CORRELATION UPPER RESPIRATORY INFECTION TO RHEUMATIC HEART

DISEASE
Written by:
RIFQA WILDAINI
030.0.!"#
Le$t%rer:
Dr. O&t'(i'n%) C* )'+i,. MS
FACULTY OF MEDICINE TRISA-TI UNI.ERSITY
/A-ARTA !0"!
A0STRACT
Rheumatic heart disease is cardiac inflammation and scarring triggered by an
autoimmune reaction to infection with group A streptococci. In the acute stage, this condition
consists of pancarditis, involving inflammation of the myocardium, endocardium, and
epicardium. Chronic disease is manifested by valvular fibrosis, resulting in stenosis and/or
insufficiency.
Rheumatic fever is rare before age 5 years and after age 25 years it is most fre!uently
observed in children and adolescents. "he highest incidence is observed in children aged 5#$5
years and in underdeveloped or developing countries where antibiotics are not routinely
dispensed for pharyngitis and where compliance is low.

Streptococcus pyogenes %group A Streptococcus& is one of the most important pathogens
encountered in clinical practice. An understanding of the diverse nature of infectious disease
complications attributable to this organism is an important cornerstone of pediatric medicine. In
addition to infections of the upper respiratory tract and the s'in, S pyogenes can cause a wide
variety of invasive systemic infections, and infection with this pathogen is also causally lin'ed to
2 potentially serious nonsuppurative complications( acute rheumatic fever and acute
glomerulonephritis. Recently, infection with S pyogenes has reemerged as an important cause of
to)ic shoc' syndrome %"**&, as well as life#threatening s'in and soft tissue infections, especially
necroti+ing fasciitis.
,ey ( rheumatic fever, upper respiratory tract infection, Streptococcus pyogenes
CHAPTER I
INTRODUCTION
-pper respiratory tract infection is most common in the northern regions of the -nited *tates,
especially during winter and early spring. .y contrast, streptococcal s'in infections occur most
fre!uently during the summer %or year#round in warm climates&, when the s'in is e)posed and
abrasions and insect bites are more li'ely to occur. Interestingly, uni!ue strains characteri+ed by
/rdem and colleagues appear to predominant in 0awaii, and novel emm types are associated
with invasive disease and streptococcal#related se!uelae.
1isease in neonates is uncommon, probably in part because of the effect of protective
transplacentally ac!uired antibody. 2revalence of pharyngeal infection is highest in children
older than 3 years. Indeed, group A streptococcal pharyngitis has been described as ha+ard in
school#aged children S pyogenes also has the potential to produce outbrea's of disease in
younger children in daycare.
/vidence suggests that the fre!uency of severe, invasive group A streptococcal infections is
increasing and that strains of streptococci with increased pathogenic potential are appearing. An
increasing number of patients are being identified who have various unusually severe soft tissue
infections associated with mar'ed systemic to)icity, bacteremia, and shoc'. 4actors responsible
for the emergence of these more virulent strains of S pyogenes are not clearly defined, although
many of these outbrea's appear to be clonal in nature.
CHAPTER II
UPPER RESPIRATORY TRACT INFECTION
-pper respiratory tract infection %-RI& represents the most common acute illness evaluated in
the outpatient setting. -RIs range from the common cold##typically a mild, self#limited, catarrhal
syndrome of the nasopharyn)##to life#threatening illnesses such as epiglottitis. 5iruses account
for most -RIs. .acterial primary infection or superinfection may re!uire targeted therapy.
"he upper respiratory tract includes the sinuses, nasal passages, pharyn), and laryn), which
serve as gateways to the trachea, bronchi, and pulmonary alveolar spaces. Rhinitis, pharyngitis,
sinusitis, epiglottitis, laryngitis, and tracheitis are specific manifestations of -RI.
-RIs are the most common infectious illness in the general population. -RIs are the leading
reasons for people missing wor' or school, and they represent the leading acute diagnosis in the
office setting.

N')12*'ryn3iti)
"he incidence of the common cold varies by age. Rates are highest in children younger than 5
years. Children who attend school or daycare are a large reservoir for -RIs, and they transfer
infection to those who care for them. Children have about 3#6 viral respiratory illnesses per year.
Adolescents and adults have appro)imately 2#7 colds a year, and people older than 89 years have
fewer than $ cold per year.
