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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 DEFINITION .............................................................
II.III.II CAUSES .............................................................
II.III.III SYMPTOMS .............................................................
II.III ENDOCARDITIS
II.IV.I DEFINITION .............................................................
II.IV.II CAUSES ..........................................................................
II.IV.III SYMPTOMS .........................................................................
CHAPTER III
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III.I CORRELATION BETWEEN RHEUMATIC FEVER AND
ENDOCARDITIS ...............................................
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.
\
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Bacterial structure
Fimbrae: attachment&adherenceM protein: major virulencefactorHyaluronic acid capsule:preventsphagocytosis
Lipotechoic acid:bind epitelcell
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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 inflammatory
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-overviewAccessed on July 8 2011
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Available at : http://eurheartj.oxfordjournals.org/content/14/1/122.shortAccessed on
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3. Rheumatic Heart Disease in developing country. Margaret J.M. February 3 2004.
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