Biofilms of clinical strains of<i>Staphylococcus</i>that do not contain polysaccharide intercellular adhesin

Kogan, Grigorij; Sadovskaya, Irina; Chaignon, Philippe; Chokr, Ali; Jabbouri, Saı̈d

doi:10.1111/j.1574-6968.2005.00043.x

Cited by 119 publications

(104 citation statements)

References 30 publications

(50 reference statements)

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“…Chaieb et al [31] described icapositive S. epidermidis isolates which did not produce biofi lm and S. epidermidis which was ica-negative but was somehow able to produce biofi lm. Similar results were reported by Kogan et al [39]. In our study, two of the three biofi lm producers were IS256-positive.…”

Section: Biofilm Formation and Insertion Element Is256supporting

confidence: 81%

Genetic determinants and biofilm formation of clinicalStaphylococcus epidermidisisolates from blood cultures and indwelling devises

Mertens¹,

Ghebremedhin²

2013

European Journal of Microbiology and Immunology

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For a long time, Staphylococcus epidermidis, as a member of the coagulase-negative staphylococci, was considered as part of the physiological skin flora of the human being with no pathogenic significance. Today, we know that S. epidermidis is one of the most prevalent causes for implant-associated and nosocomial infections. We performed pheno-and genotypic analysis (ica, IS256, SCCmec types, agr groups) of biofilm formation in 200 isolates. Fifty percent were genetically ica-positive and produced biofilm. Among all studied isolates, agr II and III and SCCmec type I were the most prevalent, whereas within the selected multi-resistant isolates (29%), agr I and III and SCCmec type II dominated. SCCmec type I and mecA-negative S. epidermidis isolates were associated with agr II. The majority of the blood culture and biopsy isolates were assigned to agr III and SCCmec type I, whereas agr II was predominantly detected in mecA-negative S. epidermidis isolated from catheter and implant materials. MLST analysis revealed the major clonal lineages of ST2, ST5, ST10, and ST242 (total 13 STs). ST2 isolates from blood cultures were icaA/D-positive and harbored SCCmec types II and III and IS256, whereas the icaA/D-and IS256-positive ST23 isolates were assigned to SCCmec types I and IV.

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Section: Biofilm Formation and Insertion Element Is256supporting

confidence: 81%

Genetic determinants and biofilm formation of clinicalStaphylococcus epidermidisisolates from blood cultures and indwelling devises

Mertens¹,

Ghebremedhin²

2013

European Journal of Microbiology and Immunology

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“…An early study reported that CoNS, isolated from paediatric shunt infections, were capable of producing a visible mucoid extracellular matrix in vitro (Bayston & Penny, 1972). However, more recent studies have demonstrated the existence of ica-independent and protein-dependent pathways (Rohde et al, 2005;Kogan et al, 2006). The variation in biofilm-forming capabilities of S. epidermidis is likely to be great, given the possible combinations of interactions between the organism itself and the surrounding environment.…”

Section: Resultsmentioning

confidence: 99%

Biofilm characteristics of Staphylococcus epidermidis isolates associated with device-related meningitis

