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Abstract

Rheumatic fever is an immunologically mediated inflammatory disease, that occurs as a delayed sequel to group A streptococcal throat infection, in genetically susceptible individuals. Chronic rheumatic heart disease remains an important public health problem in developing countries. Aetiopathogenesis and guidelines for the diagnosis, prevention and treatment of acute rheumatic fever are reviewed.

MeSH: rheumatic fever, streptococcus, rheumatic heart disease, arthritis, autoimmunity

Introduction

Rheumatic fever (RF) is a multisystem, immunologically mediated inflammatory disease, that occurs as a delayed sequel to group A streptococcal (GAS) infection. Its subsequent complication, chronic rheumatic heart disease (RHD), remains a major public health problem in developing countries.

Epidemiology

The epidemiology of RF in developed countries has changed dramatically over the past decades. In developing areas, the prevalence is still high at up to 24 per 1000 population.1 Rheumatic fever occurs most frequently among children and adolescents between 5 and 18 years,2 coinciding with the age distribution of the highest prevalence of streptococcal infections.

Aetiopathogenesis

The pathogenic mechanisms involved in the development of RF remain unclear. However, it is evident that an abnormal humoral and cellular immune response occurs. Antigenic mimicry between streptococcal antigens, mainly M-protein epitopes and human tissues, such as heart valves, myosin and tropomyosin, brain proteins, synovial tissue and cartilage has been proposed as the triggering factor leading to autoimmunity in individuals with genetic predisposition.3 Several genetic markers of susceptibility have been studied but no consistent association found.4 However, associations with different HLA class II antigens have been observed in several populations.5⁻13 Molecular mimicry was first demonstrated by humoral immune response. Streptococcal antibodies cross-react with several human tissues including heart, skin, brain, glomerular basement membrane, striated and smooth muscles.14 The presence of CD4+ T cells at lesions sites in the heart has been demonstrated, suggesting a direct role of these cells in the pathogenesis of RHD.15,16 Infiltrating T lymphocytes from heart lesions of severe RHD patients and peripheral T lynphocytes were capable of recognising immunodominant myocardium M5 peptides and valve proteins. These results showed the significance of molecular mimicry between beta hemolytic streptococci and heart tissue assessing the T-cell repertoire leading to local tissue damage in RHD.17,18 Figure 1 illustrates the events that occur during the development of RF/RHD.

Major Clinical Manifestations

Arthritis

Arthritis is the most common manifestation, present in 60-80% of patients.19,20 Itu sually affects the peripheral large joints; small joints and axial skeleton are rarely involved. Knees, ankles, elbows and wrists are the most frequently affected. In addition to arthralgia, the joints are red, warm and swollen. Arthritis is characteristically asymmetrical, migratory, and very painful, although some patients may present mild joint complaints. It usually resolves spontaneously at the most in 2 or 3 weeks. Arthritis in ARF has an excellent response to salicylates.21

Approximately one third of patients with joint involvement reported in a series of 786 cases of RF presented with "atypical" articular manifestations, considered by some as a separate entity, i.e., post-streptococcal reactive arthritis. It seems reasonable to include these manifestations as part of the spectrum of RF.19,21 Secondary prophylaxis should be recommended in these situations.

Carditis

Acute carditis was present in 50% of patients in a large recent series.19 It is a pancarditis, but valvular involvement is the rule. The commonest involved valve is the mitral, frequently associated with aortic valve involvement. Right-sided heart valves are rarely affected.

