Difference between revisions of "Rheumatic fever" - New World Encyclopedia

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'''Rheumatic fever''' is an [[inflammatory disease|inflammatory]] [[disease]] which may develop after a [[Group A streptococcal infection]] (such as [[strep throat]] or [[scarlet fever]]) and can involve the [[heart]], [[joint]]s, [[skin]], and [[brain]].  
+
'''Rheumatic fever''' is an [[inflammation|inflammatory]] [[disease]] that may develop after a [[Group A streptococcal infection]] (such as [[strep throat]] or [[scarlet fever]]) and can involve the [[heart]], [[joint]]s, [[skin]], and [[brain]]. It typically arises in children as a complication of strep throat that has been untreated or inadequately treated (Longe 2006). Rheumatic fever is often characterized by [[arthritis]] (inflammation of the joints) and/or [[carditis]] (inflammation of the heart), although other symptoms may be present.
 +
 
 +
One of the most obvious preventive actions is addressing the original Group A streptococcal infection. While treatment of this infection will usually prevent progression to rheumatic fever, it is important that the full course of prescribed [[antibiotic]]s be taken. One of the causal factors in progression to rheumatic fever is the premature discontinuation of the antibiotic treatment for strep throat.
 +
{{toc}}
 +
Treatments of rheumatic fever include anti-inflammatory medications and antibiotics. Once one has had rheumatic fever, a course of several years of antibiotics may be needed to prevent recurrence.
  
 
==General information==
 
==General information==
−
Rheumatic fever is common worldwide and is responsible for many cases of damaged [[heart valve]]s. In the Western countries, it became fairly rare since the 1950s, probably due to widespread use of antibiotics to treat [[streptococcus]] infections. While it is far less common in the [[United States]] since the beginning of the [[20th century]], there have been a few outbreaks since the [[1980s]]. Although the disease seldom occurs, it is serious and has a mortality of 2–5%.
+
 
 +
The '''Group A streptococcus bacterium''' (''Streptococcus pyogenes'', or ''GAS'') is a form of ''Streptococcus'' [[bacterium|bacteria]] responsible for most cases of streptococcal illness. Infections are largely categorized by the location of infection, including [[strep throat]] ([[pharynx]]), [[scarlet fever]] (upper body), [[impetigo]] ([[skin]] and underlying tissues). Some other [[disease]]s that can be caused by Group A streptococcus bacterium or other causal agents include [[pneumonia]] (pulmonary alveolus) and [[tonsillitis]] ([[tonsil]]s). 
 +
 
 +
[[Image:Rheumatic heart disease, gross pathology 20G0013 lores.jpg|thumb|right|]]
 +
 
 +
Rheumatic fever is particularly tied to incidents of strep throat. Since children ages 5 to 15 are particularly vulnerable to strep throat, then most are susceptible to rheumatic fever (Longe 2006). Strep throat is easily treated by a ten-day course of [[antibiotic]]s. However, when infection occurs without symptoms or when the medication is not taken for the full ten days, the individual has a 3 percent chance of developing rheumatic fever (Longe 2006). Rheumatic fever occurs approximately 20 days after strep throat or scarlet fever. In up to a third of cases, the underlying strep infection may not have caused any symptoms.
 +
 
 +
Rheumatic fever is common worldwide and is responsible for many cases of damaged [[heart valve]]s. In the Western countries, it became fairly rare since the 1950s, probably due to widespread use of antibiotics to treat [[streptococcus]] infections. While it is far less common in the [[United States]] since the beginning of the twentieth century, there have been a few outbreaks since the 1980s. Although the disease seldom occurs, it is serious and has a mortality of 2–5 percent. Heart complications may be long-term and severe, particularly if the heart valves are involved.
 
 
−
Rheumatic fever primarily affects children between ages 6 and 15 years and occurs approximately 20 days after strep throat or scarlet fever. In up to a third of cases, the underlying strep infection may not have caused any symptoms.
+
In addition, persons who have suffered a case of rheumatic fever have a tendency to develop flare-ups with repeated strep infections. The recurrence of rheumatic fever is relatively common in the absence of maintenance of low dose antibiotics, especially during the first three to five years after the first episode of rheumatic fever.
−
+
 
−
The rate of development of rheumatic fever in individuals with untreated strep infection is estimated to be 3%. The rate of development is far lower in individuals who have received antibiotic treatment. Persons who have suffered a case of rheumatic fever have a tendency to develop flare-ups with repeated strep infections.
+
==Diagnosis==
−
+
A list of diagnostic criteria have been developed, which were first published in 1944 by T. Duckett Jones, a medical doctor. These criteria have been periodically revised by the American Heart Association in collaboration with other groups.  
−
The recurrence of rheumatic fever is relatively common in the absence of maintenance of low dose antibiotics, especially during the first three to five years after the first episode of rheumatic fever. Heart complications may be long-term and severe, particularly if the heart valves are involved.
 
  
−
==Diagnosis: modified Jones criteria==
+
These modified "Jones Criteria" are categorized into two groups: Major criteria and minor criteria. For a diagnosis of rheumatic fever, two major criteria or one major and two minor criteria have to be exhibited, and there also has to be evidence of a previous infection with with streptococcus (Longe 2006; Parrillo and Parillo 2007).
−
T. Duckett Jones, MD, first published these criteria in 1944. They have been periodically revised by the [[American Heart Association]] in collaboration with other groups. '''Two major criteria, or one major and two minor criteria''', when there is also evidence of a previous strep infection support the diagnosis of rheumatic fever. p[http://www.emedicine.com/emerg/topic509.htm][http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1404745&dopt=Abstract]
 
 
 
 
 
 
===Major criteria===  
 
===Major criteria===  
−
*'''Carditis:''' inflammation of the heart muscle which can manifest as [[congestive heart failure]] with shortness of breath, [[pericarditis]] with a rub, or a new [[heart murmur]].
+
There are five major criteria. These are:
−
*'''[[Arthritis|Migratory polyarthritis]]:''' a temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards.
+
 
−
*'''[[Sydenham's chorea]] (St. Vitus' dance):''' a characteristic series of rapid movements without purpose of the face and arms. This can occur very late in the disease.
+
*''Carditis.'' [[Carditis]] is an [[inflammation]] of the [[heart]] muscle. It can manifest as congestive heart failure with shortness of breath, pericarditis, or a new heart murmur.
−
*'''[[Erythema marginatum]]:''' a long lasting rash that begins on the trunk or arms as [[macule]]s and spread outward to form a snakelike ring while clearing in the middle. This rash never starts on the face and is made worse with heat.  
+
*''Arthritis.'' [[Arthritis]], specifically migratory polyarthritis, can appear. Migratory polyarthritis is a temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards. Arthritis occurs in about 75 percent of all cases (Longe 2005).
−
*'''Subcutaneous nodules (a form of [[Aschoff bodies]]):''' painless, firm collections of collagen fibers on the back of the wrist, the outside elbow, and the front of the knees. These now occur infrequently.
+
*''Cholea.'' Sydenham's [[chorea]] (St. Vitus' dance) is a characteristic change in coordination, such as an involuntary series of rapid movements of the face and arms without purpose. This may first be noticed as a change in handwriting, and the individual may also develop a low threshold for anger and sadness (Longe 2006). Sydenham's chorea may occur very late in the disease. It occurs in about 10 pecent of all patients (Longe 2006).
−
+
*''Erythema marginatum.'' [[Erythema marginatum]] is a long lasting rash that begins on the trunk or arms as [[macule]]s and spreads outward to form a snakelike ring, while clearing in the middle. This rash never starts on the face and is made worse with heat. *''Subcutaneous nodules.'' Sucutaneous nodules (a form of Aschoff bodies) is a painless, firm collections of [[collagen]] fibers on the back of the wrist, the outside elbow, and the front of the knees. These now occur infrequently.
 +
 
 
===Minor criteria===  
 
===Minor criteria===  
−
*'''[[Fever]]''': temperature elevation
+
There are six minor criteria that may be recognized. These are:
−
*'''[[Arthralgia]]:''' Joint pain without swelling
 
−
*'''Laboratory abnormalities:''' increased [[Erythrocyte sedimentation rate]], increased [[C reactive protein]], [[leukocytosis]]
 
−
*'''[[Electrocardiogram]]''' abnormalities: a prolonged PR interval
 
−
*'''Evidence of Group A Strep infection:''' positive culture for Group A Strep, elevated or rising [[Antistreptolysin O titre]]
 
−
*'''Previous rheumatic fever or inactive heart disease'''
 
