Rheumatic fever pathophysiology: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Rheumatic fever}} | {{Rheumatic fever}} | ||
{{CMG}}; Lance Christiansen, D.O.; {{AE}} {{CZ}} | {{CMG}}; Lance Christiansen, D.O.; {{AE}} {{CZ}} {{AG}} | ||
==Pathophysiology== | ==Pathophysiology== | ||
Rheumatic fever is the result of an autoimmunological sequela to a virulent [[Streptococcus pyogenes]] infection in a patient who was immunologically sensitized from prior infections. The systemic disease affects the periarteriolar connective tissue and can occur after an untreated Group A streptococcal [[pharyngeal]] infection. It is believed to be caused by antibody [[cross-reactivity]] which is a [[Hypersensitivity#Type 2 - antibody-dependent|Type II hypersensitivity reaction]], often termed molecular mimicry. | |||
Usually, self reactive [[B cell]]s remain anergic in the periphery without [[T cell]] co-stimulation. During a streptococcal infection, activated antigen presenting cells, such as [[macrophage]]s, present the bacterial antigen to helper T cells. [[Helper T cell]]s subsequently activate B cells and induce the production of antibodies against the cell wall of [[streptococcus]]. However the antibodies may also act against the myocardium and joints, producing the symptoms of rheumatic fever. | |||
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Contrary to the immunological protection developed during most infections, infections by Streptococcus pyogenes cause both a protective immunological and pathological autoimmunological stimulation. Repeated infections by ''Streptococcus pyogenes'' will cause both a heightened protective and pathological immune response. The immune response helps in combating the streptococcal infection. However, the autoimmunological response causes an inflammatory, systemic, disease process, rheumatic fever. | |||
Group A ''[[streptococcus pyogenes]]'' have a [[cell wall]] composed of branched [[polymers]] which sometimes contain M proteins that are highly [[antigenic]]. The antibodies which the immune system generates against the M proteins may cross-react with cardiac myofiber [[sarcolemma]] and smooth muscle cells of arteries, inducing [[cytokine]] r | |||
Group A ''[[streptococcus pyogenes]]'' | |||
In acute rheumatic fever, these lesions may occur in endocardium, myocardium or pericardium. The inflammation may cause a serofibrinous pericardial exudates described as “bread-and-butter” [[pericarditis]], which usually resolves without sequelae. Involvement of the endocardium typically results in [[fibrinoid necrosis]] and verrucae formation along the lines of closure of the left heart valves. Warty projections arise from the deposition, while subendothelial lesions may induce irregular thickenings called [[MacCallum plaques]]. | In acute rheumatic fever, these lesions may occur in endocardium, myocardium or pericardium. The inflammation may cause a serofibrinous pericardial exudates described as “bread-and-butter” [[pericarditis]], which usually resolves without sequelae. Involvement of the endocardium typically results in [[fibrinoid necrosis]] and verrucae formation along the lines of closure of the left heart valves. Warty projections arise from the deposition, while subendothelial lesions may induce irregular thickenings called [[MacCallum plaques]]. | ||
==Pathological Findings== | ==Pathological Findings== | ||
Revision as of 17:50, 12 October 2015
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Lance Christiansen, D.O.; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2] Anthony Gallo, B.S. [3]
Pathophysiology
Rheumatic fever is the result of an autoimmunological sequela to a virulent Streptococcus pyogenes infection in a patient who was immunologically sensitized from prior infections. The systemic disease affects the periarteriolar connective tissue and can occur after an untreated Group A streptococcal pharyngeal infection. It is believed to be caused by antibody cross-reactivity which is a Type II hypersensitivity reaction, often termed molecular mimicry.
Usually, self reactive B cells remain anergic in the periphery without T cell co-stimulation. During a streptococcal infection, activated antigen presenting cells, such as macrophages, present the bacterial antigen to helper T cells. Helper T cells subsequently activate B cells and induce the production of antibodies against the cell wall of streptococcus. However the antibodies may also act against the myocardium and joints, producing the symptoms of rheumatic fever.
Contrary to the immunological protection developed during most infections, infections by Streptococcus pyogenes cause both a protective immunological and pathological autoimmunological stimulation. Repeated infections by Streptococcus pyogenes will cause both a heightened protective and pathological immune response. The immune response helps in combating the streptococcal infection. However, the autoimmunological response causes an inflammatory, systemic, disease process, rheumatic fever.
Group A streptococcus pyogenes have a cell wall composed of branched polymers which sometimes contain M proteins that are highly antigenic. The antibodies which the immune system generates against the M proteins may cross-react with cardiac myofiber sarcolemma and smooth muscle cells of arteries, inducing cytokine r
In acute rheumatic fever, these lesions may occur in endocardium, myocardium or pericardium. The inflammation may cause a serofibrinous pericardial exudates described as “bread-and-butter” pericarditis, which usually resolves without sequelae. Involvement of the endocardium typically results in fibrinoid necrosis and verrucae formation along the lines of closure of the left heart valves. Warty projections arise from the deposition, while subendothelial lesions may induce irregular thickenings called MacCallum plaques.
Pathological Findings
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Aortic Stenosis (Tricuspid aorta): Gross, good example of aortic stenosis due to rheumatic fever -
Gross, an excellent example of mitral scarring due to rheumatic fever (healing phase of an infectious lesion). -
Rheumatic mitral valvulitis: Gross, an excellent example of fibrosis, chorda thickening and shortening has thrombus around the large left atrium
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Mitral valve: acute rheumatic fever -
Aschoff bodies in rheumatic heart disease
courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology