CORRELATION BETWEEN RHEUMATIC FEVER AND ENDOCARDITIS

By : DIAZ RAHMADI 030.08.082

FACULTY OF MEDICINE TRISAKTI UNIVERSITY JAKARTA 7 JULI 2011

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PREFACE

First of all, I would say million thanks to ALLAH SWT who always watches over me in every time I breath. Then, hopefully the peace is always upon Mohammad, the Prophet who leads us to the truth. I also thanks to Dr.dr.Maskito A.Soerjoasmoro,MS, for his time in helping me. With his guidance and assisstance, this paper is the best that it can be. This paper about correlations between rheumatic fever and endocarditis, was prepared to fulfill the assignment in connection with English III, as subject in 6 th semester at the Faculty of Medicine Trisakti University. If there are many mistakes that I had, I really sorry. Nevertheless, I have tried my best to finish this paper and I hope that this paper could be useful for others.

Jakarta, July 8th 2011

Diaz Rahmadi

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CONTENTS PREFACE ................................................................................................. i

ABSTRACT ................................................................................................. ii CONTENTS ................................................................................................. iii CHAPTER I I.I INTRODUCTION ..................................................................................... 1

CHAPTER II II.I STREPTOCOCCUS B HEMOLYTICUS GROUP A II.I.I IDENTIFICATION .........................................................................

II.I.II PATHOGENESYS AND CLINICAL PICTURE................................ II.II RHEUMATIC FEVER II.III.I II.III.II II.III.III II.III DEFINITION CAUSES SYMPTOMS ............................................................. ............................................................. .............................................................

ENDOCARDITIS II.IV.I II.IV.II II.IV.III DEFINITION CAUSES ............................................................. ..........................................................................

SYMPTOMS .........................................................................

CHAPTER III
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III.I

CORRELATION ENDOCARDITIS

BETWEEN

RHEUMATIC

FEVER

AND

...............................................

CHAPTER IV IV.I CONCLUSION ....................................................................................

REFERENCES

.................................................................................................

ABSTRACT

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Rheumatic heart disease is the most serious complication of rheumatic fever. Acute rheumatic fever follows 0.3% of cases of group A beta-hemolytic streptococcal pharyngitis in children. As many as 39% of patients with acute rheumatic fever may develop varying degrees of pancarditis with associated valve insufficiency, heart failure, pericarditis, and even death. With chronic rheumatic heart disease, patients develop valve stenosis with varying degrees of regurgitation, atrial dilation, arrhythmias, and ventricular dysfunction. Chronic rheumatic heart disease remains the leading cause of mitral valve stenosis and valve replacement in adults in the United States. Acute rheumatic fever and rheumatic heart disease are thought to result from an autoimmune response, but the exact pathogenesis remains unclear. Although rheumatic heart disease was the leading cause of death 100 years ago in people aged 5-20 years in the United States, incidence of this disease has decreased in developed countries, and the mortality rate has dropped to just above 0% since the 1960s. Worldwide, rheumatic heart disease remains a major health problem. Chronic rheumatic heart disease is estimated to occur in 5-30 million children and young adults; 90,000 individuals die from this disease each year. The mortality rate from this disease remains 1-10%. A comprehensive resource provided by the World Health Organization (WHO) addresses the diagnosis and treatment Objective: The aim of this paper was to explore the possible correlations rheumatic fever and endocarditis. Methods: Writer searches the references from article and medical journal. Then, writer mades the review from the references. Conclusions: Cardiac involvement in rheumatic fever can be on any network component. the occurrence of endocarditis in patients with rheumatic fever caused by germs sterptococcus beta hemolitycus group that causes strep throat. body reacts to this, by producing antibodies. because the antigens of the bacteria streptococcus beta hemolitycus almost similar to those in the heart. Rather, the endocarditis in rheumatic fever is caused by an autoimmune process that affects many parts of the body in
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addition to the heart, and is triggered by a reaction to the streptococcal bacteria in strep throat. Rheumatic heart disease ends up affecting about half the people who have rheumatic fever with carditis