P*'ryn3iti)
Acute pharyngitis accounts for $: of all ambulatory office visits. "he incidence of viral and
bacterial pharyngitis pea's in children aged 7#; years.
R*in1)in%)iti)
*inusitis is common in persons with viral -RIs. "ransient changes in the paranasal sinuses are
noted on C" scans in more than 69: of patients with uncomplicated viral -RIs. 0owever,
bacterial rhinosinusitis occurs as a complication in only about 2: of persons with viral -RIs.
E2i3+1ttiti)
/piglottitis occurs at a rate of 8#$7 cases per $99,999 children, based on estimates from other
countries. "his condition typically occurs in children aged 2#; years and has a pea' incidence in
those aged 3 years. /piglottitis is estimated to occur at annual incidence of <.; cases per million
adults. "he occurrence of epiglottitis has decreased dramatically in the -nited *tates since the
introduction of the Haemophilus influenzae type . %0ib& vaccine.
L'ryn3iti) 'n4 +'ryn31tr'$*eiti)
Croup, or laryngotracheobronchitis, may affect people of any age, but usually occurs in children
aged 8 months to 8 years. "he pea' incidence is in the second year of life. "hereafter, the
enlarging caliber of the airway reduces the severity of the manifestations of subglottic
inflammation. 5accination has dramatically reduced rates of pertussis, including whooping
cough. 0owever, the incidence of whooping cough cases in the -nited *tates has increased in
recent years, reaching 5.3 cases per $99,999 population in 2998. Adolescents and infants younger
than 5 months account for many of these cases. In 2997, adults aged $<#87 years accounted for
;,996 %2;:& of 25,62; reported cases of pertussis in the -nited *tates. Challenges in laboratory
diagnosis and overreliance on polymerase chain reaction %2CR& tests have resulted in reports of
respiratory illness outbrea's mista'enly attributed to pertussis.
-RIs involve direct invasion of the mucosa lining the upper airway. 2erson#to#person
spread of viruses accounts for most -RIs. 2atients with bacterial infections may present in
similar fashion, or they may present with a superinfection of a viral -RI. Inoculation by bacteria
or viruses begins when secretions are transferred by touching a hand e)posed to pathogens to the
nose or mouth or by directly inhaling respiratory droplets from an infected person who is
coughing or snee+ing.
After inoculation, viruses and bacteria encounter several barriers, including physical,
mechanical, humoral, and cellular immune defenses. 0air lining the nose filters and traps some
pathogens. =ucus coats much of the upper respiratory tract, trapping potential invaders. "he
angle resulting from the >unction of the posterior nose to the pharyn) causes large particles to
impinge on the bac' of the throat. Ciliated cells lower in the respiratory tract trap and transport
pathogens up to the pharyn) from there they are swallowed into the stomach.
Adenoids and tonsils contain immune cells that respond to pathogens. 0umoral immunity
%immunoglobulin A& and cellular immunity act to reduce infections throughout the entire
respiratory tract. Resident and recruited macrophages, monocytes, neutrophils, and eosinophils
coordinate to engulf and destroy invaders. A host of inflammatory cyto'ines mediates the
immune response to invading pathogens. ?ormal nasopharyngeal flora, including various
staphylococcal and streptococcal species, help defend against potential pathogens. 2atients with
suboptimal humoral and phagocytic immune function are at increased ris' for contracting a -RI,
and they are at increased ris' for a severe or prolonged course of disease.
5iral agents include a vast number of serotypes, which undergo fre!uent changes in
antigenicity, posing challenges to immune defense. 2athogens resist destruction by a variety of
mechanisms, including the production of to)ins, proteases, and bacterial adherence factors, as
well as the formation of capsules that resist phagocytosis.
Incubation times before the appearance of symptoms vary among pathogens.
Rhinoviruses and group A streptococci may incubate for $#5 days, influen+a and parainfluen+a
may incubate for $#7 days, and respiratory syncytial virus %R*5& may incubate for a wee'.
2ertussis typically incubates for ;#$9 days or even as long as 2$ days before causing symptoms.
1iphtheria incubates for $#$9 days. "he incubation period of /pstein#.arr virus %/.5& is 7#8
wee's.
