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{{Rheumatic fever}}
{{Rheumatic fever}}
{{CMG}}; Lance Christiansen, D.O.; '''Associate Editor(s)-in-Chief:''' {{CZ}}
{{CMG}}; Lance Christiansen, D.O.; {{AE}} {{CZ}}; {{AG}}
 
==Overview==
[[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]]. During a streptococcal [[infection]], activated [[antigen-presenting cell]]s, such as [[macrophage]]s, 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]] also act against the [[myocardium]] and [[joint]]s, producing the [[symptoms]] of rheumatic fever.


==Pathophysiology==
==Pathophysiology==
===Pathogenesis===
*Rheumatic fever is the result of an autoimmunological sequelae to a virulent ''[[Streptococcus pyogenes]]'' infection in a [[patient]] who was immunologically sensitized from prior [[infections]], affecting [[periarteriolar]] [[connective tissue]].
*During a [[streptococcal infection]], activated [[antigen-presenting cell]]s, such as [[macrophage]]s, present the [[bacterial]] [[antigen]] to [[helper T cell]]s.
**[[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.
**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
===Acute rheumatic fever===
*[[Lesions]] may occur in [[endocardium]], [[myocardium]], or [[pericardium]].
**The [[inflammation]] may cause 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 [[heart valve]]s.
**These warty projections and irregular thickenings are known as [[MacCallum plaques]].<ref name="pmid18306530">{{cite journal| author=Chopra P, Gulwani H| title=Pathology and pathogenesis of rheumatic heart disease. | journal=Indian J Pathol Microbiol | year= 2007 | volume= 50 | issue= 4 | pages= 685-97 | pmid=18306530 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18306530  }} </ref>


[[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.'' 
===Chronic rheumatic fever===
*[[Lesions]] may occur in the [[mitral valve]].
*[[Valve]] thickening may result in [[stenosis]] or [[regurgitation]].


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<ref>Abbas and Lechtman. m'''Basic Immunology: Functions and Disorders of the Immune System'''. Elsevier Inc. 2004.</ref>, producing the symptoms of Rheumatic fever.
===Gross===
On [[gross]] [[pathology]], the following are characteristic findings of rheumatic fever:<ref name="LIBRE"> Rheumatic Heart Disease. Libre Pathology (2015). http://librepathology.org/wiki/index.php/Heart_valves#Rheumatic_heart_disease Accessed on October 12, 2015 </ref>
*"Fish-mouth appearance"
**Slit-like [[morphology]]; elliptical cross-sectional flow area ([[mitral valve]]) with abnormally small semi-minor axis
*Significant [[valvular]] thickening
*Thickening and shortening of the [[chorda tympani]]


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]].<ref>Kumar et al.  '''Robbins and Cotran Pathologic Basis of Disease'''.  Elsevier Inc. 2005</ref>
===Microscopic histopathological analysis===
On [[microscopic]] [[histopathological]] [[analysis]], the following are characteristic findings of rheumatic fever:<ref name="LIBRE"> Rheumatic Heart Disease. Libre Pathology (2015). http://librepathology.org/wiki/index.php/Heart_valves#Rheumatic_heart_disease Accessed on October 12, 2015 </ref><ref name="robbins">{{cite book |author=Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Robbins, Stanley L.; Abbas, Abul K. |title=Robbins and Cotran pathologic basis of disease |publisher=Elsevier Saunders |location=St. Louis, MO |year=2005 |pages= |isbn=0-7216-0187-1 |oclc= |doi=}}</ref>
*[[Anitschkow cell|Caterpillar cells]]
**Abundant [[eosinophilic]] [[cytoplasm]]
**Moderately-poorly defined [[cell]] border
**Well-defined central [[ovoid]] [[nucleus]] with a prominent wavy ribbon-like [[chromatin]]
*[[Aschoff bodies]] found within the [[heart]]
**Jumbled, [[eosinophilic]] [[collagen]]
**Surrounded by [[T cells]]