Keywords : Rheumatic Heart Disease, Rheumatic Fever, group A beta-hemolytic streptococcal, epidemiology

CHAPTER I INTRODUCTION

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I.1

BACKGROUND

Rheumatic fever causes chronic progressive damage to the heart and its valves. Until 1960, it was a leading cause of death in children and a common cause of structural heart disease. The disease has been known for many centuries. Baillou (1538-1616) first distinguished acute arthritis from gout. Sydenham (1624-1668) described chorea but did not associate it with acute rheumatic fever (ARF). In 1812, Charles Wells associated rheumatism with carditis and provided the first description of the subcutaneous nodules. In 1836, Jean-Baptiste Bouillaud and, in 1889, Walter Cheadle published classic works on the subject. The association between sore throat and rheumatic fever was not made until 1880. The connection with scarlet fever was made in the early 1900s. In 1944, the Jones criteria were formulated to assist disease identification. These criteria, with some modification, remain in use today. The introduction of antibiotics in the late 1940s allowed for the development of treatment and preventive strategies. Dramatic declines in the incidence of rheumatic fever are thought to be largely due to antibiotic treatment of streptococcal infection. However, there are pockets where the incidence is significant, especially in tropic areas. However, research into the subtypes of streptococci has made it clear that differences among those types are also responsible for both the decline in overall US incidence and isolated outbreaks. The most recent advance is the recognition that there is genetic predisposition to development of acute rheumatic fever, though the exact reason is still a matter of research.(1) Rheumatic heart disease (RHD) continues to be a common health problem in the developing world, causing morbidity and mortality among both children and adults. Although little longitudinal data are available, evidence suggests that there has been little if any decline in
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the occurrence of RHD over the past few decades. Recent reports from the developing world have documented rheumatic fever (RE) incidence rates as high as 206/100 000 and RHD prevalence rates as high as 18.6/1000. The high frequency of RHD in the developing world necessitates aggressive prevention and control measures.(2) I.2 PROBLEM

Rheumatic heart disease is the most dreaded complication of rheumatic fever. The term "rheumatic heart disease" refers to the chronic heart valve damage that can occur after a person has had an episode of acute rheumatic fever. This valve damage can eventually lead to heart failure. In economically developed countries, rheumatic fever and rheumatic heart disease have become uncommon health problems. In contrast, in Third World areas such as India, the Middle East, sub-Saharan Africa, and Latin America, rheumatic fever remains the leading cause of heart disease in children and young adults. The epidemiology of rheumatic fever and rheumatic heart disease in South Africa is particularly interesting because both of these disparate trends exist simultaneously in the same country. Among the white minority, who have experienced a more privileged socioeconomic and health care status under the apartheid system, rheumatic fever has decreased, as it has in economically developed countries. Among the sociopolitically deprived black majority, the trends are comparable with those of Third World communities. Twenty-one years ago, a screening study for rheumatic heart disease among 12 050 school children in Soweto (the large black ghetto area near Johannesburg) showed the highest reported prevalence of this disease at the time: 6.9 per 1000 children overall, with a maximum of 20 per 1000 among 7th and 8th grade children. The investigators concluded that a comprehensive prevention campaign is urgently needed, directed at both primary and secondary prevention of rheumatic heart disease.(3) I.3 LIMITATION OF PROBLEM
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According the background above, writer can formula the following problems are Rheumatic Fever. How to diagnose the Rheumatic Fever, the complications and treatment also description in this paper. Writer will talk not just about the Rheumatic Fever, but also Endocarditis. I.4 OBJECTIVE This paper will explain Rheumatic Fever. How to diagnose the Rheumatic Fever, the complications and treatment will be also explained in this paper. How Rheumatic Fever can be cause Endocarditis will be explained in this paper too. I.5 METHOD OF WRITING Writer searches the references from article and medical journal, which have any relationship to this topic. Writer tooks the references from Internet. Writer tooks it from some medical website and some science website which have any relation with this topic. Then, writer mades the review from the references. Because of writer mades this paper as a review from the references, it's mean writer tooks the Literature Review as the method of writing for this working paper.