=ost symptoms of -RIs, including local swelling, erythema, edema, secretions, and
fever, result from the inflammatory response of the immune system to invading pathogens and
from to)ins produced by pathogens. An initial nasopharyngeal infection may spread to ad>acent
structures, resulting in sinusitis, otitis media, epiglottitis, laryngitis, tracheobronchitis, and
pneumonia. Inflammatory narrowing at the level of the epiglottis and laryn) may result in a
dangerous compromise of airflow, especially in children, in whom a small reduction in the
luminal diameter of the subglottic laryn) and trachea may be critical. .eyond childhood,
laryngotracheal inflammation may also pose serious threats to individuals with congenital or
ac!uired subglottic stenosis.
TREATMENT
"he treatment of upper respiratory infections often is directed at symptom control while the body
fights the virus causing the infection. Antibiotics are not effective against viruses and are usually
not prescribed unless the health care practitioner believes that a bacterial infection is present in
addition to the cold.
1rin' plenty of fluids to prevent dehydration, which also moistens the nose and sinus
membranes.
An air humidifier to 'eep the air moist will assist in 'eeping the nose and sinus membranes
moist. 0owever, use caution to avoid scalding burns due to hot water when humidifying air. Cool
mist humidifiers may be a better option. Acetaminophen or ibuprofen may be used to relieve
minor fevers or facial soreness. Aspirin should not be used in children or teenagers because of
the ris' of Reye@s syndrome.
According to the American Academy of 2ediatrics, over#the#counter %A"C& cold medications
should not be used in infants and children because of their lac' of effectiveness in controlling
symptoms and the potential for significant side effects. 4or infants with stuffy noses, saline nose
drops used with a bulb syringe may be helpful in clearing the nasal passages.
Aver#the#counter cold medications should be used with caution is adults as well. "hese
preparations may contain multiple active ingredients that can increase blood pressure, cause
heart palpitations, and promote sleepiness. Alcohol is one of the active ingredients in many A"C
cold medications.
Read the labels before ta'ing any medications and discuss any !uestions or concerns with a
pharmacist or health care practitioner in regard to potential side effects. Alternative treatments
such as vitamin C, echinacea, and +inc have been used by some individuals however, their
benefits have not been scientifically proven.
=edications are usually not prescribed for upper respiratory infections. Antibiotics are not
effective in fighting viral infections. 0owever, antibiotics are appropriate if the health care
practitioner suspects that a bacterial infection e)ists, for e)ample in cases of otitis media %ear
infections&, bacterial sinusitis, and strep throat.
In some cases, where there is significant inflammation of the upper airways, for e)ample croup
in infants and children, corticosteroid medications such as prednisone %=eticorten, *terapred,
*terapred 1*& or de)amethasone %1ecadron, A,#1e), Acu#1e)& may be prescribed to decrease
that inflammation.
CHAPTER III
RHEUMATIC HEART DISEASE
Rheumatic heart disease is cardiac inflammation and scarring triggered by an autoimmune
reaction to infection with group A streptococci. In the acute stage, this condition consists of
pancarditis, involving inflammation of the myocardium, endocardium, and epicardium. Chronic
disease is manifested by valvular fibrosis, resulting in stenosis and/or insufficiency.
Rheumatic fever is rare before age 5 years and after age 25 years it is most fre!uently observed
in children and adolescents. "he highest incidence is observed in children aged 5#$5 years and in
underdeveloped or developing countries where antibiotics are not routinely dispensed for
pharyngitis and where compliance is low.
Acute rheumatic fever is a multisystem disease characteri+ed by involvement of the heart, >oints,
central nervous system %C?*&, subcutaneous tissues, and s'in. /)cept for the heart, most of these
organs are only mildly and transiently affected. "he clinical diagnosis depends on criteria
involving these systems as well as laboratory findings indicative of recent streptococcal
infection, the so#called Bones criteria.
Rheumatic heart disease is the predominant cause of mitral stenosis. A history of rheumatic fever
can be elicited from appro)imately 89: of patients presenting with pure mitral stenosis.

"here is
a 2($ female#to#male incidence. In developed countries, the disease has a latent period of 29#79
years, with another period of almost a decade before symptoms re!uire surgical intervention.
Ance significant limiting symptoms occur, there is a 9#$5: $9#year survival rate without
treatment. *evere pulmonary hypertension is a bad prognostic sign. "he mean age of presentation
in ?orth America is in the Cfth to si)th decade, and more than one third of patients undergoing
valve repair or replacement are older than 85 years.