On pathological examination, the valves are thickened and display rows of small vegetations along their apposing surfaces ( Figure 2 ). Myocarditis is characterised by infiltration of mononuclear cells, vasculitis and degenerative changes of the interstitial connective tissue.22 The pathognomonic lesion is the Aschoff body in the proliferative stage, present in 30 to 40 per cent of biopsies of patients with acute RF.23 It is seen mainly in the interstitial connective tissue of the myocardium, particularly perivascularly ( Figure 3 ).22 Inflammation of the valves consists of oedema and mononuclear cell infiltration of the valvular tissue and the chordae tendineae in the acute phase; fibrosis and calcification occur with maintenance of the inflammatory process.22

The clinical picture includes high pulse rate, congestive heart failure, arrhytmias and pericardial friction rubs. On the first attack, valvulitis is suspected in the presence of a new apical systolic murmur of mitral regurgitation (associated or not with an apical mid-diastolic murmur) and/or a basal diastolic murmur of aortic regurgitation.24 Cardiomegaly is noted on X-Ray ( Figure 4 ) and on echocardiogram. Myocarditis and/or pericarditis in the absence of valvular involvement is unlikely due to acute RF.24 It is contentious if myocardial disfunction in acute RF is valvular or myocardial in origin.25 In fact, in a subset of patients, the initial presentation may be quite severe, with overt heart failure, fever and toxaemia, making the differential diagnosis with infective endocarditis very difficult, in particular in patients with recurrent rheumatic heart disease.

The valvular lesions in RF often result in residual damage. Nevertheless, in milder forms of rheumatic carditis patients may recover from valvulitis without sequelae.1 In the first attack, the lesions are predominantly regurgitant, due to ring dilatation, swollen cusps, chordal rupture or papillary muscle dysfunction. In the chronic phase, obstructive lesions are more frequent. Figures ​Figures5 5 - 7 depict aspects of the chronic valvar involvement on echocardiography. Figures ​Figures8 8 - 10 show examples of the pathological presentation of chronic rheumatic valve disease.

Sydenham's chorea

Sydenham's chorea is characterized by involuntary movements, specially of the face and limbs, muscle weakness, disturbances of speech and gait. Children usually exhibit concomitant psycologic dysfunction, especially obsessive-compulsive disorder, increased emotional lability, hyperactivity, irritablility and age-regressed behavior.26⁻28 It is usually a delayed manifestation, and is often the sole manifestation of ARF. However, chorea may occur in association with other major manifestations of RF, particularly in the first attack.29 Evidence of a recent GAS infection is often difficult to document. Most of the patients experience resolution of the symptomatology after a few months.3,24 However, a recurrence rate up to 32% has been described, despite the regular use of secondary benzathine penicillin prophylaxis. Some believe that these episodes represent exacerbations rather than distinct attacks of acute RF.29,30

Subcutaneous nodules

Subcutaneous nodules are rarely seen and when present, they are usually associated with severe carditis. They are painless, firm, movable, measuring around 0.5 to 2 cm. They are usually located over extensor surfaces of the joints, particularly knees, wrists and elbows ( Figure 11 ).24

Erythema marginatum

This is an evanescent, erythematous, non-pruritic rash with pale centers and rounded or serpiginous margins. Lesions occur mainly on the trunk and proximal extremities and may be induced by application of heat ( Figure 12 ).24,31

Diagnosis

With the exception of Sydenham's chorea, which has a latency period of several months, the clinical manifestations of acute RF present after about 3 weeks following the streptococcal throat infection. It usually begins with nonspecific symptoms, such as fever, malaise and persistent pallor.3

There is no specific clinical or laboratory test that establishes the diagnosis of RF. Diagnosis is based on the revised Jones Criteria24 ( Table 1 ). Arthritis, carditis, chorea, and less frequently, subcutaneous nodules and erythema marginatum are major manifestations of RF. If supported by evidence of preceding streptococcal infection, the presence of two major manifestations or one major and two minor manifestations indicates a high probability of acute RF. The two exceptions to this requirement are Sydenham's chorea and indolent carditis. Other manifestations include arthralgia, serositis and involvement of the kidneys and lungs.3

Table 1

Differential diagnosis

The differential diagnosis is extensive because of the lack of specificity of many of the clinical and laboratory findings in RF and also the unavailability of a laboratory test to confirm the diagnosis. Several diseases need to be considered. Table 2 includes those more often presenting clinical difficulties to the clinician. Juvenile rheumatoid arthritis (JRA) and other connective tissue diseases often should be considered. The articular involvement in JRA usually lasts longer than in RF. It is generally polyarticular and symmetrical, typically affecting the small joints of the hands. Patients complain of increased pain in the morning or after long periods of immobility. Arthritis of the cervical spine occurs in about half of the cases but is also quite frequent in acute RF.3