I.6

FRAME OF WRITING This paper contents five chapters. Chapter I is about Introduction. Its include

background, problems, limitation of problems, objectives, methode of writing and frame of writing. In chapter II, writer will talk about Streptococcus B hemolitycus group A, which is include identification the bacteria. Rheumatic feverwhich is include definition, cause, and symptoms. Endocarditisi which is include definition, causes, and symptoms. The correlation

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between rheumatic fever and endocarditis will be explained in chapter III. The conclusion will be discussed in chapter IV.

CHAPTER II II.I. STREPTOCOCCUS B HEMOLYTICUS GROUP A II.I.I IDENTIFICATION Germs are round or oval, sometimes resembling sticks, lined up like a chain composed. Chain length varies and is largely determined olehfaktor environment. Will be longer chains in
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liquid media than in media solid. In the old growth or dead germs gram positive nature will be lost and a gram negative Streptococcal coccus with a diameter of 0.5 to 1 m. In the form of chains typical, slightly elongated coccus chain axis in the direction. Streptococcal pathogens if seed planted in a suitable liquid or solid form long chains often which consists of 8 pieces coccus or more. Streptococci that cause infections in humans are gram positive, but certain varieties are exiled from the feces of human and animal tissues there is a gram negative. In the new seed gram positive bacteria, when the seed has been a few days old can turn into a negative gram. Does not form spores, except for some strains of life saprofitik. Negative motion. Virulent strains create a sheath that contains hyaluronic acid and type specific M protein.

Bacterial structure Fimbrae: attachment &adherence M protein: major virulence factor Hyaluronic acid capsule: prevents phagocytosis Lipotechoic acid:bind epitel cell iii

Source : http://wwwmikrobia.files.wordpress.com/2008/03/streptococcus.pdf

II.I.II PATHOGENESYS AND CLINICAL PICTURE Onset of streptococcal infection can be influenced by various factors, among other biological properties of bacteria, how the host responds, and port d'entre germs.Disease caused by streptococcal bacteria can be divided into several categories, as follows

Source : http://wwwmikrobia.files.wordpress.com/2008/03/streptococcus.pdf A. DISEASES THAT OCCUR DUE TO INFECTION Streptoccocus beta hemolyticus grup A

Port d'entree greatly influence the clinical picture. In each case may occurs rapidly expanding cellulitis which diffuse into the surrounding tissue and ducts lymph nodes, but its localized inflammation itself occurs only lightly. Of lymph tract infection quickly spread into the bloodstream, so that bacteremia occurred.
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Erisipelas If a port d'entree of his skin or mucous membranes may occur erysipelas, a superficial cellulitis lesions with strict limits, endamatous, red bright and very painful. Patients appear severely ill with high fever. On examination found lekositosis, more than 15,000 leucocytes. ASO titers rise after 7-10 days. Germs are not found in blood vessels, but in lymph fluid from the edge of the lesions were widespread, especially in the network subcutaneous. In this disease can occur causing bacteremia yamg metastatic infection in other organs. Mortality with the use of antibiotics can be suppressed, but the infants, the elderly who debil and in patients who received treatment with corticosteroids, the disease can develop so quickly that the resulting fatal. This disease tends to recur in the same place, resulting in blockage of the lymph channels which are chronic. Local skin grows irregularly, causing elephantiasis verrucosa nostras. If localization in the mouth can occur macrocheilia, a swelling of the lips persiten nature.

