Hasegawa Tadao, Matsumoto Masakado, Hata Nanako, Yano Hisako, Isaka Masanori, Tatsuno Ichiro
Department of Bacteriology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Department of Microbiology and Medical Zoology, Aichi Prefectural Institute of Public Health, Nagoya, Japan.
APMIS. 2019 Feb;127(2):87-92. doi: 10.1111/apm.12914.
Streptococcal toxic shock syndrome (STSS) is primarily caused by Streptococcus pyogenes, but it may also be caused by Streptococcus dysgalactiae subsp. equisimilis (SDSE). The analyses of S. pyogenes have revealed the important roles of NAD -glycohydrolase (Nga) and CovR/CovS, a two-component regulatory system. We examined these factors in SDSE by analyzing mainly two isogenic SDSE strains (12-10-1 and 12-10-3) from the blood of a patient with STSS. The Nga activities were measured and the nucleotide sequences of covR and covS genes were determined. We detected one nucleotide difference between the covR gene of 12-10-1 and that of 12-10-3, and the Nga activity of 12-10-1 was approximately 6.8-fold more than that of 12-10-3. The introduction of covR of 12-10-3 into 12-10-1 significantly reduced the Nga activity, but the introduction of 12-10-1 covR into itself had only a little effect. In addition, the knockout of covR or covS of 12-10-3 remarkably increased the Nga activity. We are the first to report that strains with wild-type and mutated covR were isolated simultaneously from an SDSE STSS patient and that the CovR/CovS two-component regulatory system is involved in the Nga activity in SDSE as well as in S. pyogenes.
链球菌中毒性休克综合征(STSS)主要由化脓性链球菌引起,但也可能由马链球菌兽疫亚种(SDSE)引起。对化脓性链球菌的分析揭示了NAD-糖水解酶(Nga)以及双组分调节系统CovR/CovS的重要作用。我们通过主要分析来自一名STSS患者血液中的两株同基因SDSE菌株(12-10-1和12-10-3),研究了SDSE中的这些因素。测定了Nga活性,并确定了covR和covS基因的核苷酸序列。我们检测到12-10-1的covR基因与12-10-3的covR基因之间存在一个核苷酸差异,并且12-10-1的Nga活性比12-10-3的Nga活性高约6.8倍。将12-10-3的covR导入12-10-1可显著降低Nga活性,但将12-10-1的covR导入其自身仅有轻微影响。此外,敲除12-10-3的covR或covS可显著提高Nga活性。我们首次报道从一名SDSE STSS患者中同时分离出具有野生型和突变型covR的菌株,并且CovR/CovS双组分调节系统在SDSE以及化脓性链球菌中均参与Nga活性的调控。