Streptococcal toxic shock syndrome secondary to group A Streptococcus vaginitis

2015 ◽  
Vol 21 (12) ◽  
pp. 873-876 ◽  
Author(s):  
Mayu Hikone ◽  
Ken-ichiro Kobayashi ◽  
Takuya Washino ◽  
Masayuki Ota ◽  
Naoya Sakamoto ◽  
...  
2021 ◽  
Vol 22 (21) ◽  
pp. 11617
Author(s):  
Nina Tsao ◽  
Ya-Chu Chang ◽  
Sung-Yuan Hsieh ◽  
Tang-Chi Li ◽  
Ching-Chen Chiu ◽  
...  

Streptococcus pyogenes (group A Streptococcus (GAS) is an important human pathogen that can cause severe invasive infection, such as necrotizing fasciitis and streptococcal toxic shock syndrome. The mortality rate of streptococcal toxic shock syndrome ranges from 20% to 50% in spite of antibiotics administration. AR-12, a pyrazole derivative, has been reported to inhibit the infection of viruses, intracellular bacteria, and fungi. In this report, we evaluated the bactericidal activities and mechanisms of AR-12 on GAS infection. Our in vitro results showed that AR-12 dose-dependently reduced the GAS growth, and 2.5 μg/mL of AR-12 significantly killed GAS within 2 h. AR-12 caused a remarkable reduction in nucleic acid and protein content of GAS. The expression of heat shock protein DnaK and streptococcal exotoxins was also inhibited by AR-12. Surveys of the GAS architecture by scanning electron microscopy revealed that AR-12-treated GAS displayed incomplete septa and micro-spherical structures protruding out of cell walls. Moreover, the combination of AR-12 and gentamicin had a synergistic antibacterial activity against GAS replication for both in vitro and in vivo infection. Taken together, these novel findings obtained in this study may provide a new therapeutic strategy for invasive GAS infection.


2015 ◽  
Vol 04 (03) ◽  
pp. 295-299
Author(s):  
Sanjeev Gupta ◽  
Jarrod Brumby ◽  
Joanna Burton ◽  
Susan Moloney ◽  
Benjamin Kenny

2018 ◽  
Vol 8 (3) ◽  
pp. 265-268
Author(s):  
Roman Deniskin ◽  
Brittany Shah ◽  
Flor M Muñoz ◽  
Anthony R Flores

Abstract We report here 18 cases of pediatric group A streptococcal toxic shock syndrome, associated clinical findings, and bacterial molecular genetic characteristics discovered through whole-genome sequencing. This comparative whole-genome sequencing revealed unique gene content (speK) and polymorphisms (dpiB) in emm87 group A Streptococcus, the relative contributions of which, in combination with the host response, in the development of streptococcal toxic shock syndrome remain to be elucidated.


2012 ◽  
Vol 23 (3) ◽  
pp. e69-e70 ◽  
Author(s):  
R Holden ◽  
A Wilmer ◽  
T Kollman

Primary peritonitis remains a rare disease in otherwise healthy children, with group A Streptococcus (GAS) being a particularly unusual cause. A case involving a 14-year-old girl, who presented with an ‘acute abdomen’ and was taken to the operating room for urgent laparoscopy, is reported. Abdominal and pelvic structures were only minimally inflamed, as was the appendix. Peritoneal fluid and blood cultures both grew pure cultures of GAS. The patient’s course was complicated by streptococcal toxic shock syndrome. She fortunately made a full recovery. The present report highlights the diagnostic and treatment dilemmas associated with GAS primary peritonitis.


2014 ◽  
Vol 143 (4) ◽  
pp. 864-872 ◽  
Author(s):  
T. IKEBE ◽  
K. TOMINAGA ◽  
T. SHIMA ◽  
R. OKUNO ◽  
H. KUBOTA ◽  
...  

SUMMARYStreptococcal toxic shock syndrome (STSS) is a severe invasive infection characterized by the sudden onset of shock, multi-organ failure, and high mortality. In Japan, appropriate notification measures based on the Infectious Disease Control law are mandatory for cases of STSS caused byβ-haemolytic streptococcus. STSS is mainly caused by group A streptococcus (GAS). Although an average of 60–70 cases of GAS-induced STSS are reported annually, 143 cases were recorded in 2011. To determine the reason behind this marked increase, we characterized theemmgenotype of 249 GAS isolates from STSS patients in Japan from 2010 to 2012 and performed antimicrobial susceptibility testing. The predominant genotype was found to beemm1, followed byemm89,emm12,emm28,emm3, andemm90. These six genotypes constituted more than 90% of the STSS isolates. The number ofemm1,emm89,emm12, andemm28isolates increased concomitantly with the increase in the total number of STSS cases. In particular, the number ofmefA-positiveemm1isolates has escalated since 2011. Thus, the increase in the incidence of STSS can be attributed to an increase in the number of cases associated with specific genotypes.


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