Methicillin resistance and virulence genes in invasive and nasal Staphylococcus epidermidis isolates from neonates

Salgueiro, Vivian C.; Iório, Natalia Lopes Pontes; Ferreira, Mariana; Chamon, Raiane Cardoso; Santos, Kátia Regina Netto dos

doi:10.1186/s12866-017-0930-9

Cited by 38 publications

(36 citation statements)

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“…In contrast, bhp , a gene homologous to bap and assumed to promote biofilm formation ( Becker et al, 2014 ), was found more frequent among sesI -negative isolates than sesI -positive isolates. Taken together, our data showed that sesI -positive S. epidermidis invasive isolates harbored more virulence-associated genes relative to sesI -negative isolates, which is similar to the previous study ( Salgueiro et al, 2017 ).…”

Section: Discussionsupporting

confidence: 91%

“…In this present study, the prevalence of icaA among sesI -positive S. epidermidis isolates was higher relative to sesI -negative isolates. The accumulation-associated protein (Aap) encoded by aap confers intercellular adhesion and plays a role in skin colonization by its N-terminal domain A mediating adherence to human corneocytes ( Macintosh et al, 2009 ; Salgueiro et al, 2017 ). The positive rate of aap among sesI -positive isolates was significantly higher than that among sesI -negative isolates (56.6%) ( P < 0.05) in the present study.…”

Section: Discussionmentioning

confidence: 99%

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SesI May Be Associated with the Invasiveness of Staphylococcus epidermidis

Jin

Duan

et al. 2018

Front. Microbiol.

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Staphylococcus epidermidis is a commensal bacterium which widely colonizes in human skin and mucous membrane and rarely causes clinically manifested infections. S. epidermidis surface protein I (SesI) is considered to be the major virulence factor of S. epidermidis infection, but its pathogenesis is not clear. Here, we demonstrated that the prevalence of sesI among S. epidermidis invasive isolates (20.8%, 26/125) was significantly higher than that among colonizing isolates (3.8%, 4/106). The positive rates of biofilm-associated genes (aap, icaA, IS256) and resistance-associated genes mupA among the sesI-positive isolates were significantly higher than those among sesI-negative isolates (p < 0.05). And antimicrobial susceptibility testing showed that the resistance rates of sesI-positive isolates to ciprofloxacin, gentamicin and trimethoprim/sulfamethoxazole were significantly higher than those among sesI-negative isolates. Interestingly, 80.8% (21/26) of sesI-positive isolates belong to ST2 determined by MLST, while ST2 was not found among any of the 99 sesI-negative invasive isolates, indicating that there is a strong association between carriage of sesI and ST2 clone. In order to further study the role of sesI gene in pathogenesis, the sesI gene mutant (S. epidermidis RP62AΔsesI) and complementary expression strain (S. epidermidis RP62AΔsesI-C) were successfully constructed. All experimental data indicated that sesI may promote S. epidermidis to adhere and aggregate, but it had no obvious effect on the mature stage of biofilm formation. Taken together, these results suggest that sesI, along with antimicrobial and other biofilm-associated genes enables S. epidermidis easier for colonization and adhesion and contributes to the spread of S. epidermidis, especially ST2 clone.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

SesI May Be Associated with the Invasiveness of Staphylococcus epidermidis

Jin

Duan

et al. 2018

Front. Microbiol.

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“…It is carried on the mobile genetic element, staphylococcal cassette chromosome mec (SCC mec ), of which several types have been identified for S. epidermidis (Miragaia et al, 2005 ). MRSE have been found to be common in infection-causing isolates (70–87% of all S. epidermidis isolates) (Cherifi et al, 2013 ; Farina et al, 2016 ; Morgenstern et al, 2016c ; Salgueiro et al, 2017 ), and even higher (90%) in specific patient cohorts (Morgenstern et al, 2016b ). MRSE prevalence in healthy individuals is low (3–18% of S. epidermidis commensal isolates) (Rolo et al, 2012 ; Cherifi et al, 2013 ; Farina et al, 2016 ), although prevalence is increased for individuals exposed to the healthcare system, as observed in hospitalized patients or in healthcare workers (Rohde et al, 2004 ; Morgenstern et al, 2016a ; Widerstrom et al, 2016 ).…”

