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Abstract

Streptococcal toxic shock syndrome (STSS) is a re-emerging infectious disease in many developed countries. Recent studies have suggested that mutations in CovRS, a two-component regulatory system in , play important roles in the pathogenesis of STSS. However, evidence of the significance of CovRS in human infections has not been fully demonstrated. We investigated five strains isolated simultaneously from the pharynx, sputum, knee joint, cerebrospinal fluid and blood of a single STSS patient. All were 89-type strains, and multilocus sequence typing (MLST) analysis revealed that the strains of pharynx and blood were isogenic. The growth rates of the strains from pharynx and sputum were faster than those of the other strains. Protein profiles of the culture supernatants of strains from the pharynx and sputum were also different from those of the other strains. Sequence analyses revealed that strains from the knee joint, cerebrospinal fluid and blood contained a single nucleotide difference in the coding region, resulting in one amino acid change, compared with the other strains. Introduction of a plasmid containing the gene from the pharynx strain to the blood strain increased the production of SpeB protein. This suggests that the one amino acid alteration in CovS was relevant to pathogenesis. This report supports the idea that mutated CovS plays important roles in the dissemination of from the upper respiratory tract of human to aseptic tissues such as blood and cerebrospinal fluid.

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2014-04-01
2019-10-23
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References

  1. Akesson P., Sjöholm A. G., Björck L.. ( 1996;). Protein SIC, a novel extracellular protein of Streptococcus pyogenes interfering with complement function. . J Biol Chem 271:, 1081–1088. [CrossRef][PubMed]
    [Google Scholar]
  2. Ato M., Ikebe T., Kawabata H., Takemori T., Watanabe H.. ( 2008;). Incompetence of neutrophils to invasive group A streptococcus is attributed to induction of plural virulence factors by dysfunction of a regulator. . PLoS ONE 3:, e3455. [CrossRef][PubMed]
    [Google Scholar]
  3. Bohach G. A., Hauser A. R., Schlievert P. M.. ( 1988;). Cloning of the gene, speB, for streptococcal pyrogenic exotoxin type B in Escherichia coli. . Infect Immun 56:, 1665–1667.[PubMed]
    [Google Scholar]
  4. Cole J. N., Pence M. A., von Köckritz-Blickwede M., Hollands A., Gallo R. L., Walker M. J., Nizet V.. ( 2010;). M protein and hyaluronic acid capsule are essential for in vivo selection of covRS mutations characteristic of invasive serotype M1T1 group A Streptococcus.. MBio 1:, e00191. [CrossRef][PubMed]
    [Google Scholar]
  5. Cunningham M. W.. ( 2000;). Pathogenesis of group A streptococcal infections. . Clin Microbiol Rev 13:, 470–511. [CrossRef][PubMed]
    [Google Scholar]
  6. Engleberg N. C., Heath A., Miller A., Rivera C., DiRita V. J.. ( 2001;). Spontaneous mutations in the CsrRS two-component regulatory system of Streptococcus pyogenes result in enhanced virulence in a murine model of skin and soft tissue infection. . J Infect Dis 183:, 1043–1054. [CrossRef][PubMed]
    [Google Scholar]
  7. Enright M. C., Spratt B. G., Kalia A., Cross J. H., Bessen D. E.. ( 2001;). Multilocus sequence typing of Streptococcus pyogenes and the relationships between emm type and clone. . Infect Immun 69:, 2416–2427. [CrossRef][PubMed]
    [Google Scholar]
  8. Federle M. J., McIver K. S., Scott J. R.. ( 1999;). A response regulator that represses transcription of several virulence operons in the group A streptococcus. . J Bacteriol 181:, 3649–3657.[PubMed]
