The Majority of a Collection of U.S. Endocarditis Enterococcus faecalis Isolates Obtained from 1974 to 2004 Lack Capsular Genes and Belong to Diverse, Non-Hospital-Associated Lineages

Chowdhury, Shahreen; Nallapareddy, Sreedhar R.; Arias, César A.; Murray, Barbara E.

doi:10.1128/jcm.02763-13

Cited by 10 publications

(10 citation statements)

References 61 publications

(95 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition, in line with a previous investigation that reported a low correlation between the presence of capsule among E. faecalis clinical isolates and the ability to establish infection (53), our data showed that the distributions of cell wall polysaccharides are equal at all levels of E. faecalis virulence, and no significant difference in C. elegans pathogenicity was observed.…”

Section: Discussionsupporting

confidence: 80%

A Genomic Virulence Reference Map of Enterococcus faecalis Reveals an Important Contribution of Phage03-Like Elements in Nosocomial Genetic Lineages to Pathogenicity in a Caenorhabditis elegans Infection Model

et al. 2015

Self Cite

View full text Add to dashboard Cite

eIn the present study, the commensal and pathogenic host-microbe interaction of Enterococcus faecalis was explored using a Caenorhabditis elegans model system. The virulence of 28 E. faecalis isolates representing 24 multilocus sequence types (MLSTs), including human commensal and clinical isolates as well as isolates from animals and of insect origin, was investigated using C. elegans strain glp-4 (bn2ts); sek-1 (km4). This revealed that 6 E. faecalis isolates behaved in a commensal manner with no nematocidal effect, while the remaining strains showed a time to 50% lethality ranging from 47 to 120 h. Principal component analysis showed that the difference in nematocidal activity explained 94% of the variance in the data. Assessment of known virulence traits revealed that gelatinase and cytolysin production accounted for 40.8% and 36.5% of the observed pathogenicity, respectively. However, coproduction of gelatinase and cytolysin did not increase virulence additively, accounting for 50.6% of the pathogenicity and therefore indicating a significant (26.7%) saturation effect. We employed a comparative genomic analysis approach using the 28 isolates comprising a collection of 82,356 annotated coding sequences (CDS) to identify 2,325 patterns of presence or absence among the investigated strains. Univariate statistical analysis of variance (ANOVA) established that individual patterns positively correlated (n ‫؍‬ 61) with virulence. The patterns were investigated to identify potential new virulence traits, among which we found five patterns consisting of the phage03-like gene clusters. Strains harboring phage03 showed, on average, 17% higher killing of C. elegans (P ‫؍‬ 4.4e ؊6 ). The phage03 gene cluster was also present in gelatinase-and-cytolysinnegative strain E. faecalis JH2-2. Deletion of this phage element from the JH2-2 clinical strain rendered the mutant apathogenic in C. elegans, and a similar mutant of the nosocomial V583 isolate showed significantly attenuated virulence. Bioinformatics investigation indicated that, unlike other E. faecalis virulence traits, phage03-like elements were found at a higher frequency among nosocomial isolates. In conclusion, our report provides a valuable virulence map that explains enhancement in E. faecalis virulence and contributes to a deeper comprehension of the genetic mechanism leading to the transition from commensalism to a pathogenic lifestyle. Enterococcus faecalis is a Gram-positive commensal bacterium of the mammalian gastrointestinal (GI) tract (1) and a leading cause of nosocomial infections worldwide (2). In humans, the normal abundance of E. faecalis in the intestinal lumen ranges between 10 5 and 10 8 CFU/g of feces without causing any obvious deleterious effects on the host (3, 4). However, if either perturbations of the host/commensal balance that weaken the host immune system or environmental factors such as use of antibiotics that inadvertently facilitate outgrowth of resistant E. faecalis occur, life-threatening infections might arise. Moreover, the intri...

show abstract

Section: Discussionsupporting

confidence: 80%

A Genomic Virulence Reference Map of Enterococcus faecalis Reveals an Important Contribution of Phage03-Like Elements in Nosocomial Genetic Lineages to Pathogenicity in a Caenorhabditis elegans Infection Model

et al. 2015

Self Cite

View full text Add to dashboard Cite

show abstract

“…Differences in the accessory genomes of ST16 and ST179 (a SLV of ST16 confined to humans) reflect different patterns of recombination. Differences in accessory genomes were also observed for members of the hierBAPS wgsEFS‐B that encompasses ST55 (wgsEFS‐4) and ST40 (wgsEFS‐5, wgsEFS‐6), which has been detected in wild birds and humans, and also ST26 (wgsEFS‐7), which is common in healthy humans (Freitas et al ., ; Chowdhury et al ., ; Tedim et al ., ; Zischka et al ., ). The third large hierBAPS group, wgsEFS‐C, was overrepresented in the human‐associated ST6 and ST2 lineages, but has also been recovered from foodborne animals (Freitas et al ., ) and rodents (Lozano et al ., ).…”

Section: Discussionmentioning

confidence: 99%

Phylogenomics of Enterococcus faecalis from wild birds: new insights into host‐associated differences in core and accessory genomes of the species