Section: S Epidermidis As a Pathogenmentioning

confidence: 99%

Pathogenic Mechanisms and Host Interactions in Staphylococcus epidermidis Device-Related Infection

et al. 2017

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Staphylococcus epidermidis is a permanent member of the normal human microbiota, commonly found on skin and mucous membranes. By adhering to tissue surface moieties of the host via specific adhesins, S. epidermidis is capable of establishing a lifelong commensal relationship with humans that begins early in life. In its role as a commensal organism, S. epidermidis is thought to provide benefits to human host, including out-competing more virulent pathogens. However, largely due to its capacity to form biofilm on implanted foreign bodies, S. epidermidis has emerged as an important opportunistic pathogen in patients receiving medical devices. S. epidermidis causes approximately 20% of all orthopedic device-related infections (ODRIs), increasing up to 50% in late-developing infections. Despite this prevalence, it remains underrepresented in the scientific literature, in particular lagging behind the study of the S. aureus. This review aims to provide an overview of the interactions of S. epidermidis with the human host, both as a commensal and as a pathogen. The mechanisms retained by S. epidermidis that enable colonization of human skin as well as invasive infection, will be described, with a particular focus upon biofilm formation. The host immune responses to these infections are also described, including how S. epidermidis seems to trigger low levels of pro-inflammatory cytokines and high levels of interleukin-10, which may contribute to the sub-acute and persistent nature often associated with these infections. The adaptive immune response to S. epidermidis remains poorly described, and represents an area which may provide significant new discoveries in the coming years.

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“…Whole genome sequencing (WGS) provides the ability for high-resolution genetic typing analysis that can be used in epidemiological investigations whilst simultaneously providing information on an isolate's gene content. Previous studies to provide STEC serogroup phylogenies have been limited through the analysis of WGS data from a limited number of serogroup-specific strains [41][42][43], or from datasets biased towards human isolates [44], causing wide-ranging serogroup-specific diversity to be over looked.…”

Section: Plos Onementioning

confidence: 99%

“…The detection of stxbacteriophage insertion sites in serogroup O145 isolates is problematic due to multiple potential insertion sites, variations in prophage structure and variation between integration sites, including between phage which encode the same Stx subtype [44]. In addition, "Stx 2 -like" prophage, which appear to be defective as a result of nonsense mutations in the stx 2 A subunit or absent stx 2 A and stx 2 B genes, have been detected in serogroup O145 strains [42], further complicating the detection of stx-bacteriophage insertion sites in this serogroup.…”

Section: Plos Onementioning

confidence: 99%

Genomic epidemiology and carbon metabolism of Escherichia coli serogroup O145 reflect contrasting phylogenies

et al. 2020

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Shiga toxin-producing Escherichia coli (STEC) are a leading cause of foodborne outbreaks of human disease, but they reside harmlessly as an asymptomatic commensal in the ruminant gut. STEC serogroup O145 are difficult to isolate as routine diagnostic methods are unable to distinguish non-O157 serogroups due to their heterogeneous metabolic characteristics, resulting in under-reporting which is likely to conceal their true prevalence. In light of these deficiencies, the purpose of this study was a twofold approach to investigate enhanced STEC O145 diagnostic culture-based methods: firstly, to use a genomic epidemiology approach to understand the genetic diversity and population structure of serogroup O145 at both a local (New Zealand) (n = 47) and global scale (n = 75) and, secondly, to identify metabolic characteristics that will help the development of a differential media for this serogroup. Analysis of a subset of E. coli serogroup O145 strains demonstrated considerable diversity in carbon utilisation, which varied in association with eae subtype and sequence type. Several carbon substrates, such as D-serine and D-malic acid, were utilised by the majority of serogroup O145 strains, which, when coupled with current molecular and culture-based methods, could aid in the identification of presumptive E. coli serogroup O145 isolates. These carbon substrates warrant subsequent testing with additional serogroup O145 strains and non-O145 strains. Serogroup O145 strains displayed extensive genetic heterogeneity that was correlated with sequence type and eae subtype, suggesting these genetic markers are good indicators for distinct E. coli phylogenetic lineages. Pangenome analysis identified a core of 3,036 genes and an open pangenome of >14,000 genes, which is consistent with the identification of distinct phylogenetic lineages. Overall, this study highlighted the phenotypic and genotypic heterogeneity within E. coli serogroup O145, suggesting that the development of a differential media targeting this serogroup will be challenging.

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Methicillin resistance and virulence genes in invasive and nasal Staphylococcus epidermidis isolates from neonates

Cited by 38 publications

References 50 publications

SesI May Be Associated with the Invasiveness of Staphylococcus epidermidis

SesI May Be Associated with the Invasiveness of Staphylococcus epidermidis

Pathogenic Mechanisms and Host Interactions in Staphylococcus epidermidis Device-Related Infection

Genomic epidemiology and carbon metabolism of Escherichia coli serogroup O145 reflect contrasting phylogenies

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