Capsular polysaccharide phase variation in Vibrio vulnificus.

Tamara Hilton, Tom Rosche, Brett Froelich, Benjamin Smith, James Oliver
Author Information
  1. Tamara Hilton: University of North Carolina at Charlotte, 9201 University City Blvd., Charlotte, NC 28223, USA.

Abstract

Commonly found in raw oysters, Vibrio vulnificus poses a serious health threat to immunocompromised individuals and those with serum iron overload, with a fatality rate of approximately 50%. An essential virulence factor is its capsular polysaccharide (CPS), which is responsible for a significant increase in virulence compared to nonencapsulated strains. However, this bacterium is known to vary the amount of CPS expressed on the cell surface, converting from an opaque (Op) colony phenotype to a translucent (Tr) colony phenotype. In this study, the consistency of CPS conversion was determined for four strains of V. vulnificus. Environmental conditions including variations in aeration, temperature, incubation time, oxidative stress, and media (heart infusion or modified maintenance medium agar) were investigated to determine their influence on CPS conversion. All conditions, with the exception of variations in media and oxidative stress, significantly affected the conversion of the population, with high ranges of CPS expression found even within cells from a single colony. The global quorum-sensing regulators RpoS and AI-2 were also examined. While RpoS was found to significantly mediate phenotypic conversion, quorum sensing was not. Finally, 12 strains that comprise the recently found clinical (C) and environmental (E) genotypes of V. vulnificus were examined to determine their rates of population conversion. C-genotype strains, which are most often associated with infection, had a significantly lower rate of population conversion from Op to Tr phenotypes than did E-genotype strains (ca. 38% versus ca. 14%, respectively). Biofilm capabilities of these strains, however, were not correlated with increased population conversion.

References

  1. Clin Microbiol Rev. 2004 Jul;17(3):581-611, table of contents [PMID: 15258095]
  2. FEMS Microbiol Lett. 1999 May 15;174(2):207-14 [PMID: 10339810]
  3. J Bacteriol. 2000 Oct;182(19):5513-20 [PMID: 10986256]
  4. Microbiol Immunol. 2005;49(4):381-9 [PMID: 15840964]
  5. Appl Environ Microbiol. 2003 Oct;69(10):6114-20 [PMID: 14532069]
  6. J Bacteriol. 2004 Feb;186(3):889-93 [PMID: 14729720]
  7. Epidemiol Infect. 2005 Jun;133(3):383-91 [PMID: 15962544]
  8. Appl Environ Microbiol. 1999 Mar;65(3):1141-4 [PMID: 10049874]
  9. FEMS Microbiol Ecol. 2004 Nov 1;50(3):133-42 [PMID: 19712354]
  10. Infect Immun. 2001 Nov;69(11):6893-901 [PMID: 11598064]
  11. Mol Microbiol. 2003 Jun;48(6):1647-64 [PMID: 12791145]
  12. Mol Microbiol. 1998 Oct;30(2):295-304 [PMID: 9791175]
  13. Microbiology (Reading). 2001 Sep;147(Pt 9):2517-2528 [PMID: 11535791]
  14. J Bacteriol. 2001 Sep;183(17):5187-97 [PMID: 11489873]
  15. Infect Immun. 2004 Aug;72(8):4905-10 [PMID: 15271959]
  16. J Bacteriol. 2005 Apr;187(7):2519-25 [PMID: 15774896]
  17. Appl Environ Microbiol. 2004 Apr;70(4):2520-4 [PMID: 15066853]
  18. Microbiol Immunol. 2005;49(6):513-9 [PMID: 15965298]
  19. Appl Environ Microbiol. 2006 Feb;72(2):1445-51 [PMID: 16461698]
  20. Microbes Infect. 2000 Feb;2(2):177-88 [PMID: 10742690]
  21. J Clin Microbiol. 2003 Jan;41(1):442-6 [PMID: 12517889]
  22. Mol Microbiol. 2000 May;36(4):940-54 [PMID: 10844680]
  23. Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):15196-201 [PMID: 10611361]
  24. J Bacteriol. 1998 Jun;180(12):3166-73 [PMID: 9620967]
  25. Microbiology (Reading). 2003 Jul;149(Pt 7):1923-1933 [PMID: 12855743]
  26. Microbiology (Reading). 2003 Sep;149(Pt 9):2627-2634 [PMID: 12949186]
  27. J Bacteriol. 2004 Jun;186(11):3304-12 [PMID: 15150215]
  28. Microbiol Mol Biol Rev. 2002 Sep;66(3):373-95, table of contents [PMID: 12208995]
  29. Nat Rev Microbiol. 2006 Feb;4(2):113-20 [PMID: 16415927]
  30. Infect Immun. 1985 Feb;47(2):446-51 [PMID: 2578434]
  31. J Bacteriol. 2006 Mar;188(5):1987-98 [PMID: 16484211]
  32. Appl Environ Microbiol. 1999 Sep;65(9):4285-7 [PMID: 10473455]
  33. Infect Immun. 2003 Mar;71(3):1091-7 [PMID: 12595419]
  34. Infect Immun. 1987 Jan;55(1):269-72 [PMID: 2432016]

MeSH Term

Animals
Bacterial Capsules
Bacterial Proteins
Culture Media
Gene Expression Regulation, Bacterial
Genotype
Humans
Oxidative Stress
Phenotype
Sigma Factor
Signal Transduction
Temperature
Time Factors
Vibrio vulnificus

Chemicals

Bacterial Proteins
Culture Media
Sigma Factor
sigma factor KatF protein, Bacteria

Word Cloud

Created with Highcharts 10.0.0conversionstrainsCPSfoundvulnificuspopulationcolonysignificantlyVibrioratevirulencepolysaccharideOpphenotypeTrVconditionsvariationsoxidativestressmediadetermineRpoSexaminedcaCommonlyrawoystersposesserioushealththreatimmunocompromisedindividualsserumironoverloadfatalityapproximately50%essentialfactorcapsularresponsiblesignificantincreasecomparednonencapsulatedHoweverbacteriumknownvaryamountexpressedcellsurfaceconvertingopaquetranslucentstudyconsistencydeterminedfourEnvironmentalincludingaerationtemperatureincubationtimeheartinfusionmodifiedmaintenancemediumagarinvestigatedinfluenceexceptionaffectedhighrangesexpressionevenwithincellssingleglobalquorum-sensingregulatorsAI-2alsomediatephenotypicquorumsensingFinally12compriserecentlyclinicalCenvironmentalEgenotypesratesC-genotypeoftenassociatedinfectionlowerphenotypesE-genotype38%versus14%respectivelyBiofilmcapabilitieshowevercorrelatedincreasedCapsularphasevariation

Similar Articles

Cited By