Glucose Mediates Niche-Specific Repression of Staphylococcus aureus Toxic Shock Syndrome Toxin-1 through the Activity of CcpA in the Vaginal Environment.

Staphylococcus aureus chronically colonizes up to 30% of the human population on the skin or mucous membranes, including the nasal tract or vaginal canal. While colonization is often benign, this bacterium also has the capability to cause serious infections. Menstrual toxic shock syndrome (mTSS) is a serious toxinosis associated with improper use of tampons, which can induce an environment that is favorable to the production of the superantigen known as toxic shock syndrome toxin-1 (TSST-1).

Neighborhood Contexts and Oral Health Outcomes in a Pediatric Population: An Exploratory Study.

Aims: This study aimed to explore the impacts of neighborhood-level socioeconomic contexts on the therapeutic and preventative dental quality outcome of children under 16 years.

Materials And Methods: Anonymized billing data of 842 patients reporting to a university children's dental over three years (March 2017-2020) met the inclusion criteria. Their access to care (OEV-CH-A), topical fluoride application (TFL-CH-A) and dental treatment burden (TRT-CH-A) were determined by dental quality alliance (DQA) criteria.

Regulation of toxic shock syndrome toxin-1 by the accessory gene regulator in Staphylococcus aureus is mediated by the repressor of toxins.

Toxic shock syndrome toxin-1 (TSST-1) is a superantigen (SAg) produced by Staphylococcus aureus thought to be responsible for essentially all cases of menstrual-associated toxic shock syndrome (TSS). As a potent exotoxin, it is not surprising that S. aureus has evolved multiple systems to control expression of TSST-1.