and is involved in hemagglutination and bacterial aggregation (7,19,20). In animal models, PIA-negative mutants were significantly less likely to cause catheter-associated infections than their PIA-positive isogenic counterparts (27). Epidemiological studies have clearly shown that the majority of commensal Staphylococcus epidermidis isolates lack the ica operon, whereas clinical strains obtained from device-associated infections harbor the genetic information for biofilm ...

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“…Some authors attributed the absence of biofilm production in some staphylococcal isolates, despite the presence of the ica operon, to the insertion of a 1332-bp sequence element, known as IS256, in icaA causing its inactivation (Ziebuhr et al, 1997;Cho et al, 2002;Kiem et al, 2004) . However, the transposition of IS256 into the ica operon has been found to be a reversible process, as after repeated passages of the PIA negative insertional mutants, the biofilm-forming phenotype could be restored (Ziebuhr et al, 1999).…”

Section: Strainmentioning

confidence: 99%

Detection of biofilm formation, icaADBC gene and investigation of toxin genes in Staphylococus spp. strain from dental unit waterlines, University Hospital Center (UHC) Tlemcen Algeria

Lachachi¹,

Hassaïne²,

Nayme³

et al. 2014

Afr. J. Microbiol. Res.

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The formation of biofilms on pieces of equipment and dental chair unit waterlines has attracted more interest and concern. This study aimed to assess the reliability of two phenotypic methods used to detect the presence of biofilms and the icaADBC operon, and identify various toxin genes by multiplex polymerase chain reaction (PCR) in clinical staphylococcal isolates. A total of thirty-one (31) staphylococcal strains were isolated from waterline tubings in the dental unit. Two phenotypic methods were used for the detection of biofilm production. PCR detected the presence of the ica operon, and a multiplex PCR assay for the detection of staphylococcal toxin genes was done. Biofilm production was detected in twenty-six (83.87%) isolates by tissue culture plate method (TCP). The CRA method indicated that twenty (64.51%) of these strains could produce slime. By using the ica operon test, the genotypic ability to form biofilm in was identified in fourteen (45.16%) strains. Five (16.12%) strains of Staphylococcus warneri harbored one or more toxin genes detected by PCR multiplex. The presence of ica operon gene does not always have relationship with in vitro biofilm formation and genes encoding the staphylococcal toxin. Among the strains studied, few of them had the ica operon, toxin gene, and phenotypic ability to form a biofilm at the same time.

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Detection of the icaADBC gene cluster and biofilm formation in Staphylococcus epidermidis isolates from catheter-related urinary tract infections

Cited by 72 publications

References 18 publications

Tricarboxylic Acid Cycle-Dependent Regulation of Staphylococcus epidermidis Polysaccharide Intercellular Adhesin Synthesis

Tricarboxylic Acid Cycle-Dependent Regulation of Staphylococcus epidermidis Polysaccharide Intercellular Adhesin Synthesis

Clonal Analysis of Staphylococcus epidermidis Isolates Carrying or Lacking Biofilm-Mediating Genes by Multilocus Sequence Typing

Detection of biofilm formation, icaADBC gene and investigation of toxin genes in Staphylococus spp. strain from dental unit waterlines, University Hospital Center (UHC) Tlemcen Algeria

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