Table 2

Cardiac involvement presents primarily as pericarditis therefore infective endocarditis should be considered in patients with recurrent RF presenting with persistent fever of unknown origin. Sometimes the differential diagnosis can be difficult, especially in those presenting with a more severe clinical presentation. Splenomegaly, vascular and immmunologic phenomena, demonstration of vegetations on echocardiogram and positive blood cultures are indicative of infective endocarditis. Gallium-67 cardiac scintigraphy can be helpful in this setting.

Systemic lupus erythematosus (SLE) shares clinical characteristics with acute RF. Arthralgia and transient arthritis are common. SLE affects multiple organs, including kidney, central nervous system, skin, and blood. Diagnosis is made on clinical grounds and confirmed by serologic studies.32

Laboratory studies

Acute phase reactants are useful in helping to recognize acute RF and also to exclude other diseases. C-reactive protein and erythrocyte sedimentation rates are helpful in monitoring inflammatory activity.24

Laboratory evidence of a preceding GAS infection should be sought, either by demonstration of GAS in the throat by culture or rapid streptoccocal antigen test, or using streptococcal antibody tests. Elevated or rising titers of antistreptolysin O (ASO) occur in more than 80% of patients with acute GAS pharyngitis.24 There is a remarkable response during the acute phase of RF. The test specificity has been shown to be 93% with ASO titers above 960 IU/ml.33

Prolonged P-R interval relative to heart rate is a nonspecific finding, present in more than one third of the patients. Low-voltage QRS complexes and ST segment changes may be found in the presence of pericarditis and pericardial effusion.3

Endomyocardial biopsy is invasive and does not appear to provide additional diagnostic information where there is a clinical consensus about the diagnosis of RF, with a diagnostic sensitivity in one relatively large study of 27%. It should be limited to clinical investigation.23,34

Cardiac scanning scintigraphy has been shown to be a reliable method distinguishing acute from chronic, inactive RHD and also in the follow-up of active carditis ( Figure 13 ).35⁻37

The role of echocadiography to diagnose valvulitis without auscultatory findings has been debated.34,38⁻41 At present, subauscultatory valve regurgitation is not considered a diagnostic criterion for RF.24

Treatment

Prevention

Prevention of initial attacks of RF (primary prevention) requires the eradication of GAS from the pharynx. Table 3 shows the currently recommended treatment schedules.42 Emphasis should be given to the need of eradication of GAS as part of the treatment of acute RF.

Antibiotic prophylaxis is the safest way to prevent recurrent attacks of acute RF and is recommended for patients with well-documented RF. The recommendations from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young of the American Heart Association are shown on Table 4 .42

Arthritis

Salicylates remain the first-line drugs in the treatment of arthritis. The response is usually excellent. Treatment should be started at 80 to 100 mg/kg/day (maximum, 4g daily) for 3-4 weeks. Naproxen (10-15mg/kg/day, bid) is an alternative drug, with very good response. Other nonsteroidal antiinflammatory drugs also can be used.

Carditis

Moderate to severe carditis is usually an indication for cortiscoteroids although efficacy in reducing sequelae has not been proven so far. Albert at al. performed a meta-analysis of the literature on the treatment of rheumatic carditis, comparing corticosteroids and salicylates in preventing valvular damage. It seems clear that corticosteroids are superior to salicylates in rapidly resolving acute manifestations, but the advantage of the former in preventing a pathologic murmur at 1 year posttreatment was not statistically significant.43 Prednisone, 2mg/kg/day (maximum, 60mg/day) is used for two weeks and after that, the dose is gradually tapered, reducing 20 to 25% of the previous dose every week. Some advocate the concomitant use of salicylates to avoid rebound. In severe carditis, therapy may be initiated with intravenous methylprednisolone.44,45 Intravenous immunoglobulin seems not to alter the extent and severity of carditis or decrease chronic morbitidy.46

