2.) What is the Pathophysiology of Rheumatic Fever/ Rheumatic Heart Disease?
Organism Factors • Based on evidence, ARF is exclusively caused by URTI ( Group A Streptococci). • It has been postulated that a series of preceding streptococcal infections is needed to “prime” the immune system to the final infection that directly causes the disease.
The Immune Response • Susceptible host encounters a group A streptococcus • Auto immune reaction occurs • Leads to human tissue damage as a result of cross-reactivity between epitopes on the organism and host.
Molecular mimicry • Group A Streptococci- has epitopes present in the M protein • Similar molecules – human myosin, tropomyosin, keratin, actin, laminin, vimentin, and NAG. • Basis for Autoimmune response • T cell sensitization • T cells recalled following subsequent exposure
Valvular Damage • Laminin- found in cardiac endothelium and is recognized by anti-myosin, anti-M protein, T cells. • Antibodies to cardiac valve cross react with NAG
Infective Endocarditis • Prototypic lesion- vegetation • Infection most commonly involves the heart valve • Organisms that cause this generally enter the bloodstream from mucosal surfaces, the skin, or sites of focal infection.
Infective Endocarditis • Etiologies: • Health Care Associated – bacteremia arising from IV catheterizations, nosocomial wound, UTI’s, chronic invasive procedures • Prosthetic Valve endocarditis- intraoperative contamination • Injection drug users-
Infective Endocarditis • Highly variable clinical manifestations • Causative microorganism primarily responsible for acute course incluse B-hemolytic streptococci, S. aureus, and Pneumococci. • Febrile patient with valvular abnormalities or behavior pattern that predispose ( injection drug use) • Bacteremia with organisms that frequently causes endocarditis
Infective Endocarditis • 39.4-40 degrees Celcius fever for the acute course • Fever may be blunted or absent in patients who are elderly or severely debilitated.