Stevens

Greene

O’Gara

et al. 2009

Journal of Medical Microbiology

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Staphylococcus epidermidis biofilm causes device-related meningitis in neurosurgical patients. This study assessed the contribution of polysaccharide and protein to the development of a strong biofilm-positive phenotype in four S. epidermidis isolates associated with probable device-related meningitis, under varying environmental conditions. RT-PCR analysis of the intercellular adhesion operon (icaADBC) and assessment of polysaccharide intercellular adhesin (PIA) production indicated a correlation between increased icaA transcription and PIA production in ica + isolates grown in medium with 4 % ethanol and 4 % NaCl. Treatment of biofilm with sodium metaperiodate caused dispersion of adhered cells (P ,0.0001), indicating involvement of PIA. Transcriptional levels of protein factors revealed that atlE transcription levels were similar in all isolates, whilst aap levels were variable, with induction being seen in two isolates following growth in the presence of alcohol or salt. Transcription of agr did not influence protein expression and RNAIII transcription varied among the strains. Although aap transcription was induced, the treatment of biofilm with proteinase K did not always disperse the biofilm. Our data suggest that, among the three ica + S. epidermidis isolates clinically associated with meningitis that were studied, PIA contributed to the strong biofilm-positive phenotype, whereas protein factors appeared to have a secondary role. INTRODUCTIONSuccessful treatment and prevention of hydrocephalus, a common neurosurgical condition, often involves the insertion of an external ventricular drain (EVD) or a shunt. However, this can be complicated by infections such as meningitis, often caused by coagulase-negative staphylococci (CoNS), with Staphylococcus epidermidis being isolated most frequently (Diaz-Mitoma et al., 1987). Mounting evidence suggests that such infections are a result of biofilm formation on the device (Diaz-Mitoma et al., 1987;Tojo et al., 1988;Kockro et al., 2000).Staphylococcal biofilm formation involves both host and bacterial factors. Early investigations have shown that production of polysaccharide is a primary mechanism employed by S. epidermidis (Peters et al., 1987;Tojo et al., 1988; Christensen et al., 1990;Mack et al., 1992). The polysaccharide is a polymeric homoglycan consisting of repeating units of b-1,6-N-acetylglucosamine (Mack et al., 1996; McKenney et al., 1998;Maira-Litran et al., 2002;Sadovskaya et al., 2005), termed polysaccharide intercellular adhesin (PIA). Synthesis of PIA is linked to the biosynthetic enzyme-coding genes located in the intercellular adhesion operon (icaADBC) (Heilmann et al., 1996), and biofilm production involving PIA is known to be ica-dependent and is considered the primary mechanism employed by staphylococci (Stevens et al., 2008).Other ica-independent mechanisms of biofilm development in staphylococci have been identified and protein factors such as the major cell-wall autolysin (AtlE) have been found to promote the initial adhesion of S. epiderm...

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“…According to an alternative hypothesis, these processes may also be accomplished by enzymatic degradation of biofilm matrix molecules. In that regard, recent research indicated that staphylococcal biofilm formation is accomplished by protein and/or exopolysaccharide biofilm matrix components (24,25). Hypothetically, enzymatic degradation of these polymers may thus contribute to biofilm maturation; and a proteolytic detachment mechanism has been proposed for protein-dependent biofilms of S. aureus (28).…”

Section: Discussionmentioning

confidence: 99%

“…Biofilm formation in staphylococci has been shown to be exopolysaccharide dependent or independent (24,25). To analyze whether PSMβ peptides mediate biofilm detachment in both exopolysaccharide-dependent and -independent S. epidermidis biofilms, we first determined presence of the ica genes responsible for production of the main biofilm exopolysaccharide polysaccharide intercellular adhesin (PIA, or poly-N-acetylglucosamine [PNAG]) in the 24 agr-negative S. epidermidis strains.…”

Section: Figurementioning

confidence: 99%

Staphylococcus epidermidis surfactant peptides promote biofilm maturation and dissemination of biofilm-associated infection in mice

et al. 2011

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Biofilms are surface-attached agglomerations of microorganisms embedded in an extracellular matrix. Biofilm-associated infections are difficult to eradicate and represent a significant reservoir for disseminating and recurring serious infections. Infections involving biofilms frequently develop on indwelling medical devices in hospitalized patients, and Staphylococcus epidermidis is the leading cause of infection in this setting. However, the molecular determinants of biofilm dissemination are unknown. Here we have demonstrated that specific secreted, surfactant-like S. epidermidis peptides -the β subclass of phenol-soluble modulins (PSMs) -promote S. epidermidis biofilm structuring and detachment in vitro and dissemination from colonized catheters in a mouse model of device-related infection. Our study establishes in vivo significance of biofilm detachment mechanisms for the systemic spread of biofilm-associated infection and identifies the effectors of biofilm maturation and detachment in a premier biofilm-forming pathogen. Furthermore, by demonstrating that antibodies against PSMβ peptides inhibited bacterial spread from indwelling medical devices, we have provided proof of principle that interfering with biofilm detachment mechanisms may prevent dissemination of biofilm-associated infection.

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Biofilms of clinical strains ofStaphylococcusthat do not contain polysaccharide intercellular adhesin

Cited by 119 publications

References 30 publications

Genetic determinants and biofilm formation of clinicalStaphylococcus epidermidisisolates from blood cultures and indwelling devises

Genetic determinants and biofilm formation of clinicalStaphylococcus epidermidisisolates from blood cultures and indwelling devises

Biofilm characteristics of Staphylococcus epidermidis isolates associated with device-related meningitis

Staphylococcus epidermidis surfactant peptides promote biofilm maturation and dissemination of biofilm-associated infection in mice

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