Heart failure usually responds to steroids. Bed rest is always recommended and should be planned on an individual basis. Diuretics and vasodilators may be used in patients with more severe haemodynamic decompensation. Digoxin should be used with caution because of the risk of toxicity in the presence of active myocarditis.47 Surgical treatment in the acute stage should be considered when clinical therapy is ineffective to control cardic failure. Valve repair, although technically more difficult, is the first choice for younger patients.48

Chorea

Treatment with haloperidol (initial dose of 0.5 to 1mg/kg/day, maximum, 5mg/day)49 or valproic acid (15-20 mg/kg/day)50,51 are helpful in decreasing the severity of involuntary movements but may not improve the behavioral symptoms. Carbamazepine has also been suggested as a first-line treatment for Sydenham's chorea.52 Alternatively, phenobarbital also may be used, 5-7mg/kg/day, tid. Treatment is usually maintained for 8-12 weeks. Intravenous immunoglobulin therapy has been suggested.26

Acknowledgments

The authors would like to acknowledge the assistance of Dr. Clovis Artur Almeida da Silva, from the Department of Paediatrics, Rheumatology Unity (director), University of Sao Paulo Medical School, who provided invaluable help with the illustrations and suggestions on the text. We would also like to thank Prof. Maria de Lourdes Higuchi, director of the Laboratory of Pathology, Heart Institute (InCor), University of Sao Paulo Medical School, for the pictures on the pathological specimens.

References

20. Kiss MHB. Articular involvement in rheumatic fever. Rev.Soc.Cardiol.Estado de Sao Paulo. 1993;3:26-31. [ Google Scholar]

22. Pomerance A. Cardiac involvement in rheumatic and 'collagen' diseases. In: Pomerance A, Davies MJ, editors. The pathology of the heart. Oxford: Blackwell Scientific Publications; 1975. pp. 279-306. [ Google Scholar]

35. Soares J, Jr, Snitcowsky R, Meneghetti JC, Hironaka FH, Assis RVC, Giorgi MCP, et al. Gallium-67 imaging in the diagnosis and follow-up of rheumatic carditis. Eur.J.Nucl.Med. 1990;16:S5. [ Google Scholar]

36. Soares J, Jr, Snitcowsky R, Assis RV, Izaki M, Giorgi MCP, Meneghetti JC, et al. Carditis in rheumatic fever - importance of scintigraphic diagnosis. J.Nucl.Med. 1992;33:995. [ Google Scholar]

Articles from Images in Paediatric Cardiology are provided here courtesy of Images in Paediatric Cardiology

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Rheumatic fever is an immunologically mediated inflammatory disease, that occurs as a delayed sequel to group A streptococcal throat infection, in genetically susceptible individuals. Chronic rheumatic heart disease remains an important public health problem in developing countries. Aetiopathogenesis and guidelines for the diagnosis, prevention and treatment of acute rheumatic fever are reviewed.

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Complete explanation of Rheumatic Fever by Emmanuel Rusingiza

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Complete explanation of Rheumatic Fever by Emmanuel Rusingiza

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"Acute Rheumatic Fever" by Emmanuel Rusingiza, MD, for OPENPediatrics

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Rheumatic fever is an inflammatory reaction that can develop as a complication of a Group A streptococcal infection, such as strep throat or scarlet fever. It occurs when the infection has been untreated or undertreated.

Not everyone who has a streptococcal infection will develop rheumatic fever (RF), but if RF does develop, symptoms normally appear after infection.

It most commonly affects boys and girls aged 5 to 15 years, but it can occur in adults and younger children. Neurologic complications seem to be more common in females.

RF can have long-term complications, the most common being rheumatic heart disease (RHD) which develops in 30 to 45 percent of those with RF. Worldwide, RHD is responsible for 230,000 - 500,000 deaths per year.

Before the widespread introduction of antibiotics, RF was a leading cause of acquired heart disease in developed nations, but it is now relatively rare in these countries. Thanks to routine treatment of Strep throat, RF now only occurs in about cases per every 1,000 children in mainland U.S.