  
−
===Other signs and symptoms===  
+
*''Fever.'' [[Fever]] (temperature elevation) may occur.  
−
*[[Abdominal pain]]  
+
*''Arthralgia.'' [[Arthralgia]] is joint pain without swelling.
−
*[[Nosebleed]]s
+
*''Laboratory evidence.'' Such abnormalities may occur as increased erythrocyte sedimentation rate, increased C reactive protein, or [[leukocytosis]].  
 +
*''Electrical changes in the heart.'' Electrical changes in the heart may be observed by use of an electrocardiogram (EKG) that can measure the electrical characteristics of the heart's functioning.
 +
*''Evidence of Group A strep infection.'' Group A strep infection may be observed through a positive culture for Group A Strep, or elevated or rising [[Antistreptolysin O titre]].
 +
Other signs and symptoms include abdominal pain and nosebleeds.
  
−
==Pathophysiology==
+
==Causes==
−
Rheumatic fever is a systemic disease affecting the peri-arteriolar connective tissue which occurs 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 become anergic in the periphery because they fail to receive T cell costimulation.  In the case of a Strep infection activated antigen presenting cells against the bacterial antigen activate helper T cells, thereby breaking the T cell anergy and subsequently B cell anergy.  The B cells are now free to produce antibodies that react against the bacterial cell wall and in addition the mycardium and joints (Abbas and Lechtman).
+
Rheumatic fever is a systemic [[disease]] affecting the peri-arteriolar [[connective tissue]], which occurs after an untreated Group A streptococcal pharyngeal infection. There are two basic theories for how the bacterial infection can lead to rheumatic fever (Longe 2006). One theory, less well supported by research, is that the bacteria produce a [[toxin]] (poisonous chemical) that circulates through the body in the bloodstream (Longe 2005). The more supported theory is that the causes is related to a problem within the body's [[immune system]], whereby [[antibody|antibodies]], designed to destroy invading agents, mistakenly attack the body itself, being unable to distinguish the Group A streptococcus bacteria's antigens from antigens present in the body's own cells (Longe 2006).
  
−
Group A ''[[streptococcus pyogenes]]'' has a [[cell wall]] that is composed of branched [[polymers]] which sometimes contain "''M proteins''" that are highly [[antigenic]]. The antibodies 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 recruiment 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 [[delayed hypersensitivity]] reaction as these lesions predominantly contain [[T-helper]] cells and [[macrophages]] (Kumar et al).
+
Specifically, it is believed that rheumatic fever is caused by [[antibody]] cross-reactivity. This cross-reactivity is a Type II hypersensitivity reaction and is termed "molecular mimicry." Usually self reactive [[B cell]]s become anergic in the periphery because they fail to receive [[T cell]] co-stimulation.  In the case of a strep infection, activated [[antigen]], presenting cells against the bacterial antigen, activate helper T cells, thereby breaking the T cell anergy and subsequently B cell anergy. The B cells are now free to produce antibodies that react against the bacterial cell wall, and in addition, the mycardium and joints (Abbas and Lichtman 2004).
  
−
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” pericarditits, which generally resolves without sequalea. 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 call MacCallum plaques.
+
Group A ''[[streptococcus pyogenes]]'' has a [[cell wall]] that is composed of branched polymers, which sometimes contain "M proteins" that are highly [[antigenic]]. The antibodies 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 [[leukocyte|neutrophils]] and macrophages.  Characteristic Aschoff bodies, composed of swollen [[leukocyte|eosinophilic]] [[collagen]] surrounded by [[lymphocyte]]s and macrophages can be seen on light microscopy.  The larger macrophages may become Aschoff giant cells. Acute rheumatic valvular lesions may also involve a [[delayed hypersensitivity]] reaction as these lesions predominantly contain [[T-helper]] cells and [[macrophages]] (Kumar et al. 2005).
−
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.
+
 
−
[http://www.robbinspathology.com/]
+
In acute rheumatic fever, 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” pericarditits, which generally resolves without sequalea. 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 percent of mitral stenosis often resulting in a “fish mouth” appearance (Kumar 2005).
  
