Rheumatic fever pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
It was first thought that individuals developed an allergic response to the bacteria, but later it was determined that rheumatic fever was an autoimmunological sequela to a virulent Streptococcus pyogenes infection in a patient who had adequate rheumatic sensitivity from prior infections by Streptococcus pyogenes. | |||
The development of a rheumatic fever episode depends on the involved host being highly autoimmunologically sensitized to autoantigens exhibited by Streptococcus pyogenes to its host during prior Streptococcus pyogenes infectious episodes, so a decrease in the frequency and virulence of infections by Streptococcus pyogenes in a society can cause rheumatic fever, as a disease entity, to be less frequent and less severe. | |||
Scarlet fever and rheumatic fever are, primarily, the same disease. The somewhat typical rash of scarlet fever develops if an individual contracts an infecton from a strain of Streptococcus pyogenes that secretes erythrotoxin A, B, and C, and if the individual involved has not had an infection by that particular strain previously, since during a previous infection antibodies will have been developed against the erythrogenic toxin of interest. Repeated infections by strains of Streptococcus pyogenes that have, and do not have, erythrotoxin A, B, and C can reinforce each other in the development of autoimmunological reactions by a host, since they all have certain autoantigens and secreted toxic products, other than erythrotoxin A, B, and C, in commonk. If a person, usually a child, develops an infection from Streptococcus pyogenes that secretes A, B, or C erythrotixin they will develop a mild infectious/autoimmunological disease and the classic, mild rash of scarletina, the diminuative term for scarlet fever, will often develop. | |||
Since the development of rheumatic fever depends upon a prior, high-level of autoimmunological stimulation, which itself depends upon an individual, in the past, experiencing many infectious episodes by Streptococcus pyogenes, and since Streptococcus pyogenes are endemic in human and domestic animal populations (information from the Russian Encyclopedia (V.Nasonova,E. Talahaev), it must be understood that all individuals experience pathological, autoimmunological stimulation during Streptococcus pyogenes infections. | |||
[[Rheumatic fever]] is a systemic disease affecting the peri-arteriolar connective tissue and can occur after an untreated Group A streptococcal pharyngeal infection. It is believed to be caused by antibody [[cross-reactivity]]. This cross-reactivity is a Type II hypersensitivity reaction and is termed ''molecular mimicry.'' | [[Rheumatic fever]] is a systemic disease affecting the peri-arteriolar connective tissue and can occur after an untreated Group A streptococcal pharyngeal infection. It is believed to be caused by antibody [[cross-reactivity]]. This cross-reactivity is a Type II hypersensitivity reaction and is termed ''molecular mimicry.'' | ||
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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]
Pathophysiology
It was first thought that individuals developed an allergic response to the bacteria, but later it was determined that rheumatic fever was an autoimmunological sequela to a virulent Streptococcus pyogenes infection in a patient who had adequate rheumatic sensitivity from prior infections by Streptococcus pyogenes.
The development of a rheumatic fever episode depends on the involved host being highly autoimmunologically sensitized to autoantigens exhibited by Streptococcus pyogenes to its host during prior Streptococcus pyogenes infectious episodes, so a decrease in the frequency and virulence of infections by Streptococcus pyogenes in a society can cause rheumatic fever, as a disease entity, to be less frequent and less severe.
Scarlet fever and rheumatic fever are, primarily, the same disease. The somewhat typical rash of scarlet fever develops if an individual contracts an infecton from a strain of Streptococcus pyogenes that secretes erythrotoxin A, B, and C, and if the individual involved has not had an infection by that particular strain previously, since during a previous infection antibodies will have been developed against the erythrogenic toxin of interest. Repeated infections by strains of Streptococcus pyogenes that have, and do not have, erythrotoxin A, B, and C can reinforce each other in the development of autoimmunological reactions by a host, since they all have certain autoantigens and secreted toxic products, other than erythrotoxin A, B, and C, in commonk. If a person, usually a child, develops an infection from Streptococcus pyogenes that secretes A, B, or C erythrotixin they will develop a mild infectious/autoimmunological disease and the classic, mild rash of scarletina, the diminuative term for scarlet fever, will often develop.
Since the development of rheumatic fever depends upon a prior, high-level of autoimmunological stimulation, which itself depends upon an individual, in the past, experiencing many infectious episodes by Streptococcus pyogenes, and since Streptococcus pyogenes are endemic in human and domestic animal populations (information from the Russian Encyclopedia (V.Nasonova,E. Talahaev), it must be understood that all individuals experience pathological, autoimmunological stimulation during Streptococcus pyogenes infections. Rheumatic fever is a systemic disease affecting the peri-arteriolar connective tissue and can occur after an untreated Group A streptococcal pharyngeal infection. It is believed to be caused by antibody cross-reactivity. This cross-reactivity is a Type II hypersensitivity reaction and is termed molecular mimicry.
Usually, self reactive B cells remain anergic in the periphery without T cell co-stimulation. During a Strep. 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 react against the myocardium and joints[1], producing the symptoms of Rheumatic fever.
Group A streptococcus pyogenes has 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 release and tissue destruction. This inflammation occurs through direct attachment of complement and Fc receptor-mediated recruitment of neutrophils and macrophages. Characteristic Aschoff bodies, composed of swollen eosinophilic collagen surrounded by lymphocytes and macrophages can be seen on light microscopy. The larger macrophages may become Aschoff giant cells. Acute rheumatic valvular lesions may also involve a cell-mediated immunity reaction as these lesions predominantly contain T-helper cells and macrophages.[2]
In acute RF, these lesions can be found in any layer of the heart and is hence called pancarditis. 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-sided heart valves. Warty projections arise from the deposition, while subendothelial lesions may induce irregular thickenings called MacCallum plaques.
Chronic rheumatic heart disease is characterized by repeated inflammation with fibrinous resolution. The cardinal anatomic changes of the valve include leaflet thickening, commissural fusion and shortening and thickening of the tendinous cords. RHD cause 99% of mitral stenosis often resulting in a “fish mouth” gross appearance.[3]
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
References
- ↑ Abbas and Lechtman. mBasic Immunology: Functions and Disorders of the Immune System. Elsevier Inc. 2004.
- ↑ Kumar et al. Robbins and Cotran Pathologic Basis of Disease. Elsevier Inc. 2005
- ↑ "Robbins & Cotran Pathologic Basis of Disease".