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Detection of invasive protein profile of Streptococcus pyogenes M1 isolates from pharyngitis patients
Author(s) -
HASEGAWA TADAO,
OKAMOTO AKIRA,
KAMIMURA TAKUYA,
TATSUNO ICHIRO,
HASHIKAWA SHINNOSUKE,
YABUTANI MITSUTAKA,
MATSUMOTO MASAKADO,
YAMADA KEIKO,
ISAKA MASANORI,
MINAMI MASAAKI,
OHTA MICHIO
Publication year - 2010
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1600-0463.2009.02574.x
Subject(s) - streptococcus pyogenes , pharyngitis , microbiology and biotechnology , serotype , toxic shock syndrome , biology , exotoxin , pulsed field gel electrophoresis , streptococcus , gel electrophoresis , group a , virology , bacteria , genetics , medicine , staphylococcus aureus , genotype , gene , toxin , pathology
Hasegawa T, Okamoto A, Kamimura T, Tatsuno I, Hashikawa S‐N, Yabutani M, Matsumoto M, Yamada K, Isaka M, Minami M, Ohta M. Detection of invasive protein profile of Streptococcus pyogenes M1 isolates from pharyngitis patients. APMIS 2010; 118: 167–78. Streptococcal toxic shock syndrome (STSS) is a re‐emerging infectious disease in Japan and many other developed countries. Epidemiological studies have revealed that the M1 serotype of Streptococcus pyogenes is the most dominant causative isolate of STSS. Recent characterization of M1 isolates revealed that the mutation of covS , one of the two‐component regulatory systems, plays an important role in STSS by altering protein expression. We analyzed the M1 S. pyogenes clinical isolates before or after 1990 in Japan, using two‐dimensional gel electrophoresis (2‐DE) and pulsed‐field gel electrophoresis (PFGE). PFGE profiles were different between the isolates before and after 1990. Markedly different profiles among isolates after 1990 from STSS and pharyngitis patients were detected. Sequence analysis of two‐component regulatory systems showed that covS mutations were detected not only in STSS but also in three pharyngitis isolates, in which proteins from the culture supernatant displayed the invasive type. The mutated CovS detected in the pharyngitis isolates had impaired function on the production of streptococcal pyrogenic exotoxin B (SpeB) analyzed by 2‐DE. These results suggest that several covS mutations that lead to the malfunction of the CovS protein occurred even in pharyngeal infection.

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