Source ; http://wwwmikrobia.files.wordpress.com/2008/03/streptococcus.pdf

SEPSIS PUERPURALIS

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Streptococcus germs into the uterus after childbirth. Septikimia occur because the wound is infected, namely in the form of endometritis. SEPSIS Sepsis occurs because the incision or due to trauma, infection with streptococcus germs. Some call this disease as a surgical scarlet fever.

B. DISEASES THAT OCCUR DUE TO LOCAL INFECTION Beta hemolytic streptococcus group A Sore throat A disease that almost everyone has felt it. Due to Streptococcal beta hemolyticus.pada infants and small children arise as nasofaringitis subacute with serous secretions and a slight fever, and the infection tends to expand into the middle ear, mastoid process and the lining of the brain. Lymph nodes cervical usually enlarged. The disease can last for weeks.

In children more than adults, the illness lasts nasofaringitis and more acute with severe tonsillitis, the mucous membranes hiperemis and swollen with a purulent exudate. Cervical lymph nodes enlarged and painful, usually accompanied by high fever. Twenty percent of these infections causes no symptoms (asymptomatic). If germs can make can make erythrogenic toxin, may arise scarlet fever rash. In the rash of scarlet fever germs present in the pharynx, but the toxin erythrogenic it generates causes the reddish diffuse. Erythema began to arise in the neck, extends to the body, then spread to extremities. In histopatologik visible presence of leukocyte extravasation polymorphonuclear cells and red blood cells of small blood vessels into the skin.
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Anti erythrogenic can prevent rash, but no effect on infection streptococcus germs. If severe inflammation, abscess can arise peritonsiler or Ludwig's angina, with massive swelling in the floor of the mouth can clog breathing. With Schult-Charlton reaction could be demonstrated if a rash occurs due to erythrogenic toxin or not. Streptococcal bacterial infection in the upper respiratory tract is usually not of the lungs. Pneumonia due to Streptococcus beta hemolyticus usually occurs after a viral infection such as influenza or morbili.

Sand paper like in scarlet fever

Strawberry tongue in scarlet fever Source : http://wwwmikrobia.files.wordpress.com/2008/03/streptococcus.pdf C. BACTERIAL ENDOCARDITIS Bacterial endocarditis akuta This disease occurs in bacteremia by Streptococcus beta hemolyticus, pneumococcus, stefilokokus, or coliform gram negative organisms. on addict narcotics, staphylococci and candida is a major cause endocarditis. This disease can affect the heart valves are normal and has been deformed, and cause bacterial endocarditis Acute ulcerative.

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Heart valve destruction that occurs rapidly and rupture chordae tendinae, seringksli cause death within several days or several weeks.

Source : http://wwwmikrobia.files.wordpress.com/2008/03/streptococcus.pdf

Bacterial endocarditis subakuta The disease is primarily about an abnormal heart valve, rheumatic lesion, calcification of heart disease or continental. The cause is primarily Streptococcus viridans and Streptococcus faecalis; Staphylococcal can sometimes be be the cause, but denying any microorganisms, including fungi can be the cause.

D. POST-INFECTIOUS DISEASES HEMOLITYC GROUP A BETA STREPTOCOCCUS after a group A streptococcal infection, particularly strep throat, can followed by a latent period for 2-3 weeks, after which may arise nephritis or rheuma fever fever. The existence of this latent period suggests that the disease occur after streptococcal