 
==Treatment==  
 
==Treatment==  
−
The management of acute rheumatic fever is geared toward the reduction of inflammation with [[anti-inflammatory medication]]s such as [[aspirin]] or [[corticosteroid]]s. Individuals with positive cultures for strep throat should also be treated with [[antibiotic]]s. Another important cornerstone in treating rheumatic fever includes the continuous use of low dose antibiotics (such as [[penicillin]], [[sulfadiazine]], or [[erythromycin]]) to prevent recurrence.
+
The management of acute rheumatic fever is geared toward the reduction of [[inflammation]] with anti-inflammatory medications, such as [[aspirin]] or [[steroid|corticosteroid]]s. Individuals with positive cultures for strep throat should also be treated with [[antibiotic]]s. Another important cornerstone in treating rheumatic fever includes the continuous use of low dose antibiotics (such as [[penicillin]], [[sulfadiazine]], or [[erythromycin]]) to prevent recurrence.  
  
−
===Infection===
 
 
Patients with positive cultures for ''streptococcus pyogenes'' should be treated with penicillin as long as [[allergy]] is not present. This treatment will not alter the course of the acute disease.
 
Patients with positive cultures for ''streptococcus pyogenes'' should be treated with penicillin as long as [[allergy]] is not present. This treatment will not alter the course of the acute disease.
−
===Inflammation===
+
 
 
Patients with significant symptoms may require [[corticosteroids]]. [[Salicylates]] are useful for pain.   
 
Patients with significant symptoms may require [[corticosteroids]]. [[Salicylates]] are useful for pain.   
−
===Heart failure===
+
 
−
Some patients develop significant [[carditis]] which manifests as [[congestive heart failure]]. This requires the usual treatment for heart failure: [[diuretics]], [[digoxin]], [[etcetera]]. Unlike normal heart failure, rheumatic heart failure responds well to [[corticosteroids]].
+
Some patients develop significant [[carditis]], which manifests as [[congestive heart failure]]. This requires the usual treatment for heart failure: [[Diuretics]], [[digoxin]],and so forth. Unlike normal heart failure, rheumatic heart failure responds well to corticosteroids.
 +
 
 +
There are no proven effective alternative remedies for rheumatic fever, but there are some methods that may help with [[pain]] relief, cardiac function, and other symptoms (Longe 2005). Among these are massage; aramatherapy (oils of rosemary, benzoin, German chamomile, camphor, juniper, or lavender to relieve pain and oils of cypress, fennel, lemon, and wintergreen to reduce inflammation); acupuncture; and osteopathy (Longe 2005).
  
 
==Prevention==
 
==Prevention==
−
Prevention of recurrence is achieved by eradicating the acute infection and [[prophylaxis]] with antibiotics. The [[American Heart Association]] recommends prophylaxis continue at least 10 years.
+
The most important preventative action is addressing the original Group A streptococcal infection. Treatment of this infection with antibiotics will usually prevent progression to rheumatic fever. If an individual has a sore throat that persists longer than 24 hours, it is recommended that the person see a physician. It is important that the full course of antibiotics be taken. One of the causal factors in progression to rheumatic fever is discontinuing the antibiotics prematurely.
 +
 
 +
Prevention of recurrence is achieved by eradicating the acute infection and [[prophylaxis]] with antibiotics. A regime of antibiotics for five years or until the patient reaches 18 years of age, whichever comes first, is recommended by some practitioners (Longe 2006). The American Heart Association recommends prophylaxis continue at least 10 years.
  
 
Nurses also have a role in prevention, primarily in screening school-aged children for sore throats that may be caused by group A streptococci.
 
Nurses also have a role in prevention, primarily in screening school-aged children for sore throats that may be caused by group A streptococci.
  
 
==References==
 
==References==
−
*Jones TD. The diagnosis of rheumatic fever. ''[[Journal of the American Medical Association|JAMA]]''. 1944; 126:481–484
+
 