    [Google Scholar]
  9. Ferretti J. J., McShan W. M., Ajdic D., Savic D. J., Savic G., Lyon K., Primeaux C., Sezate S., Suvorov A. N.. & other authors ( 2001;). Complete genome sequence of an M1 strain of Streptococcus pyogenes. . Proc Natl Acad Sci U S A 98:, 4658–4663. [CrossRef][PubMed]
    [Google Scholar]
  10. Garcia A. F., Abe L. M., Erdem G., Cortez C. L., Kurahara D., Yamaga K.. ( 2010;). An insert in the covS gene distinguishes a pharyngeal and a blood isolate of Streptococcus pyogenes found in the same individual. . Microbiology 156:, 3085–3095. [CrossRef][PubMed]
    [Google Scholar]
  11. Graham M. R., Smoot L. M., Migliaccio C. A., Virtaneva K., Sturdevant D. E., Porcella S. F., Federle M. J., Adams G. J., Scott J. R., Musser J. M.. ( 2002;). Virulence control in group A Streptococcus by a two-component gene regulatory system: global expression profiling and in vivo infection modeling. . Proc Natl Acad Sci U S A 99:, 13855–13860. [CrossRef][PubMed]
    [Google Scholar]
  12. Hasegawa T., Minami M., Okamoto A., Tatsuno I., Isaka M., Ohta M.. ( 2010a;). Characterization of a virulence-associated and cell-wall-located DNase of Streptococcus pyogenes. . Microbiology 156:, 184–190. [CrossRef][PubMed]
    [Google Scholar]
  13. Hasegawa T., Okamoto A., Kamimura T., Tatsuno I., Hashikawa S. N., Yabutani M., Matsumoto M., Yamada K., Isaka M.. & other authors ( 2010b;). Detection of invasive protein profile of Streptococcus pyogenes M1 isolates from pharyngitis patients. . APMIS 118:, 167–178. [CrossRef][PubMed]
    [Google Scholar]
  14. Ichikawa M., Minami M., Isaka M., Tatsuno I., Hasegawa T.. ( 2011;). Analysis of two-component sensor proteins involved in the response to acid stimuli in Streptococcus pyogenes. . Microbiology 157:, 3187–3194. [CrossRef][PubMed]
    [Google Scholar]
  15. Ikebe T., Ato M., Matsumura T., Hasegawa H., Sata T., Kobayashi K., Watanabe H.. ( 2010;). Highly frequent mutations in negative regulators of multiple virulence genes in group A streptococcal toxic shock syndrome isolates. . PLoS Pathog 6:, e1000832. [CrossRef][PubMed]
    [Google Scholar]
  16. Levin J. C., Wessels M. R.. ( 1998;). Identification of csrR/csrS, a genetic locus that regulates hyaluronic acid capsule synthesis in group A Streptococcus. . Mol Microbiol 30:, 209–219. [CrossRef][PubMed]
    [Google Scholar]
  17. Okada N., Tatsuno I., Hanski E., Caparon M., Sasakawa C.. ( 1998;). Streptococcus pyogenes protein F promotes invasion of HeLa cells. . Microbiology 144:, 3079–3086. [CrossRef][PubMed]
    [Google Scholar]
  18. Sumby P., Whitney A. R., Graviss E. A., DeLeo F. R., Musser J. M.. ( 2006;). Genome-wide analysis of group A streptococci reveals a mutation that modulates global phenotype and disease specificity. . PLoS Pathog 2:, e5. [CrossRef][PubMed]
    [Google Scholar]
  19. Tanaka M., Hasegawa T., Okamoto A., Torii K., Ohta M.. ( 2005;). Effect of antibiotics on group A Streptococcus exoprotein production analyzed by two-dimensional gel electrophoresis. . Antimicrob Agents Chemother 49:, 88–96. [CrossRef][PubMed]
    [Google Scholar]
  20. Tatsuno I., Okada R., Zhang Y., Isaka M., Hasegawa T.. ( 2013;). Partial loss of CovS function in Streptococcus pyogenes causes severe invasive disease. . BMC Res Notes 6:, 126. [CrossRef][PubMed]
    [Google Scholar]
  21. Walker M. J., Hollands A., Sanderson-Smith M. L., Cole J. N., Kirk J. K., Henningham A., McArthur J. D., Dinkla K., Aziz R. K.. & other authors ( 2007;). DNase Sda1 provides selection pressure for a switch to invasive group A streptococcal infection. . Nat Med 13:, 981–985. [CrossRef][PubMed]
    [Google Scholar]
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