León‐Sampedro

Campo

Rodríguez-Baños

et al. 2019

Environmental Microbiology

View full text Add to dashboard Cite

Summary Wild birds have been suggested to be reservoirs of antimicrobial resistant and/or pathogenic Enterococcus faecalis (Efs) strains, but the scarcity of studies and available sequences limit our understanding of the population structure of the species in these hosts. Here, we analysed the clonal and plasmid diversity of 97 Efs isolates from wild migratory birds. We found a high diversity, with most sequence types (STs) being firstly described here, while others were found in other hosts including some predominant in poultry. We found that pheromone‐responsive plasmids predominate in wild bird Efs while 35% of the isolates entirely lack plasmids. Then, to better understand the ecology of the species, the whole genome of fivestrains with known STs (ST82, ST170, ST16 and ST55) were sequenced and compared with all the Efs genomes available in public databases. Using several methods to analyse core and accessory genomes (AccNET, PLACNET, hierBAPS and PANINI), we detected differences in the accessory genome of some lineages (e.g. ST82) demonstrating specific associations with birds. Conversely, the genomes of other Efs lineages exhibited divergence in core and accessory genomes, reflecting different adaptive trajectories in various hosts. This pangenome divergence, horizontal gene transfer events and occasional epidemic peaks could explain the population structure of the species.

show abstract

“…Besides, their multilocus sequence typing (MLST)-based strain lineages (sequence types [STs]) were not yet defined. Alternatively, the sequence types in some genome-sequenced strains are available from previous reports (42,43), and we could partially investigate the correlations of Bac41 types with ST clonal lineages (Table 6; see also Recombinant His-tagged BacL 1 and BacA proteins derived from pYI14 (rBacL 1pYI14 and rBacA pYI14 ), pYI12 (rBacL 1pYI12 and rBacA pYI12 ), or pMGT421 (rBacL 1pMGT421 and rBacA pMGT421 ) proteins (400 ng) were separated by SDS-PAGE and stained with Coomassie brilliant blue (CBB). (B) Combinations of recombinant His-tagged BacL 1 and BacA proteins derived from pYI14 (rBacL 1pYI14 and rBacA pYI14 ), pYI12 (rBacL 1pYI12 and rBacA pYI12 ), or pMGT421 (rBacL 1pMGT421 and rBacA pMGT421 ) proteins (25 ng each) were spotted onto THB soft-agar (0.75%) plates containing the indicator strains.…”

Section: Discussionmentioning

confidence: 99%

Partial Diversity Generates Effector Immunity Specificity of the Bac41-Like Bacteriocins of Enterococcus faecalis Clinical Strains

2016

View full text Add to dashboard Cite

Bacteriocin 41 (Bac41) is the plasmid-encoded bacteriocin produced by the opportunistic pathogen Enterococcus faecalis. Its genetic determinant consists of bacL 1 (effector), bacL 2 (regulator), bacA (effector), and bacI (immunity). The secreted effectors BacL 1 and BacA coordinate to induce the lytic cell death of E. faecalis. Meanwhile, the immunity factor BacI provides self-resistance to the Bac41 producer, E. faecalis, against the action of BacL 1 and BacA. In this study, we demonstrated that more than half of the 327 clinical strains of E. faecalis screened had functional Bac41 genes. Analysis of the genetic structure of the Bac41 genes in the DNA sequences of the E. faecalis strains revealed that the Bac41-like genes consist of a relatively conserved region and a variable region located downstream from bacA. Based on similarities in the variable region, the Bac41-like genes could be classified into type I, type IIa, and type IIb. Interestingly, the distinct Bac41 types had specific immunity factors for self-resistance, BacI1 or BacI2, and did not show cross-immunity to the other type of effector. We also demonstrated experimentally that the specificity of the immunity was determined by the combination of the C-terminal region of BacA and the presence of the unique BacI1 or BacI2 factor. These observations suggested that Bac41-like bacteriocin genes are extensively disseminated among E. faecalis strains in the clinical environment and can be grouped into at least three types. It was also indicated that the partial diversity results in specificity of self-resistance which may offer these strains a competitive advantage. IMPORTANCEBacteriocins are antibacterial effectors produced by bacteria. In general, a bacteriocin-coding gene is accompanied by a cognate immunity gene that confers self-resistance on the bacteriocin-producing bacterium itself. We demonstrated that one of the bacteriocins, Bac41, is disseminated among E. faecalis clinical strains and the Bac41 subtypes with partial diversity. The Bac41-like bacteriocins were found to be classified into type I, type IIa, and type IIb by variation of the cognate immunity factors. The antibacterial activity of the respective effectors was specifically inhibited by the immunity factor from the same type of Bac41 but not the other types. This specificity of effector-immunity pairs suggests that bacteriocin genes might have evolved to change the immunity specificity to acquire an advantage in interbacterial competition. Enterococcus faecalis is a Gram-positive commensal bacterium present in the intestinal tract of healthy humans or animals, but it is also a causative agent of opportunistic infectious diseases, including urinary infectious disease, bacteremia, infective endocarditis, and others (1-4). As represented by the development of drug resistance, the acquisition of new genes via mobile genetic elements (MGEs), such as plasmids, raises the concern of increased severity of these enterococcal diseases (5). Enterococcal plasmids also encode various bact...

show abstract

The Majority of a Collection of U.S. Endocarditis Enterococcus faecalis Isolates Obtained from 1974 to 2004 Lack Capsular Genes and Belong to Diverse, Non-Hospital-Associated Lineages

Cited by 10 publications

References 61 publications

A Genomic Virulence Reference Map of Enterococcus faecalis Reveals an Important Contribution of Phage03-Like Elements in Nosocomial Genetic Lineages to Pathogenicity in a Caenorhabditis elegans Infection Model

A Genomic Virulence Reference Map of Enterococcus faecalis Reveals an Important Contribution of Phage03-Like Elements in Nosocomial Genetic Lineages to Pathogenicity in a Caenorhabditis elegans Infection Model

Phylogenomics of Enterococcus faecalis from wild birds: new insights into host‐associated differences in core and accessory genomes of the species

Partial Diversity Generates Effector Immunity Specificity of the Bac41-Like Bacteriocins of Enterococcus faecalis Clinical Strains

Contact Info

Product

Resources

About