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infection is not a direct result of spread of bacteria, but is a hypersensitivity reaction rather than the organ exposed to an anti-streptococcal RHEUMATIC HEART DISEASE Rheuma fever or rheumatic fever is a streptococcal infection sequelae hemolyticus the most serious, because it can cause damage to the muscle and heart valves. Pathogenesis of rheuma unclear but some have claimed that streptococcus group A has a structure similar to the muscle glycoprotein and human heart valves. Rheuma fever is usually preceded by infection streptococcus group A 2-3 weeks before. Perhaps only a mild infection without give symptoms. Streptococcal infections that do not get treatment, in 0.3 - 3% of patients can cause fever, rheuma. Criteria for rheuma cardiac diagnosis from Jones which has been modified are: A. Major criteria:1. Carditis 2. Khorea Sydenham 3. Subcutaneous nodules 4. Erythema marginatum 5. Polyarthritis migrans. B. Minor criteria: 1. Fever 2. Poliartralgia 3. Extension of P-R interval on ECG 4. Increasing erythrocyte sedimentation rate and C-protein reaktive 5. Evidence of streptococcal infection hemolyticus previous beta. 6. A history of rheuma fever or rheumatic valve lesions Rheuma cardiac diagnosis is almost certain if found two major criteria or more. In this disease there is thickening and deformity of the heart valves, and the formation of Aschoff bodies in the myocardium, in the form of granuloma perivaskuler tiny hereinafter replaced by scar tissue. Rheuma heart has a tendency to be active again in the presence of streptococcal infection, whereas the nephritis there is no properties like this. On The first attack of rheuma heart arises only little damage to the heart, but the damage continues to increase in subsequent attacks. So important is to prevent the occurrence of beta streptococcal infections in patients with group A hemolyticus concerned, namely by providing a dose of

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penicillin in eradication. If no penicillin-resistant patients can be given eritromosin. Prophylactic treatment be continued until age 25 or even a lifetime.(4)

II RHEUMATIC FEVER II.II.I DEFINITION Rheumatic fever is a multisystem collagen vascular disease occurring after group A streptococcal infection in individuals who have predisposing factors. This disease is still the most important cause of acquired heart disease (acquired heart disease) in children and young adults in many countries, especially developing countries. Involvement of the cardiovascular disease is characterized by inflammation of endocardium and myocardium via an autoimmune process that causes tissue damage

II.II.II CAUSE Rheumatic fever, as with other diseases are caused by the interaction of individuals, the cause of disease and environmental factors. Streptococcus infection in group A beta hemolyticus throat always precede the occurrence of rheumatic fever, both in the first attack and repetition attack. To cause an attack of rheumatic fever, streptococcus group A should lead to infection in the pharynx, not just the superficial colonization. Unlike the glumeronefritis associated with Streptococcus infection in the skin and in the respiratory tract, rheumatic fever does not seem related to Streptococcus infection in skin.(5) II.II.III SYMPTOMS Symptoms vary, depending on the inflamed body part.
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Symptoms usually occur a few weeks after a sore throat caused by streptococcus disappeared. The main symptoms are Joint pain (arthritis), Chest pain or palpitations (heart pounding) because carditis, Shock / twitch out of consciousness (Corea Sydenham), Skin rash (erythema marginatum), Small lumps under the skin (nodules). Initial symptoms are most often found are joint pain and fever. One or several joints suddenly become sore and painful when touched. Joints may also appear red, felt warm and swollen and may contain fluid.The most commonly affected are the ankle joint, knee, elbow and wrist; sometimes also attack the shoulder joint arthritis, hip and small joints in the hands and feet. If the pain in the joints disappeared, then there will be pain in other joints, especially in children who did not undergo rest breaks and not getting anti-inflammatory drugs. Sometimes joint pain is very mild in nature. Fever arise suddenly and simultaneously with the onset of joint pain; fever is going up and down. Joint pain and fever usually lasts for 2 weeks and rarely lasted more than a month. Inflammation of the heart often occur along with joint pain and fever. Initially, cardiac inflammation does not cause symptoms. Inflammation of the sac causing cardiac chest pain. Heart failure can occur, with symptoms like Shortness of breath, Nausea, Vomiting, Stomach pain, Dry cough. Inflammation of the heart causing the child susceptible to fatigue.
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Carditis beratahap disappear, usually within 5 months. But the possible permanent damage to the heart valves leading to rheumatic heart disease. The most commonly affected is the valve between the atrium and left ventricle (mitral valve). Leakage could occur at Katu (mitral valve regurgitation) or narrowing (stenosis mitral valve) or both. Sydenham Korea develop gradually, usually within 1 month korea heavier. Child shows rapid movement and is not intended, which disappeared during sleep. The movement involves every muscle except the eye muscles. His face often grinned. In mild cases the child looks a bit stiff and have difficulty in dressing and eating. In severe cases, children often do things to hurt himself (flailing arms or legs alone). Koreans usually disappear gradually after 4 months, but sometimes lasts for 6-8 months. At the other symptoms disappear, a rash of flat with wavy edges and are not accompanied by pain. The rash lasts shorter, sometimes less than 24 hours. In children suffering from heart inflammation is usually found a small lump under the skin. These nodules are usually painless and will disappear by itself.(6)