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Rheumatic fever is a complication of some types of streptococcal infection.

RF is caused by a reaction to the bacteria that cause strep throat, so that diagnosis and treatment of this condition can prevent it from developing into RF.

Symptoms of strep throat include:

sore throat

swollen, tender lymph nodes

trouble swallowing

nausea and vomiting

red skin rash

high temperature

swollen tonsils

abdominal pain

Signs and symptoms generally develop 2 to 4 weeks after a streptococcal infection.

Some individuals will experience just one or two of the following symptoms, but others may experience most of them:

rapid heart rate

decreased ability to exercise

joint pain and swelling

fever

splotchy rash

uncontrollable twitching and movements

Arthritis, or pain and swelling in the joints, affects 75 percent of patients. It normally starts in the larger joints, such as the knees, ankles, wrists, and elbows, before moving to other joints. This inflammation normally resolves within 4-6 weeks, without causing permanent damage.

Inflammation of the heart can lead to chest pain, palpitations, a sensation that the heart is fluttering or pounding hard, panting, and shortness of breath, and fatigue.

On average, around of patients develop carditis or valvulitis, a potentially fatal inflammation of the heart that can have serious, long-term effects. Younger children are more susceptible.

Inflammation of the nerves can lead to symptoms of Sydenham's chorea, including:

chorea, the uncontrollable jerking of knees, elbows, wrists, and ankles

inappropriate crying or laughing

irritability and moodiness

difficulty controlling fine hand movements

problems with balance

Symptoms usually pass within a few months but can last up to 2 years. They are not normally permanent.

Other symptoms include a red, blotchy, skin rash, which appears in 1 in 10 cases. Less common are nosebleeds, abdominal pain, bumps and lumps, or nodules, under the skin, and a high fever over 102 degrees Fahrenheit.

The inflammation may also lead to headache, sweating, vomiting, and weight loss.

Treatment aims to destroy the bacteria, relieve symptoms, control inflammation, and prevent recurrences of RF.

Antibiotics, such as penicillin, may be given to destroy any remaining strep bacteria in the body. Further antibiotics may be prescribed, to prevent recurrence. This may continue for depending on the age of the person and whether or not the heart is affected.

Long-term, and even lifelong, preventive antibiotics may be necessary to prevent recurring inflammation of the heart.

It is important to remove all traces of streptococcal bacteria, as any remaining bacteria can lead to repeated occurrences of RF and a significantly higher risk of heart damage, which can become permanent.

Anti-inflammatory drugs: Naproxen, for example, may help to reduce pain, inflammation, and fever.

Corticosteroids: Prednisone may be given if the patient does not respond to first-line anti-inflammatory medications, or if there is inflammation of the heart.

Aspirin: This is not usually recommended for children aged under 16 years because of the risk of developing Reye's syndrome, which can cause liver and brain damage, and even death, but an exception is usually made in cases of RA because the benefits are greater than the risks.

Anticonvulsant medications: These can treat severe chorea symptoms. Examples include valproic acid (Depakene or Stavzor), carbamazepine (Carbatrol or Equetro), haloperidol (Haldol) and risperidone (Risperdal).

Anyone who has RF as a child will need to inform their doctor as they get older because heart damage can appear many years later.

The doctor will ask about the patient's symptoms and recent medical history. They will pay particular attention to any recent illness along with the following:

swelling, pain, and stiffness in the joints

any jerky, involuntary movements

a red or pink skin rash

small nodules or lumps and bumps under the skin, especially on the elbows, ankles, knees, and knuckles

irregular heart rhythm

Tests may include:

Electrocardiogram (EKG): An electrical tracing of the heart to detect abnormal heart rhythms suggesting inflammation

Echocardiography: An ultrasound of the heart to look for inflammation or heart valve damage

Blood tests

Additional tests can detect specific strep infections.

Symptoms of RF, and specifically inflammation, may persist for weeks, months, or longer, causing long-term problems.

Rheumatic heart disease (RHD) is the most common and most serious complication.

Globally, RHD is estimated to affect more than 15 million people per year and cause more than deaths.

