Staphylococcus aureus TSST-1 and β-toxin contribute to infective endocarditis via multiple mechanisms

Staphylococcus aureus is a gram positive bacterium found on a significant portion of the population. Its commonness, large quantity of virulence factors, and ability to easily obtain antibiotic resistance contribute to its capacity to be such a harmful pathogen. There are at least 70 million infections in the United States that can be attributed to S. aureus. It is capable of causing a broad range of infections including pneumonia, toxic shock syndrome, skin infections, sepsis, food poisoning, and infective endocarditis. Infective endocarditis is an infection of the heart characterized by the growth of bacteria and host factors on the aortic valve into what is termed a “vegetation”. Vegetation size often correlates with the seriousness of the disease. This infection is highly lethal resulting in death in up to 66% of S. aureus infective endocarditis patients. Infective endocarditis can also result in a variety of complications including, strokes, infarcts, and kidney injury.

One of the many virulence factors that S. aureus produces is β-toxin. β-toxin is capable of digesting a lipid commonly found on cell membranes, and also helps build biofilms. In my work, I determined the importance of β-toxin in the development of infective endocarditis. More specifically, I assessed which of its activities contribute to disease. I determined that β-toxin increases lethality in infective endocarditis. Additionally, I found β-toxin increases the size of vegetations that make the infection worse. This is the first time the activity responsible for its ability to build biofilms was characterized, and each activity of the toxin was studied individually. To combat this extremely aggressive infection, determining what and how S. aureus virulence factors are acting during disease progression must be revealed to define the best route for treatment.