ENDOCARDITIS II.III.I DEFINITION Endocarditis is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves (native or prosthetic valves). Other structures that may be involved include the interventricular septum, the chordae tendineae, the mural endocardium, or even
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on intracardiac devices. Endocarditis is characterized by a prototypic lesion, the vegetation, which is a mass of platelets, fibrin, microcolonies of microorganisms, and scant inammatory cells. In the subacute form of infective endocarditis, the vegetation may also include a center of granulomatous tissue, which may fibrose or calcify Endocarditis is an infection of the inner lining of your heart (endocardium). Endocarditis typically occurs when bacteria or other germs from another part of your body, such as your mouth, spread through your bloodstream and attach to damaged areas in your heart. Left untreated, endocarditis can damage or destroy your heart valves and can lead to life-threatening complications. Treatments for endocarditis include antibiotics and, in severe cases, surgery. Endocarditis is uncommon in people with healthy hearts. People at greatest risk of endocarditis have a damaged heart valve, an artificial heart valve or other heart defects.(7) II.III.II CAUSES Endocarditis caused by bacterial growth in one of the heart valves, leading to an infected mass called "vegetation". Infection may be introduced during the brief periods of having the bacteria in the bloodstream, such as after dental work, colonoscopy, and other similar procedures. Endocarditis can involve the heart muscle, heart valves, or lining of the heart. Most people who develop endocarditis have have some abnormality of a heart valve. Risk factors for developing endocarditis include Injection drug use, Permanent central venous access line, Prior valve surgery, Recent dental surgery, Weakened valves

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Bacterial infection is the most common source of endocarditis. However, it can also be caused by fungi. In some cases, no cause can be identified. In infective endocarditis, the bacteria cluster on and around the heart valves; this may impair their ability to function properly. Although bacterial endocarditis may occur in anyone at any time, it is unusual in persons who do not have valvular heart disease. Valves deformed by a previous attack of rheumatic fever were once a major predisposing factor, but this is less so today since rheumatic fever has become much less common Other predisposing factors include artificial heart valves, some congenital heart disorders, hypertrophic cardiomyopathy, and mitral valve prolapse with regurgitation. People with such risk factors are more likely to develop endocarditis when exposed to an infection from any source. Dental surgery, urologic or gynecologic surgery, colonoscopy, and skin infections increase the risk of endocarditis, even if there is no pre-existing anatomic valve deformity. Intravenous drug users are also at significant risk.(8)