The inflammation causes permanent damage to the heart, most commonly the mitral valve, the valve between the upper and lower chambers of the left side of the heart.

This can lead to:

Valvular stenosis: The valve narrows, causing a drop in blood flow

Valvular regurgitation: Blood flows in the wrong direction because of a leak

Heart muscle damage: Inflammation weakens the heart muscle so that the heart cannot pump properly

Other conditions that may develop if there is damage to heart tissue, the mitral valve, or other heart valves include:

Heart failure: This is a serious condition in which the heart is not pumping blood throughout the body efficiently. This can affect the left side, the right side, or both sides of the heart.

Atrial fibrillation: An abnormal heart rhythm where the upper chambers of the heart (the atria) do not coordinate with the lower part of the heart (the ventricles). This causes the heart muscle to contract irregularly, excessively fast, or both making its pumping ability inefficient. This abnormal rhythm can also lead to a stroke.

RF is now rare in developed countries, but it remains a risk elsewhere. Researchers continue to seek effective ways to prevent RF and its complications.

The main cause of RF is Group A streptococcus (GAS), a bacteria that can cause infections such as Strep throat with or without scarlet fever and skin infections like impetigo, and cellulitis.

However, not all strains of streptococcal bacteria will lead to RF, and not everyone who has a GAS infection will develop RF.

Genetic factors may increase the risk. The chance of having RF appears to be higher if another family member has had it.

The exact link between group A strep infection and RF remains unclear, but scientists believe that it is not the bacteria itself that causes the disease, but rather the immune system's faulty reaction to it.

Strep bacteria have a protein that resembles one found in some body tissues. Immune system cells that would usually target the bacteria may start attacking the body's own tissues instead, as if they are toxins or infectious agents.

In RF, the tissues that they attack are those of the heart, joints, central nervous system (CNS) and skin. These tissues react by becoming inflamed.

If a patient with Strep bacteria takes a complete course of antibiotic treatment, the chances of RF developing are very low.

In 8 out of 10 cases, the signs and symptoms of RF resolve within 12 weeks. Between 30 and 45 percent of people with RF will develop heart problems. Recurrences of rheumatic fever often occur within 5 years.

In the past, RF was a major cause of mortality, but now this is rare in industrialized countries. However, RF is fatal in 1.5 percent of cases worldwide.

Environmental factors, such as overcrowding, poor sanitation, and poor access to healthcare increase the risk of developing RF.

Leaving strep throat or scarlet fever untreated or partially treated by not finishing a complete course of antibiotics increases the risk of RF significantly.

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Rheumatic fever: Causes, symptoms, and treatment

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Rheumatic fever is an inflammatory reaction. It occurs when infections, including those that cause strep throat and scarlet fever, go untreated. Rheumatic fever is most common in children under 16, and it can lead to severe, lasting complications. In this article, learn about risk factors, diagnosis, and more.

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Lisa Cauthen

Lisa is a Registered Nurse with a 14 years of experience and a Masters Degree in Nursing Education. She has certifications in CPN, ACLS, PALS, and NRP.

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Christianlly Cena

Christianlly has taught college Physics, Natural science, Earth science, and facilitated laboratory courses. He has a master's degree in Physics and is currently pursuing his doctorate degree.

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Both scarlet and rheumatic fevers are childhood illnesses associated with the group-A strep bacteria. This lesson will explore both scarlet fever and rheumatic fever while focusing on what differs them. Updated: 06/20/2021

A Boy and a Bunny

In the classic children's story, The Velveteen Rabbit, a boy is so in love with his stuffed rabbit that the rabbit becomes 'real'. Unfortunately, the boy becomes sick with scarlet fever and all his possessions, including the cherished rabbit, must be destroyed. Would the story have ended any differently if the boy had been diagnosed with rheumatic fever rather than scarlet fever? Would it end differently if it happened today, rather than the early 20th century? Let's meet Max and Joey and follow their experiences to find out.

