Biofilm formation by Staphylococcus hominis strains isolated from human clinical specimens

Szczuka, Ewa; Telega, Kinga; Kaznowski, Adam

doi:10.1007/s12223-014-0332-4

Cited by 28 publications

(28 citation statements)

References 24 publications

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“…The presence of adhesins in S. hominis strains was not tested, which is a limitation of this work. Our earlier results revealed that all S. hominis strains tested in this study harbour the ica ADBC genes encoding the polysaccharide intercellular adhesin (PIA) (Szczuka et al 2015). …”

Section: Discussionmentioning

confidence: 89%

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Multifactorial mechanisms of the pathogenesis of methicillin-resistant Staphylococcus hominis isolated from bloodstream infections

Szczuka

Krzymińska

Bogucka

et al. 2017

Antonie van Leeuwenhoek

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Staphylococcus hominis is a species of the coagulase-negative staphylococci. It has been designated as a potential pathogen but so far the pathogenic mechanisms of this bacterium have not been determined. We studied 30 clinical isolates of methicillin-resistant S. hominis, which were previously examined for biofilm forming properties. The results of this study revealed that all these S. hominis strains had the ability to adhere to HeLa cells. Over 40% of the S. hominis strains invaded epithelial cells. The invasion index ranged from 0 to 41.5%. All isolates exhibited the cytotoxic activity of extracellular factors, which caused the destruction of epithelial cells. More than 90% of these methicillin-resistant strains contained at least one aminoglycosides resistance gene. The ant(4′)-I gene was found in 63% of the isolates, aac(6′)/aph(2″) in 20% and aph(3′)-IIIa in 47%. Two strains were assigned to SCCmec type VIII and three to SCCmec type III. The remaining isolates (83%) harboured a non-typeable SCCmec type. The mec complex A was predominant in this species. The results indicate that the pathogenicity of S. hominis may be multifactorial, involving adhesion, invasion and the activity of extracellular toxins, which cause damage to the host epithelium.

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Section: Discussionmentioning

confidence: 89%

“…Isolates were stored at − 70 °C. Previously, these strains were tested for biofilm forming properties (Szczuka et al 2015). Resistance to methicillin was determined by a cefoxitin disc test.…”

Section: Methodsmentioning

confidence: 99%

Multifactorial mechanisms of the pathogenesis of methicillin-resistant Staphylococcus hominis isolated from bloodstream infections

Szczuka

Krzymińska

Bogucka

et al. 2017

Antonie van Leeuwenhoek

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“…hominis biofilm production, their architecture and icaADBC frequency. [ 22 ] However, compared to other CoNS species, S . hominis is not categorised as a strong biofilm producer.…”

Section: Introductionmentioning

confidence: 99%

Antibiotic Susceptibility of Biofilm Cells and Molecular Characterisation of Staphylococcus hominis Isolates from Blood

et al. 2015

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ObjectivesWe aimed to characterise the staphylococcal cassette chromosome mec (SCCmec) type, genetic relatedness, biofilm formation and composition, icaADBC genes detection, icaD expression, and antibiotic susceptibility of planktonic and biofilm cells of Staphylococcus hominis isolates from blood.MethodsThe study included 67 S. hominis blood isolates. Methicillin resistance was evaluated with the cefoxitin disk test. mecA gene and SCCmec were detected by multiplex PCR. Genetic relatedness was determined by pulsed-field gel electrophoresis. Biofilm formation and composition were evaluated by staining with crystal violet and by detachment assay, respectively; and the biofilm index (BI) was determined. Detection and expression of icaADBC genes were performed by multiplex PCR and real-time PCR, respectively. Antibiotic susceptibilities of planktonic cells (minimum inhibitory concentration, MIC) and biofilm cells (minimum biofilm eradication concentration, MBEC) were determined by the broth dilution method.ResultsEighty-five percent (57/67) of isolates were methicillin resistant and mecA positive. Of the mecA-positive isolates, 66.7% (38/57) carried a new putative SCCmec type. Four clones were detected, with two to five isolates each. Among all isolates, 91% (61/67) were categorised as strong biofilm producers. Biofilm biomass composition was heterogeneous (polysaccharides, proteins and DNA). All isolates presented the icaD gene, and 6.66% (1/15) isolates expressed icaD. This isolate presented the five genes of ica operon. Higher BI and MBEC values than the MIC values were observed for amikacin, vancomycin, linezolid, oxacillin, ciprofloxacin, and chloramphenicol.Conclusions S. hominis isolates were highly resistant to methicillin and other antimicrobials. Most of the detected SCCmec types were different than those described for S. aureus. Isolates indicated low clonality. The results indicate that S. hominis is a strong biofilm producer with an extracellular matrix with similar composition of proteins, DNA and N-acetylglucosamine; and presents high frequency and low expression of icaD gene. Biofilm production is associated with increased antibiotic resistance.