II.II.III SYMPTOMS The presentation of infective endocarditis often includes extracardiac manifestations or findings that are associated with intracardiac extension of infection. Fever is the most common symptom and sign; however it may be absent or minimal in patients with congestive heart failure, severe debility chronic renal or liver failure, previous use of antimicrobial drugs or infective endocarditis caused by less virulent organisms. Other common symptoms of acute infective endocarditis include anorexia, weight loss, malaise and night sweats. Most
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patients with infective endocarditis have a heart murmur ( most commonly preexisting), and patients may have petechiae on the skin , conjunctinae, or oral mucosal mucosa ,as well as splenomegaly and other peripheral manifestations. Prosthetic- valve endocarditis may be manifested as an indolent illness with low grade fever, or it can be an acute febrile, toxic illness. The high frequency of invasive infection in prosthetic-valve endocarditis results in higher rates of new or changing murmurs and of congestive heart failure. Unexplained fever in patient with the prosthetic valve should prompt careful evaluation for prosthetic-valve endocarditis. Isolated right sided infective endocarditis is not associated with peripheral emboli and other peripheral vascular phenomena: instead, pulmonary findings may predominate. The onset of nosocomial infective endocarditis is usually acute, and signs of endocarditis are infrequent.The diagnosis of infective endocarditis is suggested by bacteremia persisting for days before treatment or for 72 hours or more after the removal of an infected catheter and the initiation of treatment, especially in patient with an abnormal or prosthetic valve.Among patients with the prosthetic valves or candidemia from sources other than valves carries risks of subsequent prosthetic-valve endocarditis of approximately 16% and and 11%, respectively. Acute (recent onset) IE often feels like the flu, with fever, shaking chills, sweats, aching muscles, and weakness. Chronic IE is a more subtle form of the illness, and often manifests with chronic, non-specific symptoms - such as vague aches and pains, chills, weight loss, joint pain or swelling, and weakness. People with chronic IE can also have some less common but more specific signs of the condition. These include linear red streaks under the nails (splinter hemorrhages), red spots on the palms and soles (Janeway lesions) and, painful red bumps on the pads of the fingers and toes (Osler's nodes). If the IE progresses enough to produce significant heart damage,
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patients may experience shortness of breath, swelling of the ankles, and other symptoms of heart failure.(9)

CHAPTER III III.I. CORRELATION BETWEEN RHEUMATIC FEVER AND ENDOCARDITIS In 0.3-3% of cases, infection leads to rheumatic fever several weeks after the sore throat has resolved. Only infections of the pharynx initiate or reactivate rheumatic fever. The organism spreads by direct contact with oral or respiratory secretions, and spread is enhanced by crowded living conditions. Patients remain infected for weeks after symptomatic resolution of pharyngitis and may serve as a reservoir for infecting others. Penicillin treatment shortens the clinical course of streptococcal pharyngitis and, more importantly, is effective in decreasing the incidence of major sequelae.(10)

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Research shows that the other components of streptococcal has reactivity with other tissues. These include immunologic cross-reaction between streptococcal carbohydrates and glycoproteins valve, between streptococcal protoplasmic membranes and nerve tissue subtalamus and caudate nuclei and between the hyaluronic capsule and articular cartilage. Multiple immunologic cross-reactivity may explain the multiple organ involvement in rheumatic fever Cardiac involvement in rheumatic fever can be on any network component. The process of inflammation during acute carditis most often limited to the endocardium and myocardium, but in patients with severe myocarditis, the pericardium may also be involved. Some with the other collagen diseases such as systemic lupus erythematosus or juvenile rheumatoid artristis (in both diseases serositas usually indicated by pericarditis), rarely found in rheumatic fever without endocarditis or myocarditis pericaditis. Pericaditis in rheumatic patients usually express a pankarditis or expansion process. Histological discovery in acute rheumatic carditis is not always specific. The level of histologic changes are not correlated with the degree of clinical need. In the early stages, when there is dilatation of the heart, histologic changes can be minimal, although impaired heart function may mencolok. With continued inflammation, exudative and proliferative changes became more apparent. This stage is characterized by changes in the network edematosa, accompanied by cellular infiltration consisting of lymphocytes and plasma cells with few granulocytes. Fibrinoid, granular material eusinofil found scattered across a basic network. This material includes collagen fibers plus granular material derived from collagen which is degenerate in a mixture of fibrin, globulin, and other materials. Other tissues affected by disease processes,