Appro)imately one fifth of patients with postrheumatic heart disease have pure insufficiency(
78: of patients have stenosis with insufficiency 37:, pure stenosis and 29:, pure
insufficiency. =itral insufficiency is more li'ely caused by floppy mitral valve, with ischemia
and endocarditis other important causes.
Rheumatic heart disease is currently an uncommon cause of aortic stenosis, occurring less
fre!uently in developed countries than senile degenerative calcific aortic valve disease, and
degenerative bicuspid valve disease. =ost patients have concomitant mitral valve disease.
Rheumatic heart disease is also an infre!uent cause of aortic insufficiency in developed
countries, less common than aortic root disease and endocarditis, depending on the patient
population. 2ure aortic stenosis is caused by postinflammatory disease in <: of patients with
surgical treatment, compared with $7: of patients with pure aortic insufficiency and $;: of
mi)ed aortic insufficiency and stenosis. "he clinical features of aortic stenosis and regurgitation
are similar to those of other pathologic causes.
"he following is an image of postinflammatory aortic valve disease.
2ostinflammatory aortic disease, resection. "he stenotic aortic
valve %flow surface& is difficult to repair and is generally replaced. In this e)ample, there is
diffuse thic'ening and scarring of the valve, with focal nodules of calcification. In contrast to
noninflammatory degenerative stenosis, there is significant commissural disease, with thic'ening
of all 3 commissures.
In the acute phase, verrucous endocarditis consists of small, uniformly si+ed thrombotic
vegetations that do not produce valve destruction. "he chronically scarred, inflamed, and
neovasculari+ed valve is most commonly encountered by pathologists. Chronically, rheumatic
fever leads to commissural fusion, valve thic'ening, and calcification. "he appearance of the
mitral valve with shortened, fused chordae and scarred commissures has been li'ened to the
mouth of a catfish %fish#mouth deformity&. "here is also diffuse scarring of the aortic valve, with
commissural fibrosis and thic'ening of the leaflets.
2ostinflammatory or postrheumatic valve disease is generally diagnosed at the time of surgery by
gross inspection of the valve by the surgeon %see the following image&. In the case of mitral
stenosis, there are few conditions in the differential diagnosis. Aortic stenosis is more fre!uently
caused by calcific valve disease, appro)imately half of which occur on congenitally bicuspid
valves. ?odular calcific stenosis is characteri+ed by calcific deposits in the sinuses of 5alsalva,
with relative sparing of the valve@s free edges and commissures.
2ostinflammatory mitral disease, autopsy. "he mitral valve is
seen from the ventricular aspect. "he anterolateral commissure %left& demonstrates scarring, with
thic'ening and focal fusion of the chordae tendineae. In contrast, the chordae of the
posteromedial commissure, toward the right of the figure, are relatively normal.
In contrast, postinflammatory aortic stenosis typically involves the leaflets, free edges, and
commissures, with fibrosis and little calcification %see the image below&. =itral insufficiency
caused by postrheumatic valve disease may be somewhat difficult to distinguish from mitral
valve prolapse, but the presence of chordal fusion, thic'ening, and shortening typically separate
postinflammatory disease from mitral valve prolapse with its thin, elongated cords and
translucent, glistening leaflets.
Acute vegetations of acute rheumatic fever show valve leaflets with surface thrombi, lac' of
underlying valve destruction, and mild edema and chronic inflammation. Chronically, rheumatic
valve disease is characteri+ed by neovasculari+ation, chronic inflammation, and relatively mild
calcification. In contrast to annular calcification, the calcium is in the leaflet itself.
0istologically, neovascularity is common in postrheumatic valve disease, but this is not a feature
of uncomplicated mitral valve prolapse. *ignificant inflammation is uncommon in rheumatic
valve disease in the chronic phase, but there is generally no inflammation in my)omatous valve
disease. In general, the diagnosis is made by the gross appearance of the valve, with clinical
history and ad>uncts in diagnosis.
Aschoff bodies are specific for postrheumatic carditis, whereas Anitsch'ow cells can be seen in a
variety of conditions. In fact, Aschoff nodules are considered pathognomonic for rheumatic heart
disease these are interstitial fibroinflammatory lesions with macrophages and collagen necrosis
%see the first image below&. Anitsch'ow cells, which have unusual wavy nuclear outlines, are
called caterpillar cells and are typically present, but they can also be seen in other conditions not
in association with Aschoff nodules %see the second image below&.
