Streptococcal Toxic Shock Syndrome Caused by Streptococcus suis Serotype 2

Jiaqi Tang(Nanjing Institute of Technology), Changjun Wang(Nanjing General Hospital of Nanjing Military Command), Youjun Feng(Institute of Microbiology), Weizhong Yang(Chinese Center For Disease Control and Prevention), Huai‐Dong Song(Ruijin Hospital), Zhihai Chen(Chinese National Human Genome Center), Hongjie Yu(Chinese Center For Disease Control and Prevention), Xiuzhen Pan(Nanjing General Hospital of Nanjing Military Command), Xiaojun Zhou(Jinling Institute of Technology), Huaru Wang(Nanjing General Hospital of Nanjing Military Command), Bo Wu(Jinling Institute of Technology), Haili Wang(Nanjing General Hospital of Nanjing Military Command), Huamei Zhao(Nanjing General Hospital of Nanjing Military Command), Ying Lin(South China University of Technology), Jianhua Yue(Nanjing General Hospital of Nanjing Military Command), Zhenqiang Wu(South China University of Technology), Xiao-Wei He(South China University of Technology), Feng Gao(Chinese Academy of Sciences), Abdul Hamid Khan(Chinese Academy of Sciences), Jian Wang(BGI Group (China)), Guoping Zhao(Chinese National Human Genome Center), Yu Wang(Chinese Center For Disease Control and Prevention), Xiaoning Wang(South China University of Technology), Chen Zhu(Ruijin Hospital), George F. Gao(Chinese Academy of Sciences)
PLoS Medicine
April 3, 2006
Cited by 464Open Access
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Abstract

BACKGROUND: Streptococcus suis serotype 2 (S. suis 2, SS2) is a major zoonotic pathogen that causes only sporadic cases of meningitis and sepsis in humans. Most if not all cases of Streptococcal toxic shock syndrome (STSS) that have been well-documented to date were associated with the non-SS2 group A streptococcus (GAS). However, a recent large-scale outbreak of SS2 in Sichuan Province, China, appeared to be caused by more invasive deep-tissue infection with STSS, characterized by acute high fever, vascular collapse, hypotension, shock, and multiple organ failure. METHODS AND FINDINGS: We investigated this outbreak of SS2 infections in both human and pigs, which took place from July to August, 2005, through clinical observation and laboratory experiments. Clinical and pathological characterization of the human patients revealed the hallmarks of typical STSS, which to date had only been associated with GAS infection. Retrospectively, we found that this outbreak was very similar to an earlier outbreak in Jiangsu Province, China, in 1998. We isolated and analyzed 37 bacterial strains from human specimens and eight from pig specimens of the recent outbreak, as well as three human isolates and two pig isolates from the 1998 outbreak we had kept in our laboratory. The bacterial isolates were examined using light microscopy observation, pig infection experiments, multiplex-PCR assay, as well as restriction fragment length polymorphisms (RFLP) and multiple sequence alignment analyses. Multiple lines of evidence confirmed that highly virulent strains of SS2 were the causative agents of both outbreaks. CONCLUSIONS: We report, to our knowledge for the first time, two outbreaks of STSS caused by SS2, a non-GAS streptococcus. The 2005 outbreak was associated with 38 deaths out of 204 documented human cases; the 1998 outbreak with 14 deaths out of 25 reported human cases. Most of the fatal cases were characterized by STSS; some of them by meningitis or severe septicemia. The molecular mechanisms underlying these human STSS outbreaks in human beings remain unclear and an objective for further study.


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