Adam Spaulding successfully defends PhD thesis

Pat and Adam with cake

Adam Spaulding successfully defended his PhD thesis, "Secreted Virulence Factors in Lethal Illness caused by Staphylococcus aureus," on Monday, April 29, 2013. Spaulding is pictured here with his mentor, Patrick Schlievert, PhD.

Staphylococcus aureus causes significant illnesses throughout the world, including toxic shock syndrome (TSS), pneumonia, and infective endocarditis. Major contributors to S. aureus illnesses are secreted virulence factors it produces, including superantigens and cytolysins. Rabbit cardiac physiology is considered similar to humans, and rabbits exhibit susceptibility to S. aureus superantigens and cytolysins. As such, rabbits are an excellent model for studying pneumonia, infective endocarditis, and sepsis.

We examined the ability of USA200, USA300 and USA400 strains to cause vegetations and lethal sepsis in rabbits. USA200, TSST-1+ strains that produce only low amounts of α-toxin, exhibited modest LD50 in sepsis colony-forming units (CFUs), and 3/4 caused significant IE. In contrast, USA300 strains were highly effective in causing lethal sepsis but were minimally capable of causing IE. USA400 strains were both highly lethal and highly effective causes of IE.

We also investigated the use of superantigens and cytolysins as staphylococcal vaccine candidates. Immunization of rabbits against toxoid variants of these superantigens and cytolysins provided complete protection from highly lethal pulmonary challenge with USA100, USA200, USA300 and USA400 S. aureus strains. Immunization against these exotoxins also protected rabbits from infective endocarditis and lethal sepsis. Passive immunization using pooled sera protects previously non-immunized rabbits from lethal pneumonia due to MNPE. These data suggest that immunization against toxoid proteins of S. aureus exotoxins protects from serious illnesses.


Adam was born in upstate New York and grew up in the city of Jacksonville, FL, graduating from Bartram Trail High School in 2003. He then moved to Athens, GA, to pursue undergraduate studies at the University of Georgia. While attending UGA, he studied genetic transfer and DMSP catabolism in Roseobacter spp. in Mary Ann Moran’s laboratory for two years, as well as working with Sidney Crow on fungal metabolism at Georgia State University. Additionally, Adam worked at Vistakon, a Johnson & Johnson company, developing an anti-microbial contact lens. Adam received his B.S. in Microbiology in 2007.

Adam entered the University of Minnesota’s Microbiology, Immunology, and Cancer Biology PhD program in August 2008, joining Pat Schlievert’s laboratory in Spring 2009 to begin research on Staphylococcus aureus superantigens and cytolysins. In August of 2011, the lab migrated to The University of Iowa, which they now call home. As a graduate student, he has published three first-author papers: One on the development of a vaccine against S. aureus; one on the comparison of S. aureus isolate to cause sepsis and infective endocarditis; and a review on superantigens. Adam currently has a first-author paper on additional vaccine development against S. aureus in preparation to be submitted to Nature Medicine. Adam has been fortunate to present his work at several meetings, including the 2012 ASM Conference, where he received a travel grant and an award for outstanding student poster; he has presented a poster at the Great Lakes Regional Center for Excellence in Biodefense and Infectious Diseases annual meeting on three occasions. He also attended the 2012 ASM Kadner Institute. Adam has been supported by the NIH and GLRCE.

Outside of lab, Adam is an avid supporter of the Georgia Bulldogs. He spends his time home-brewing, cooking with his wife, Kelsey, riding his bike, and playing guitar. Adam is a SCUBA diver, an ocean enthusiast, and (when he can get to one) general beach bum.

After finishing his work at The University of Iowa, Adam will be moving to North Carolina to begin a postdoctoral position with Rita Tamayo at UNC Chapel Hill to study the colonization-virulence transition of Clostridium difficile.