−
*Abbas and Lechtman. '''Basic Immunology: Functions and Disorders of the Immune System'''.  Elsevier Inc. 2004.
+
* Abbas, A. K., and A. H. Lichtman. 2004. ''Basic Immunology: Functions and Disorders of the Immune System.'' Philadelphia: Saunders. ISBN 072160241X
−
*Kumar et al. '''Robbins and Cotran Pathologic Basis of Disease'''.  Elsevier Inc. 2005
+
* Ferrieri, P. 2002. [http://circ.ahajournals.org/cgi/content/full/106/19/2521?ck=nck Proceedings of the Jones criteria workshop]. ''Circulation'' 106 : 2521–2523. Retrieved May 19, 2007.
−
*[http://circ.ahajournals.org/cgi/content/full/106/19/2521?ck=nck Ferrieri P. Proceedings of the Jones criteria workshop]. ''Circulation'' 2002; 106 : 2521–23
+
* Jones, T. D. 1944. The diagnosis of rheumatic fever. ''Journal of the American Medical Association''. 126: 481–484.
−
*[http://www.emedicine.com/med/topic2922.htm Acute Rheumatic Fever eMedicine]
+
* Kumar, V., A. K. Abbas, N. Fausto, S. L. Robbins, and R. S. Cotran. 2005. ''Robbins and Cotran Pathologic Basis of Disease.'' Philadelphia: Elsevier Saunders. ISBN 0721601871
−
*[http://www.emedicine.com/emerg/topic509.htm Rheumatic Fever Emergency Medicine eMedicine]
+
* Longe, J. L. 2006. ''The Gale Encyclopedia of Medicine.'' Detroit: Thomson Gale. ISBN 1414403682
−
*[http://www.emedicine.com/ped/topic2006.htm Rheumatic Fever Pediatrics eMedicine]
+
* Longe, J. L. (Ed.) 2005. ''The Gale Encyclopedia of Alternative Medicine.'' Detroit: Thomson/Gale. ISBN 0787693960
 +
* Meador, R. J., and I. J. Russell. 2005. [http://www.emedicine.com/med/topic2922.htm Acute rheumatic fever]. ''Emedicine.'' Retrieved May 18, 2007.
 +
* Parrillo, S. J., and C. V. Parrillo. 2007. [http://www.emedicine.com/emerg/topic509.htm Rheumatic fever]. ''Emedicine.'' Retrieved May 19, 2007.
  
 
==External links==
 
==External links==
−
*[http://www.nlm.nih.gov/medlineplus/ency/article/003940.htm NIH Rheumatic Fever Guide]
+
All links retrieved December 8, 2022.
−
* [http://heartcenter.seattlechildrens.org/conditions_treated/rheumatic_heart_disease.asp Rheumatic fever information] from Seattle Children's Hospital Heart Center
+
*[http://www.nlm.nih.gov/medlineplus/ency/article/003940.htm National Institutes of Health (NIH) Rheumatic Fever Guide].
 +
 
  
  
 
{{credit|131700038}}
 
{{credit|131700038}}
 
[[Category:Life sciences]]
 
[[Category:Life sciences]]
 +
[[Category:Health and disease]]
 +
[[Category:Diseases]]

Latest revision as of 20:01, 8 December 2022


Rheumatic fever
Classification and external resources
ICD-10 I00-I02
ICD-9 390–392
DiseasesDB 11487
MedlinePlus 003940
eMedicine med/3435  med/2922 emerg/509 ped/2006

Rheumatic fever is an inflammatory disease that may develop after a Group A streptococcal infection (such as strep throat or scarlet fever) and can involve the heart, joints, skin, and brain. It typically arises in children as a complication of strep throat that has been untreated or inadequately treated (Longe 2006). Rheumatic fever is often characterized by arthritis (inflammation of the joints) and/or carditis (inflammation of the heart), although other symptoms may be present.

One of the most obvious preventive actions is addressing the original Group A streptococcal infection. While treatment of this infection will usually prevent progression to rheumatic fever, it is important that the full course of prescribed antibiotics be taken. One of the causal factors in progression to rheumatic fever is the premature discontinuation of the antibiotic treatment for strep throat.

Treatments of rheumatic fever include anti-inflammatory medications and antibiotics. Once one has had rheumatic fever, a course of several years of antibiotics may be needed to prevent recurrence.

General information

The Group A streptococcus bacterium (Streptococcus pyogenes, or GAS) is a form of Streptococcus bacteria responsible for most cases of streptococcal illness. Infections are largely categorized by the location of infection, including strep throat (pharynx), scarlet fever (upper body), impetigo (skin and underlying tissues). Some other diseases that can be caused by Group A streptococcus bacterium or other causal agents include pneumonia (pulmonary alveolus) and tonsillitis (tonsils).

