sesA, sesB, sesC, sesD, sesE, sesG, sesH,andembpgenes are genetic markers that differentiate commensal isolates ofStaphylococcus epidermidisfrom isolates that cause prosthetic joint infection

Ortega‐Peña, Silvestre; Vargas-Mendoza, Carlos F.; Franco-Cendejas, Rafael; Aquino-Andrade, Alejandra; Vazquez-Rosas, Guillermo Jose; Betanzos‐Cabrera, Gabriel; Guerrero–Barajas, Claudia; Jan‐Roblero, Janet; Rodríguez‐Martínez, Sandra; Cancino-Diaz, Mario E.; Diaz, Juan C. Cancino

doi:10.1080/23744235.2019.1597276

Cited by 10 publications

(9 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…All isolates used in this work have been characterized genotypically (PFGE, agr type, and SSC mec ), showing a high diversity among them (Flores‐Páez et al, ; Ortega‐Peña et al, ). When including phenotypic data (production of protease‐independent biofilm, trypsin‐induced biofilm or no production of trypsin‐induced biofilm) in the phylogenetic trees reported, we did not find a correlation between the isolates and different phenotypes.…”

Section: Resultsmentioning

confidence: 99%

“…However, a large number of clinical and commensal isolates must be analyzed in epidemiological studies in order to establish the importance of this protease‐induced biofilms mechanism. In previous studies, we demonstrated that collections of isolates from OI and PJI are genetically different and there are no clonal associations between them; it also occurs with commensal isolates (Flores‐Páez et al, ; Ortega‐Peña et al, ). Thus, the objective of this work was to evaluate the trypsin biofilm induction capacity of genetically different S. epidermidis isolates from clinical (OI and PJI) and commensal (HS) sources.…”

Section: Introductionmentioning

confidence: 84%

“…Commensal and clinical CoNS isolates used in this work were those reported previously by our research group. Twenty‐four clinical isolates of patients with OI from 2000 to 2010 were obtained from “Instituto de Oftalmología Fundación Conde de Valenciana” (Flores‐Páez et al, ), and 64 clinical isolates of patients with PJI from 2011 to 2015 were from “Instituto Nacional de Rehabilitación Luís Guillermo Ibarra Ibarra” (Ortega‐Peña et al, ).…”

Section: Methodsmentioning

confidence: 99%

“…Non‐epidermidis CoNS was composed as follows: 11 Staphylococcus hominis ; 5 Staphylococcus warneri ; 2 as Staphylococcus capitis ; and 1 of each of Staphylococcus lentus , Staphylococcus caprae , Staphylococcus sciuri , Staphylococcus haemolyticus , and Staphylococcus lugdunensis . Genotypic features of OI, PJI, and HS‐1 isolates were previously determined (MLST, agr type, SSC me c type), showing high diversity among them (Flores‐Páez et al, ; Ortega‐Peña et al, ).…”

Section: Methodsmentioning

confidence: 99%

“…Together with Staphylococcus aureus , CoNS are the primary agents responsible for nosocomial infections and represent the most common source of infections associated with medical devices (Darouiche, ), causing a problem for the public health system. Molecular epidemiological studies reveal a sizeable genetic diversity among staphylococci (Conlan et al, ; Schoenfelder et al, ); in isolates from ocular infections (OI), prosthetic joint infections (PJI), and healthy skin (HS), there is no genetic association among them (Flores‐Páez et al, ; Ortega‐Peña et al, , in press). For the case of isolates from ocular infections (OI), biofilm formation is a discriminant biomarker compared to commensal isolates (Duggirala et al, ; Jain & Agarwal, ; Okee et al, ; Suzuki, Kawamura, Uno, Ohashi, & Ezaki, ); however, there is evidence that the number of isolates from prosthetic joint infections with biofilm formation capacity is similar to commensal isolates (Hellmark, Söderquist, Unemo, & Nilsdotter‐Augustinsson, ).…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

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

et al. 2019

View full text Add to dashboard Cite

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,

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 84%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%