Aschoff nodule. "he acute phase of rheumatic heart disease, or
rheumatic carditis, is characteri+ed by the Aschoff nodule, which is an interstitial aggregate of
macrophages and lymphocytes, with necrotic collagen, in an area of interstitial fibrosis.
Anitsch'ow cell. In the center of Aschoff nodules are Anitsch'ow
or caterpillar cells, characteri+ed by linear condensation of nuclear chromatin with undulations
reminiscent of a caterpillar %arrows&. "hese cells are not specific for rheumatic fever but are seen
in various conditions. In Aschoff nodules, the Anitsch'ow cells are macrophages, although the
same nuclear change can occur in myocytes and other connective tissue cells.
In rheumatic heart disease, C17 and C16 "#cell subsets are present within acute rheumatic fever
valves. =a>or histocompatibility comple) class 2 %=0C#2& antigens are e)pressed on vessel
endothelium and valve fibroblasts
TREATMENT
"reatment of acute rheumatic fever includes antibiotics to treat the strep infection and additional
medications to ease the inflammation of the heart and other symptoms. -sually aspirin is given
in large doses until the >oint inflammation goes away rarely, steroids are needed. Ance the acute
illness has gone away, patients need to ta'e penicillin, or an e!uivalent antibiotic, for many years
to prevent recurrences. "his is a very important treatment because the ris' of heart valve damage
increases if rheumatic fever recurs.
=ost often the valve lea' caused by the disease is mild and does not need treatment. If the lea' is
severe enough to strain and enlarge the heart, surgery may be needed to eliminate the lea'. "his
surgery may involve repair of the damaged valve. *ometimes the valve is too badly damaged to
repair, in which case it must be replaced by an artificial valve.
PRO5NOSIS
Rheumatic mitral valve disease is inconsistently reparable, and the long#term outcomes after
surgical repair are not as good as for valve repair for mitral valve prolapse due to leaDet and
chordal scarring. In addition, leaDet scarring may be progressive after repair. 0owever, rheumatic
mitral valve stenosis that is not associated with severe chordal fusion or shortening or with
calcification may be treated with either percutaneous or open mitral commissurotomy with a
high degree of long#term success.
CHAPTER I.
CORRELATION UPPER RESPIRATORY INFECTION TO RHEUMATIC HEART
DISEASE
=edical history is very important to 'now the course of the disease begins by streptococcal
throat infections, rheumatic fever onset symptoms, whether first time or if an attac' ill again.
.ecause rheumatic fever can affect multiple organs and tissues separately or together, while the
symptoms of each organ / tissue is not typical, then it might not ma'e a diagnosis based on
symptoms alone one. Re!uired some of the symptoms of each organ and the more symptoms that
are more correct diagnosis is made.
.oth the first attac' of rheumatic fever and repeated attac's are always preceded by either a
severe throat infection, moderate, mild or without symptoms. 2eriod of shoots %/ntry of the
bacteria until the onset of first symptoms& 2#7 days, ma)imum of 8 days. In a severe throat
infection which symptoms are headache, fever, vomiting, throat feels hot / pain, abdominal pain,
muscle and >oint pain, red spots on s'in, rapid pulse, sore throat clear that there is a thorough and
in throat e)udate newly arising after the first day.
-p until now still not 'nown with certainty a direct lin' between strep throat with symptoms of
acute rheumatic fever. "here are several hypotheses that may e)plain the occurrence of acute
rheumatic fever attac' are(
Reaction of antibodies that circulate in the blood against streptococcal antigen bound to
body tissues and cause damage to the networ'.
An autoimmune reaction that occurs in the patient@s body.
.eta#hemolytic streptococcus group A produces a variety of e)tracellular to)ins and en+ymes,
each of which can stimulate antibody formation but not all of them lead to immunity. "he most
fre!uently measured and it is very important to determine the presence of streptococcal infection
that precedes rheumatic fever is atibodi against streptolisin A %A*A / Asto&. In immunologic
cross#reaction occurred between the beta#hemolytic streptococcus group A with certain parts of
the heart. "hus, antibodies against streptococcal formed will react well with those parts of the
heart.
*treptococcus is 'nown to produce no less than 29 products are among the most important
e)tracellular streptolisin A, streptolisin *, hyaluronidase, strepto'inase, difosforidin
nu'leotidase, dio'siribonu'lease erytrogenic and streptococcal to)ins. "hese products stimulate
the emergence of antibodies.
