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: 2.69). 09/2009; 191(20):6203-10. DOI: 10.1128/JB.00592-09
Source: PubMed

ABSTRACT 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.

Download full-text


Available from: Vinai Chittezham Thomas, Jul 17, 2014
  • Source
    • "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). "
    Journal of Genetics and Genomics 08/2014; 42(1). DOI:10.1016/j.jgg.2014.07.002 · 2.92 Impact Factor
  • Source
    • "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 "
    [Show abstract] [Hide abstract]
    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.
    Journal of Medical Entomology 01/2014; 51(1):63-7. DOI:10.1603/ME13161 · 1.82 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The vast majority of enterococci, including species that are major agents of nosocomial infection, are peaceful inhabitants of the gastrointestinal (GI) tracts of animals that range from insects to humans. However, situations arise in which enterococci can cause serious disease. The era of modern medicine has created circumstances that facilitate the pathogenic behavior of these microbes in the following ways. First, the use, and arguable overuse, of antibiotics has selected for bacteria that are resistant to these medicines. Even though enterococci may not be as inherently virulent as some other bacterial pathogens, they are facile at collecting and exchanging antibiotic resistance determinants, in addition to being naturally resistant to many antibitoics. Such properties give enterococci a selective advantage in environments with heavy antibiotic usage, such as the hospital, and may allow them to out-compete other species that would normally keep them in check. Another factor is the increasing susceptible population of immunocompromised individuals, which includes the elderly, solid organ and bone marrow transplant patients, and cancer patients. The action of the immune system likely contributes to the commensal balance, and a severely weakened defense system may be unable to keep these species in check. Finally, there are genetic factors that contribute to the ability of enterococci to survive and cause infection in a host environment, which are defined as virulence determinants for the purpose of this discussion. Some of these factors are part of the core genome, while others are traits that can be acquired and shared. Much work has been done over the last 20 years to identify these virulence determinants, and to characterize their mechanisms of action, which is is the main focus of this chapter. Animal models have made critical contributions to our understanding of the pathogenesis of enterococcal infection. A number of advances recently have been made that allow for new and more facile models to be employed in these studies. However, since the motivation behind a given study usually relates to some aspect of human infection, it is important to understand the parallels and limitations of each model, in order to know the extent to which the results can be extrapolated to humans.
    Enterococci: From Commensals to Leading Causes of Drug Resistant Infection, Edited by Michael S Gilmore, Don B Clewell, Yasuyoshi Ike, Nathan Shankar; Massachusetts Eye and Ear Infirmary.
Show more