Rheumatic heart disease, gross pathology 20G0013 lores.jpg

Rheumatic fever is particularly tied to incidents of strep throat. Since children ages 5 to 15 are particularly vulnerable to strep throat, then most are susceptible to rheumatic fever (Longe 2006). Strep throat is easily treated by a ten-day course of antibiotics. However, when infection occurs without symptoms or when the medication is not taken for the full ten days, the individual has a 3 percent chance of developing rheumatic fever (Longe 2006). Rheumatic fever occurs approximately 20 days after strep throat or scarlet fever. In up to a third of cases, the underlying strep infection may not have caused any symptoms.

Rheumatic fever is common worldwide and is responsible for many cases of damaged heart valves. In the Western countries, it became fairly rare since the 1950s, probably due to widespread use of antibiotics to treat streptococcus infections. While it is far less common in the United States since the beginning of the twentieth century, there have been a few outbreaks since the 1980s. Although the disease seldom occurs, it is serious and has a mortality of 2–5 percent. Heart complications may be long-term and severe, particularly if the heart valves are involved.

In addition, persons who have suffered a case of rheumatic fever have a tendency to develop flare-ups with repeated strep infections. The recurrence of rheumatic fever is relatively common in the absence of maintenance of low dose antibiotics, especially during the first three to five years after the first episode of rheumatic fever.

Diagnosis

A list of diagnostic criteria have been developed, which were first published in 1944 by T. Duckett Jones, a medical doctor. These criteria have been periodically revised by the American Heart Association in collaboration with other groups.

These modified "Jones Criteria" are categorized into two groups: Major criteria and minor criteria. For a diagnosis of rheumatic fever, two major criteria or one major and two minor criteria have to be exhibited, and there also has to be evidence of a previous infection with with streptococcus (Longe 2006; Parrillo and Parillo 2007).

Major criteria

There are five major criteria. These are:

  • Carditis. Carditis is an inflammation of the heart muscle. It can manifest as congestive heart failure with shortness of breath, pericarditis, or a new heart murmur.
  • Arthritis. Arthritis, specifically migratory polyarthritis, can appear. Migratory polyarthritis is a temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards. Arthritis occurs in about 75 percent of all cases (Longe 2005).
  • Cholea. Sydenham's chorea (St. Vitus' dance) is a characteristic change in coordination, such as an involuntary series of rapid movements of the face and arms without purpose. This may first be noticed as a change in handwriting, and the individual may also develop a low threshold for anger and sadness (Longe 2006). Sydenham's chorea may occur very late in the disease. It occurs in about 10 pecent of all patients (Longe 2006).
  • Erythema marginatum. Erythema marginatum is a long lasting rash that begins on the trunk or arms as macules and spreads outward to form a snakelike ring, while clearing in the middle. This rash never starts on the face and is made worse with heat. *Subcutaneous nodules. Sucutaneous nodules (a form of Aschoff bodies) is a painless, firm collections of collagen fibers on the back of the wrist, the outside elbow, and the front of the knees. These now occur infrequently.

Minor criteria

There are six minor criteria that may be recognized. These are:

  • Fever. Fever (temperature elevation) may occur.
  • Arthralgia. Arthralgia is joint pain without swelling.
  • Laboratory evidence. Such abnormalities may occur as increased erythrocyte sedimentation rate, increased C reactive protein, or leukocytosis.
  • Electrical changes in the heart. Electrical changes in the heart may be observed by use of an electrocardiogram (EKG) that can measure the electrical characteristics of the heart's functioning.
  • Evidence of Group A strep infection. Group A strep infection may be observed through a positive culture for Group A Strep, or elevated or rising Antistreptolysin O titre.

Other signs and symptoms include abdominal pain and nosebleeds.

Causes

Rheumatic fever is a systemic disease affecting the peri-arteriolar connective tissue, which occurs after an untreated Group A streptococcal pharyngeal infection. There are two basic theories for how the bacterial infection can lead to rheumatic fever (Longe 2006). One theory, less well supported by research, is that the bacteria produce a toxin (poisonous chemical) that circulates through the body in the bloodstream (Longe 2005). The more supported theory is that the causes is related to a problem within the body's immune system, whereby antibodies, designed to destroy invading agents, mistakenly attack the body itself, being unable to distinguish the Group A streptococcus bacteria's antigens from antigens present in the body's own cells (Longe 2006).