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]].
===Images===
The following are gross and microscopic images associated with rheumatic fever:<ref name="RFPath"> Pathology Education Instructional Resource. University of Alabama at Birmingham (2014). Images courtesy of Propessor Peter Anderson DVM PhD and published with permission of PEIR, Department of Pathology, University of Alabama at Birmingham. http://www.peir.net Accessed on October 12, 2015.</ref>


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.<ref>{{cite web |url=http://www.robbinspathology.com/ |title=Robbins & Cotran Pathologic Basis of Disease |format= |work=}}</ref>
<gallery>
Image:Rheumatic fever 001.jpg|[[Aortic stenosis]] ([[Tricuspid]] aorta): gross, an example of aortic stenosis due to rheumatic fever.


==Pathological Findings==
Image:Rheumatic fever 002.jpg|[[Mitral]] scarring: gross, an example of mitral scarring due to rheumatic fever (healing phase of an infectious lesion).


[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
Image:Rheumatic mitral valvulitis.jpg|Rheumatic [[mitral]] [[valvulitis]]: gross, an example of [[fibrosis]], [[chorda tympani|chorda]] thickening and shortening with [[thrombus]] around the large left atrium.


<gallery>
Image:ARF mitral valve.jpg|Rheumatic [[mitral]] [[valvulitis]]: gross, an example of acute rheumatic fever lesion along line of closure of [[mitral valve]].
Image:Rheumatic fever 001.jpg|Aortic Stenosis (Tricuspid aorta): Gross, good example of aortic stenosis due to rheumatic fever  
Image:Rheumatic fever 002.jpg|Gross, an excellent example of mitral scarring due to rheumatic fever (healing phase of an infectious lesion).
Image:Rheumatic mitral valvulitis.jpg|Rheumatic mitral valvulitis: Gross, an excellent example of fibrosis, chorda thickening and shortening has thrombus around the large left atrium
</gallery>


Image:Rheumatic fever 003.jpg|[[Mitral]] valve: gross, acute rheumatic fever.


<gallery>
Image:Rheumatic fever 004.jpg|[[Aschoff bodies]]: microscopic histopathological analysis, [[Aschoff bodies]] in rheumatic heart disease.
Image:Rheumatic fever 003.jpg|Mitral valve: acute rheumatic fever
Image:Rheumatic fever 004.jpg|Aschoff bodies in rheumatic heart disease
</gallery>
</gallery>


==References==
==References==
{{reflist|2}}
{{Reflist|2}}


[[Category:Disease]]
[[Category:Cardiology]]
[[Category:Cardiology]]
[[Category:Infectious disease]]
[[Category:Rheumatology]]
[[Category:Bacterial diseases]]
 
{{WH}}
{{WS}}

Latest revision as of 00:00, 30 July 2020

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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]

Overview

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. 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 also act against the myocardium and joints, producing the symptoms of rheumatic fever.

Pathophysiology

Pathogenesis

Acute rheumatic fever

Chronic rheumatic fever

Gross

On gross pathology, the following are characteristic findings of rheumatic fever:[2]

Microscopic histopathological analysis

On microscopic histopathological analysis, the following are characteristic findings of rheumatic fever:[2][3]

Images

The following are gross and microscopic images associated with rheumatic fever:[4]

References

  1. ↑ Chopra P, Gulwani H (2007). "Pathology and pathogenesis of rheumatic heart disease". Indian J Pathol Microbiol. 50 (4): 685–97. PMID 18306530.
  2. ↑ 2.0 2.1 Rheumatic Heart Disease. Libre Pathology (2015). http://librepathology.org/wiki/index.php/Heart_valves#Rheumatic_heart_disease Accessed on October 12, 2015
  3. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, MO: Elsevier Saunders. ISBN 0-7216-0187-1.
  4. ↑ Pathology Education Instructional Resource. University of Alabama at Birmingham (2014). Images courtesy of Propessor Peter Anderson DVM PhD and published with permission of PEIR, Department of Pathology, University of Alabama at Birmingham. http://www.peir.net Accessed on October 12, 2015.
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