Capsular Polysaccharide Production in Enterococcus faecalis and Contribution of CpsF to Capsule Serospecificity

Division of Biology, Kansas State University, 119 Ackert Hall, Manhattan, KS 66506, USA.
Journal of bacteriology (Impact Factor: 2.81). 09/2009; 191(20):6203-10. DOI: 10.1128/JB.00592-09
Source: PubMed


Many bacterial species produce capsular polysaccharides that contribute to pathogenesis through evasion of the host innate
immune system. The gram-positive pathogen Enterococcus faecalis was previously reported to produce one of four capsule serotypes (A, B, C, or D). Previous studies describing the four capsule
serotypes of E. faecalis were based on immunodetection methods; however, the underlying genetics of capsule production did not fully support these
findings. Previously, it was shown that capsule production for serotype C (Maekawa type 2) was dependent on the presence of
nine open reading frames (cpsC to cpsK). Using a novel genetic system, we demonstrated that seven of the nine genes in the cps operon are essential for capsule production, indicating that serotypes A and B do not make a capsular polysaccharide. In
support of this observation, we showed that serotype C and D capsule polysaccharides mask lipoteichoic acid from detection
by agglutinating antibodies. Furthermore, we determined that the genetic basis for the difference in antigenicity between
serotypes C and D is the presence of cpsF in serotype C strains. High-pH anion-exchange chromatography with pulsed amperometric detection analysis of serotype C and
D capsules indicated that cpsF is responsible for glucosylation of serotype C capsular polysaccharide in E. faecalis.

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    • "antiphagocytosis genes except cdsA and uppS were absent in E. faecium T-110. These two genes were reported to play no role in capsule production and antiphagocytosis (Lance et al., 2009). Though bopD gene which is involved in biofilm formation was intact, it may not be functional due to the absence of the fsrABC operon that controls its expression (Bourgogne et al., 2006). "

    Full-text · Article · Aug 2014 · Journal of Genetics and Genomics
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    • "Clinical strain (ATCC 700802), serotype C, vancomycin-resistant, gelatinase-, and serine protease-positive Sahm et al. 1989 V583⌬gelE⌬sprE Isogenic deletion mutant of V583, gelatinase-, and serine protease-defective, tetracycline-and spectinomycin-resistant Hancock and Perego 2004 V583⌬cpsC Isogenic deletion mutant of V583, capsule serotype C-deÞcient Thurlow et al. 2009 MMH594 Epidemic clinical strain, serotype C, hemolytic, high-level gentamicin-resistant Huycke et al. 1991 OG1X Clinical strain, streptomycin-resistant, aggregation substance-, cytolysin-, and gelatinase-defective Ike et al. 1983 OG1RF A derivative of clinical strain OG1, serotype B laboratory strain (ATCC 47077), rifampicin-and fusidic acid-resistant, gelatinase-positive Dunny et al. 1978 JH2Ð2 A derivative of clinical strain JH2, plasmid-free, aggregation substance-, cytolysin-, and gelatinase-defective "
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    ABSTRACT: House flies are among the most important nonbiting insect pests of medical and veterinary importance. Larvae develop in decaying organic substrates and their survival strictly depends on an active microbial community. House flies have been implicated in the ecology and transmission of enterococci, including multi-antibiotic-resistant and virulent strains of Enterococcus faecalis. In this study, eight American Type Culture Collection type strains of enterococci including Enterococcus avium, Enterococcus casseliflavus, Enterococcus durans, Enterococcus hirae, Enterococcus mundtii, Enterococcus gallinarum, Enterococcusfaecalis, and Enterococcusfaecium were evaluated for their significance in the development of house flies from eggs to adults in bacterial feeding assays. Furthermore, the bacterial colonization of the gut of teneral flies as well as the importance of several virulence traits of E. faecalis in larval mortality was assessed. Overall survival of house flies (egg to adult) was significantly higher when grown with typically nonpathogenic enterococcal species such as E. hirae (76.0% survival), E. durans (64.0%), and E. avium (64.0%) compared with that with clinically important species E. faecalis (24.0%) and E. faecium (36.0%). However, no significant differences in survival of house fly larvae were detected when grown with E. faecalis strains carrying various virulence traits, including isogenic mutants of the human clinical isolate E. faecalis V583 with in-frame deletions of gelatinase, serine protease, and capsular polysaccharide serotype C. Enterococci were commonly detected in fly puparia (range: 75-100%; concentration: 103-105 CFU/puparium);however, the prevalence of enterococci in teneral flies varied greatly: from 25.0 (E. casseliflavus) to 89.5% (E. hirae). In conclusion, depending on the species, enterococci variably support house fly larval development and colonize the gut of teneral adults. The human pathogenic species, E. faecalis and E. faecium, poorly support larval development and are likely acquired in nature by adult flies during feeding. House fly larvae do not appear to be a suitable model organism for assessment of enterococcal virulence traits.
    Full-text · Article · Mar 2014 · Journal of Medical Entomology
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    • "Our analysis of the E. faecium TX16 genome did not identify close homologs of the cpsC-K cluster of E. faecalis. Homologs of the two genes, cpsA and cpsB, were found and well conserved in TX16, but were recently reported to not be sufficient for capsule production in E. faecalis[54]. Similarly, homologs of cpsA-cpsB but not of cpsC-K were found in the 21 other E. faecium draft genomes. "
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    ABSTRACT: Enterococci are among the leading causes of hospital-acquired infections in the United States and Europe, with Enterococcus faecalis and Enterococcus faecium being the two most common species isolated from enterococcal infections. In the last decade, the proportion of enterococcal infections caused by E. faecium has steadily increased compared to other Enterococcus species. Although the underlying mechanism for the gradual replacement of E. faecalis by E. faecium in the hospital environment is not yet understood, many studies using genotyping and phylogenetic analysis have shown the emergence of a globally dispersed polyclonal subcluster of E. faecium strains in clinical environments. Systematic study of the molecular epidemiology and pathogenesis of E. faecium has been hindered by the lack of closed, complete E. faecium genomes that can be used as references. In this study, we report the complete genome sequence of the E. faecium strain TX16, also known as DO, which belongs to multilocus sequence type (ST) 18, and was the first E. faecium strain ever sequenced. Whole genome comparison of the TX16 genome with 21 E. faecium draft genomes confirmed that most clinical, outbreak, and hospital-associated (HA) strains (including STs 16, 17, 18, and 78), in addition to strains of non-hospital origin, group in the same clade (referred to as the HA clade) and are evolutionally considerably more closely related to each other by phylogenetic and gene content similarity analyses than to isolates in the community-associated (CA) clade with approximately a 3-4% average nucleotide sequence difference between the two clades at the core genome level. Our study also revealed that many genomic loci in the TX16 genome are unique to the HA clade. 380 ORFs in TX16 are HA-clade specific and antibiotic resistance genes are enriched in HA-clade strains. Mobile elements such as IS16 and transposons were also found almost exclusively in HA strains, as previously reported. Our findings along with other studies show that HA clonal lineages harbor specific genetic elements as well as sequence differences in the core genome which may confer selection advantages over the more heterogeneous CA E. faecium isolates. Which of these differences are important for the success of specific E. faecium lineages in the hospital environment remain(s) to be determined.
    Full-text · Article · Jul 2012 · BMC Microbiology
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