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such as joint tissue, may show fibrinoid; this can also occur in the healed tissue in patients with other collagen diseases Inflammatory reaction is also about the cause endocarditis endocardium layer. The process of tissue valve endocarditis and wall endocardium. Inflammation of the valve tissue causing similar clinical manifestations of rheumatic carditis. The most frequently involved are the mitral valve, aortic valve followed. Tricuspid valve is rarely involved, and the pulmonary valve is rarely involved. Overview of the etiology of valve disease by Roberts suggests that the etiology of rheumatic 70% of the cases can be derived from pure mitral valve disease (isolated) and only 13% of cases stemming from pure aortic valve disease. In the second patient valve (mitral and aortic) are involved, the possibility of rheumatic etiology is 97%1. Early inflammation in endocarditis can cause valve insufficiency. The discovery in endocarditis consists of histological edema and cellular linfiltrasi valve tissue and chordae tendine. Lesions that are typical of rheumatic endocarditis 'patches (patch) MacCallum', thickened area of tissue found in the left atrium, namely on the basis of the posterior mitral valve leaflets. Hyaline degeneration in the affected valves will cause the formation of verruca on the edge, which would hinder the approach leaves the valve completely and prevent the closure of ostium valve. With persistent inflammation, fibrosis occurs and the classification of the valve. Microscopic classification can occur in young patients with rheumatic valve disease. If there is no reversal process and healing, this process will eventually lead to stenosis and calcification changes in the rough, which occurred several years after attack.(5)

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CHAPTER IV CONCLUSION In conclucion, Cardiac involvement in rheumatic fever can be on any network component. the occurrence of endocarditis in patients with rheumatic fever caused by germs sterptococcus beta hemolitycus group that causes strep throat. body reacts to this, by producing antibodies. because the antigens of the bacteria streptococcus beta hemolitycus almost similar to those in the heart. Rather, the endocarditis in rheumatic fever is caused by an autoimmune process that affects many parts of the body in addition to the heart, and is triggered by a reaction to the streptococcal bacteria in strep throat. Rheumatic heart disease ends up affecting about half the people who have rheumatic fever with carditis. Most of the
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time, rheumatic heart disease is diagnosed 10 to 20 years after being "triggered" by acute rheumatic fever

REFFERENCES
1. Rheumatic fever in emergency medicine. Bryant P.A. March 25 2011. Available at :

http://emedicine.medscape.com/article/808945-overview Accessed on July 8 2011 2. Rheumatic Heart Disease in the developing world. Mark J. Eisenberg. July 10 2003. Available at : http://eurheartj.oxfordjournals.org/content/14/1/122.short Accessed on July 10 2011 3. Rheumatic Heart Disease in developing country. Margaret J.M. February 3 2004. Availabel at : http://www.annals.org/content/120/3/243.full . Accessed on July 8 2011

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4. Streptococcus Beta Hemolitycus Group A . Mukti A.A. May 17 2008. Available at :

http://wwwmikrobia.files.wordpress.com/2008/03/streptococcus.pdf . Accessed on July 8 2011 5. Acute Rheumatic Fever. October 4 2008. Pahlevi R. Available at : http://usebrains.wordpress.com/2008/10/04/demam-rematik-akut/ . Accessed on July 8 2011 6. Rheumatic Fever. April 27 2008. Mumpuni S.S. Available at : http://medicastore.com/penyakit/961/Demam_Rematik.html . Accessed on July 8 2011 7. Endocarditis. August 13 2008. Sexton D.J. Available at : http://www.mayoclinic.com/health/endocarditis/DS00409 . Accessed on July 8 2011 8. Causes and risk factors of Endocarditis.July 28 2001. Available at : http://www.healthscout.com/ency/68/72/main.html#CausesandRiskFactorsofEndocar ditis . Accessed on July 8 2011 9. Infectious endocarditis . Richard N. Fogoros, M.D. January 21 2010. Available at : http://heartdisease.about.com/od/heartvalvedisease/a/Infectious_endocarditis.htm . Accessed on July 8 2011 10. Rheumatic Heart Disease. Guilherme L. August 4 2010. Available at : http://emedicine.medscape.com/article/891897-overview#a0104 . Accessed on July 8 2011

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