Lesson

Quiz

Course

The Velveteen Rabbit

Max is an 8-year-old boy who is complaining of an itchy belly and back. His mom finds a bright red, rough rash on nearly his whole body and takes his temperature, revealing 101.7 degrees Fahrenheit. At his pediatrician's office, Max is diagnosed with scarlet fever.

Scarlet fever is an illness caused by infection of group-A beta-hemolytic streptococci bacteria or group-A strep for short. Scarlet fever, also known as scarlatina, gets its name from the bright red rash that covers most of the body. The rash is usually raised, feels like sandpaper, and is often itchy. In addition to a rash, as the name suggests, a fever is usually also present. Scarlet fever is often associated with strep throat as both are caused by the same bacteria and can occur together.

Scarlet Fever

Treatment

Recalling the story of the velveteen rabbit, Max's mother becomes concerned about the treatment Max (and his toys) will need. Luckily for Max and other children today, destruction of items belonging to a person with scarlet fever is no longer necessary.

Treatment for scarlet fever includes antibiotics to kill the group-A strep bacteria. In most cases a single course, usually 10-14 days, of antibiotics is sufficient. Meditations to reduce fever and anti-itch creams or medications are also appropriate.

Rheumatic Fever

Joey is also 8 years old and is Max's best friend. Joey had the same itchy belly and rash as Max but it went away and so his mother did not take him to the pediatrician. About three weeks went by with Joey doing well until he spiked a fever and began to complain of a headache and knee pain in both legs. Joey's mom took him to the pediatrician and Joey was diagnosed with rheumatic fever.

Rheumatic fever is a systemic, inflammatory disease caused by a delayed response to group-A beta-hemolytic streptococci infection. It usually follows strep throat or scarlet fever that is untreated or undertreated. Symptoms of rheumatic fever usually appear 2-4 weeks initial exposure to the bacteria and affect many systems within the body. Symptoms include fever along with headache, abdominal pain, and nosebleeds. Chest pain or difficulty breathing can indicate cardiac, or heart, involvement. Nervous system changes such as jerky, involuntary movements may be present. Joint redness, swelling, and pain are usually present and can shift, moving from one joint to another. A rash known as erythema marginatum that is transitory (meaning it may change in appearance throughout the illness) typically appears on the torso and inner arms and legs.

Treatment

Appropriately concerned for the seriousness of the diagnosis, Joey's mother wants to know everything she can to treat her son and hopefully prevent complications from rheumatic fever.

Treatment of rheumatic fever occurs in two stages. The first stage includes a short- term course of antibiotics, usually 10 days, aimed at removing all traces of the bacteria from the body. To reduce the inflammation in the body, anti-inflammatory medications may be given. Serious cases with heart damage may require additional treatments and even surgery.

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Scarlet Fever vs. Rheumatic Fever: Identification Exercise

This activity will check your knowledge regarding the differences and similarities between scarlet and rheumatic fever.

Guidelines

Identify whether the description, symptoms, or treatment of the illness are for scarlet fever or rheumatic fever. Write SF for scarlet fever, RF for rheumatic fever, or BOTH if the two share the same symptoms or treatment. With a pencil and an eraser, neatly write your answers in the blank space provided.

_______________ 1. An illness that is a result of exposure to the group-A beta-hemolytic streptococci bacteria.

_______________ 2. Application of anti-itch creams is deemed appropriate.

_______________ 3. May occur together with strep throat as they are caused by the same bacteria.

_______________ 4. It appears 2-4 weeks after initial exposure to group-A strep, of which symptoms were untreated or undertreated.

_______________ 5. Taking antibiotics to kill the group-A strep bacteria present in the body.

_______________ 6. Fever with headache, abdominal pain, nosebleeds, and joint pain are symptoms that occur in this illness.

_______________ 7. A form of rash may appear in the body along with other symptoms.

_______________ 8. Treated with long-term, prophylactic antibiotics that are given for 5 years.

Answer Key

1. BOTH

2. SF

3. SF

4. RF

5. BOTH

6. RF

7. BOTH

8. RF

Medical Disclaimer: The information on this site is for your information only and is not a substitute for professional medical advice.

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