In patients who recovered from streptococcal infection, there are appro)imately 29 antigen#
antibody system some of them linger longer than others. Anti#1?A#ase for e)ample can persist
for several months and are useful for studies of patients who showed symptoms of ,orea as the
sole manifestation of rheumatic fever, while the other antibody levels had returned to normal.
Asto %anti#streptolisin A& is an antibody of the best 'nown and most fre!uently used indicator for
the presence of infe'sistreptococcus. Appro)imately 69: of patients with rheumatic fever /
rheumatic heart disease showed an acute rise in titer Asto this( if the e)amination on 3 antibodies
terhadapstreptococcus, then in <5: of cases of rheumatic fever / rheumatic heart disease found
e)altation or more antibodies to the streptococcus.
"here are several possibilities that can lead to rheumatic fever(
$. Eenetic factors. "hese genetic factors have long been embraced by the evidence(
a& In one family there are some people suffer from 1R.
b& Rheumatic fever is more fre!uently attac'ed one egg twins %identical& twins than two
eggs.
2. . Age factor.
a& =ost of the 1R@s first attac' occurred at age 5#$5 years, we can conclude the age
factor is an important factor.
3. socio#economic level.
=ost of the patients came from the class of very low income people with minimal
'nowledge with all its conse!uences.It is evident from studies in 1enmar' where a
decline in rheumatic fever between the years $682#$<82 with increased prosperity.
7. Ather factors such as ethnic group / race, se), nutritional status, geographic situation /
climate is still a contradiction.
An a lighter throat infections ac!uired milder symptoms include fever, mild sore throat,
abdominal pain and mild enlargement of nec' glands, throat a little red and a little on
throat e)udate. "his throat infection usually resolves after 5#; days.
After recovering the patient does not show symptoms for $#3 wee's %latent phase& and
then new symptoms arise acute rheumatic fever.
2revention of rheumatic fever can be addressed in patients with upper respiratory tract infection
by beta hemolytic streptococcus group A in order to prevent the onset of rheumatic fever
%2rimary prevention& or to prevent recurrence in patients who have never suffered from
rheumatic fever %secondary prevention&.
4or the diagnosis of primary prevention need to be enforced by a streptococcal infection of the
respiratory tract. Aften the e)amination can not be distinguished from other causes such as
infection by the virus or diphtheria infection in the throat. =oreover, it turns out that the sore
throat is usually due to infection by viruses and not bacteria. Infection by the virus does not
re!uire antibiotics and usually resolves itself after a few days.
*econdary prevention is aimed toward people who have never suffered from rheumatic fever
with the aim that no recurrence of rheumatic fever. Research shows that people who regularly
receive prevention, rarely had an attac' of rheumatic fever for the second time compared with
patients who did not receive regular preventive. ?ot always easy to provide this secondary
prevention for patients should be regularly 3 wee's or once a month should receive an in>ection
or ta'ing the same medication every day for years. In many patients discontinue their own terms
with the ris' of relapse prevention of rheumatic fever.
Complaints and symptoms vary widely from very mild to very severe with heart failure depends
on the heart are affected and the severity of inflammation of the heart
C*'2ter .
CONCLUSION
=edical history is very important to 'now the course of the disease begins by streptococcal
throat infections, rheumatic fever onset symptoms, whether first time or if an attac' ill again.
.ecause rheumatic fever can affect multiple organs and tissues separately or together, while the
symptoms of each organ / tissue is not typical, then it might not ma'e a diagnosis based on
symptoms alone one. Re!uired some of the symptoms of each organ and the more symptoms that
are more correct diagnosis is made.
.oth the first attac' of rheumatic fever and repeated attac's are always preceded by either a
severe throat infection, moderate, mild or without symptoms.
Complaints and symptoms vary widely from very mild to very severe with heart failure depends
on the heart are affected and the severity of inflammation of the heart
All patients with rheumatic fever should be treated in hospital because it re!uires intensive
treatment and after discharge still re!uire long#term monitoring in order not to relapse again,
especially the heart has not been affected. /very time the recurrence of symptoms will be more
severe than ever.
$. Eoldstein, I, 0alpern, ., and Robert, F. Immunulogi Relationship .etween *treptococcus
A 2olysaccharide Ad the *tructural Elycoproteins Af 0eart valve nature
.