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“…When this procedure was used in non‐epidermidis CoNS, the proportions of isolates that could or could not form a trypsin‐induced biofilm were not significantly different, suggesting that trypsin is not adequate for biofilm induction in these isolates. Information concerning biofilm formation in non‐epidermidis CoNS is limited, and the molecular mechanisms mediating biofilm formation are less studied (Frank & Patel, ; Fredheim et al, ; Szczuka, Telega, & Kaznowski, ; Yokoi et al, ). A mechanism concerning a protease that favors biofilm formation has not yet been found.…”

Section: Discussionmentioning

confidence: 99%

Non‐biofilm‐forming commensal Staphylococcus epidermidis isolates produce biofilm in the presence of trypsin

et al. 2019

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Epidemiological studies comparing clinical and commensal Staphylococcus epidermidisisolates suggest that biofilm formation is a discriminant biomarker. A study showed that four non-biofilm-forming clinical S. epidermidis isolates could form an induced biofilm by trypsin treatment, suggesting that S. epidermidis can form biofilms in a protease-independent way and in a trypsin-induced way. In this study, the trypsin capacity to induce biofilm formation was evaluated in non-biofilm-forming S. epidermidis isolates (n = 133) in order to support this mechanism and to establish the importance of total biofilms (meaning the sum of protease-independent biofilm and trypsin-induced biofilm). Staphylococcus epidermidis isolates from ocular infections (OI; n = 24), prosthetic joint infections (PJI; n = 64), and healthy skin (HS-1; n = 100) were screened for protease-independent biofilm formation according to Christensen's method. The result was that there are significant differences (p < .0001) between clinical (43.2%) and commensal (17%) protease-independent biofilm producers. Meanwhile, non-biofilm-forming isolates were treated with trypsin, and biofilm formation was evaluated by the same method. The number of commensal trypsin-induced biofilm producers significantly increased from 17% to 79%. In contrast, clinical isolates increased from 43.2% to 72.7%. The comparison between clinical and commensal total biofilm yielded no significant differences (p = .392). A similar result was found when different isolation sources were compared (OI vs. HS-1 and PJI vs. HS-1). The genotype icaA − /aap + was associated with the trypsin-induced biofilm phenotype; however, no correlation was observed between aap mRNA expression and the level of trypsin-induced biofilm phenotype. Studying another group of commensal S. epidermidis nonbiofilm-forming isolates (HS-2; n = 139) from different body sites, it was found that 70 have been corrected.] | MATERIAL S AND ME THODS | CoNS isolatesCommensal and clinical CoNS isolates used in this work were those reported previously by our research group. Twenty-four clinical isolates (60.3%) formed trypsin-induced biofilms. In conclusion, trypsin is capable of inducing biofilm production in non-biofilm-forming commensal S. epidermidis isolates with the icaA − /aap + genotype, and there is no significant difference in total biofilms when comparing clinical and commensal isolates, suggesting that total biofilms are not a discriminant biomarker. K E Y W O R D Snon-biofilm-forming, protease-independent biofilm, Staphylococcus epidermidis, total biofilm,

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Biofilm formation by Staphylococcus hominis strains isolated from human clinical specimens

Cited by 28 publications

References 24 publications

Multifactorial mechanisms of the pathogenesis of methicillin-resistant Staphylococcus hominis isolated from bloodstream infections

Multifactorial mechanisms of the pathogenesis of methicillin-resistant Staphylococcus hominis isolated from bloodstream infections

Antibiotic Susceptibility of Biofilm Cells and Molecular Characterisation of Staphylococcus hominis Isolates from Blood

Non‐biofilm‐forming commensal Staphylococcus epidermidis isolates produce biofilm in the presence of trypsin

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