Hemolytic uremic syndrome (HUS) is characterized by acute renal failure, thrombocytopenia, and microangiopathic hemolytic anemia. HUS occurs as a complication of childhood associated Streptococcus pneumoniae infections such as pneumonia, otitis media, and meningitis. Without proper diagnosis and treatment the outcome to HUS is almost always fatal. The bacterial factor leading to HUS has been identified as the pneumococcal neuraminidase, which exposes the Thomsen-Friedenreich antigen (T-antigen) on the surface of endothelial cells and red blood cells. The disease state occurs when antibodies to the T-antigen are present in infected individuals. My studies focus on describing the events that occur between the initial clinical presentation and the onset of HUS. I am working to mimic HUS in an animal model. I have been able to demonstrate exposure of T-antigen on kidneys and red blood cells during S. pneumoniae infection in mice. Future studies will examine the effect that localized kidney infection could contribute to the development of HUS. These studies will help physicians predict which S. pneumoniae infections will progress to become HUS and avoid practices that exacerbate HUS. ? ?

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
1F31HL077998-01
Application #
6829763
Study Section
Special Emphasis Panel (ZRG1-F10 (29))
Program Officer
Mondoro, Traci
Project Start
2004-08-01
Project End
2006-01-31
Budget Start
2004-08-01
Budget End
2005-07-31
Support Year
1
Fiscal Year
2004
Total Cost
$23,522
Indirect Cost
Name
University of Alabama Birmingham
Department
Microbiology/Immun/Virology
Type
Schools of Medicine
DUNS #
063690705
City
Birmingham
State
AL
Country
United States
Zip Code
35294