Specifically, it is believed that rheumatic fever is caused by antibody cross-reactivity. This cross-reactivity is a Type II hypersensitivity reaction and is termed "molecular mimicry." Usually self reactive B cells become anergic in the periphery because they fail to receive T cell co-stimulation. In the case of a strep infection, activated antigen, presenting cells against the bacterial antigen, activate helper T cells, thereby breaking the T cell anergy and subsequently B cell anergy. The B cells are now free to produce antibodies that react against the bacterial cell wall, and in addition, the mycardium and joints (Abbas and Lichtman 2004).

Group A streptococcus pyogenes has a cell wall that is composed of branched polymers, which sometimes contain "M proteins" that are highly antigenic. The antibodies 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 delayed hypersensitivity reaction as these lesions predominantly contain T-helper cells and macrophages (Kumar et al. 2005).

In acute rheumatic fever, 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” pericarditits, which generally resolves without sequalea. 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 percent of mitral stenosis often resulting in a “fish mouth” appearance (Kumar 2005).

Treatment

The management of acute rheumatic fever is geared toward the reduction of inflammation with anti-inflammatory medications, such as aspirin or corticosteroids. Individuals with positive cultures for strep throat should also be treated with antibiotics. Another important cornerstone in treating rheumatic fever includes the continuous use of low dose antibiotics (such as penicillin, sulfadiazine, or erythromycin) to prevent recurrence.

Patients with positive cultures for streptococcus pyogenes should be treated with penicillin as long as allergy is not present. This treatment will not alter the course of the acute disease.

Patients with significant symptoms may require corticosteroids. Salicylates are useful for pain.

Some patients develop significant carditis, which manifests as congestive heart failure. This requires the usual treatment for heart failure: Diuretics, digoxin,and so forth. Unlike normal heart failure, rheumatic heart failure responds well to corticosteroids.

There are no proven effective alternative remedies for rheumatic fever, but there are some methods that may help with pain relief, cardiac function, and other symptoms (Longe 2005). Among these are massage; aramatherapy (oils of rosemary, benzoin, German chamomile, camphor, juniper, or lavender to relieve pain and oils of cypress, fennel, lemon, and wintergreen to reduce inflammation); acupuncture; and osteopathy (Longe 2005).

Prevention

The most important preventative action is addressing the original Group A streptococcal infection. Treatment of this infection with antibiotics will usually prevent progression to rheumatic fever. If an individual has a sore throat that persists longer than 24 hours, it is recommended that the person see a physician. It is important that the full course of antibiotics be taken. One of the causal factors in progression to rheumatic fever is discontinuing the antibiotics prematurely.

Prevention of recurrence is achieved by eradicating the acute infection and prophylaxis with antibiotics. A regime of antibiotics for five years or until the patient reaches 18 years of age, whichever comes first, is recommended by some practitioners (Longe 2006). The American Heart Association recommends prophylaxis continue at least 10 years.

Nurses also have a role in prevention, primarily in screening school-aged children for sore throats that may be caused by group A streptococci.

References
ISBN links support NWE through referral fees

  • Abbas, A. K., and A. H. Lichtman. 2004. Basic Immunology: Functions and Disorders of the Immune System. Philadelphia: Saunders. ISBN 072160241X
  • Ferrieri, P. 2002. Proceedings of the Jones criteria workshop. Circulation 106 : 2521–2523. Retrieved May 19, 2007.
  • Jones, T. D. 1944. The diagnosis of rheumatic fever. Journal of the American Medical Association. 126: 481–484.
  • Kumar, V., A. K. Abbas, N. Fausto, S. L. Robbins, and R. S. Cotran. 2005. Robbins and Cotran Pathologic Basis of Disease. Philadelphia: Elsevier Saunders. ISBN 0721601871
  • Longe, J. L. 2006. The Gale Encyclopedia of Medicine. Detroit: Thomson Gale. ISBN 1414403682
  • Longe, J. L. (Ed.) 2005. The Gale Encyclopedia of Alternative Medicine. Detroit: Thomson/Gale. ISBN 0787693960
  • Meador, R. J., and I. J. Russell. 2005. Acute rheumatic fever. Emedicine. Retrieved May 18, 2007.
  • Parrillo, S. J., and C. V. Parrillo. 2007. Rheumatic fever. Emedicine. Retrieved May 19, 2007.

External links

All links retrieved December 8, 2022.


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