Elevated antistreptolysin-O Titer Research Articles

Evaluation of the Effect of Tonsillectomy on Antistreptolysin O (ASO) Titer

Background: Acute recurrent tonsillitis is a common problem worldwide and tonsillectomy is the preferable treatment for patients not responding to medical treatment. Many patients with acute recurrent tonsillitis and increased antistreptolysin O (ASO) titers are caused by group A beta hemolytic streptococcal (GABHS) tonsillitis, which can lead to serious side effects such rheumatic fever and glomerulonephritis. ‎
 Aim: To assess the consequence of tonsillectomy on ASO titer.
 Patients and Method: This prospective study was conducted to analyze the consequence of tonsillectomy on 43 patients with raised antistreptolysin O (ASO) titer out of 220 patients with acute recurrent tonsillitis, for the period from October 2015 to October 2016 at Otolaryngology department, Tertiary referring hospital at Erbil, Kurdistan/Iraq. Their Demographic characteristics, medical, drug and family history and disease extent were analyzed. Postoperative follow up were processed.
 Results: The study included 43 patients between 3 to 16 years suffering from acute recurrent tonsillitis, elevated ASO titer (≥200 IU/ml) and positive throat swab for GABHS were included in the study. Six months postoperatively had been shown that there is a significant reduction in ASO titer in comparison to preoperative measures (p < 0.001) and this is also applicable to the number of sore throat episodes.
 Conclusion: The main conclusion from this study is significant effect of tonsillectomy on decreasing ASO titer which reveals the reduction in postoperative GABHS throat infection, this supported by reduction of postoperative sore throat episodes.

Effect of Tonsillectomy on Antistreptolysin O (ASO) Titer

Abstract 
 Recurrent attacks of tonsillitis are a common worldwide problem and the best treatment of choice after failure of medical therapy is a tonsillectomy. The large numbers of patients that presented with recurrent attacks of tonsillitis and associated with high antistreptolysin O (ASO) titer level due to group A beta hemolytic streptococcal (GABHS) tonsillitis will have serious complications as glomerulonephritis and rheumatic fever. The aim of study: to evaluate the effect of tonsillectomy on elevated ASO titer.
 Patients and methods: Prospective non-randomized clinical study was performed at Al-Jumhory teaching hospital, Mosul, Iraq; for the period from January 2021 to January 2022. that included seventy patients for whom tonsillectomy was indicated. There were 45 females and 25 males, the age range from 3 to15 years old and the mean age was7.63year. Positive throat swab for group A beta hemolytic streptococcal (GABHS) and elevated ASO titer level (≥200 IU/ml). Postoperative follow up of the patients were processed for six months.
 Results: seventy patients included in the study, presented with recurrent attacks of tonsillitis, with positive throat swab for GABHS and elevated ASO titer level (≥200 IU/ml), age between 3 to 15 years old .Follow up of the patients for six months after tonsillectomy had been shown that there is a significant decrease in ASO titer level in comparison to preoperative level measures (p <0.001 )
 Conclusion: The most important conclusion from the result of our study that tonsillectomy lead to significant reduction in ASO titer level.

Elevated antistreptolysin O titer is closely related to cardiac mitral insufficiency in untreated patients with Takayasu arteritis

BackgroundThe etiology of Takayasu arteritis (TA) is unknown; however, a possible relationship between streptococcal infection and TA has been proposed. This study aimed to identify the clinical features and cardiac valvular involvement in untreated TA patients with an elevated antistreptolysin O (ASO) titer.MethodsIn this retrospective study, the clinical characteristics and features of valvular involvement were compared in TA patients with or without an elevated ASO titer.ResultsOf the 74 untreated TA patients, 13 patients were found have elevated ASO titers (17.6%). Mitral insufficiency was the most common in patients with elevated ASO (69.2%, 9/13), followed by aortic valve insufficiency (46.2%, 5/13) and tricuspid insufficiency (46.2%, 5/13), which were no significantly different than that in normal ASO group. The proportions of moderate to severe mitral (30.8% vs 1.6%, p = 0.000) and tricuspid valve (15.4% vs 1.64%, p = 0.023) insufficiency in the ASO positive group were significantly higher than those in the ASO negative group. The odds of mitral regurgitation in patients with elevated ASO titers were 3.9 times higher than those in the group with normal ASO titers (p = 0.053, OR = 3.929, 95% confidence interval [CI]: 0.983–15.694). Furthermore, the risk of moderate to severe mitral insufficiency in patients with elevated ASO titers was 41.6 times higher than that in patients with normal ASO titers (p = 0.002, OR = 41.600, 95% CI: 3.867–447.559).ConclusionsAn increase in ASO titer is related to valvular involvement in TA and is closely linked to mitral insufficiency.

High antistreptolysin O titer is associated with coronary artery lesions in patients with Kawasaki disease.

Purpose In Kawasaki disease (KD) patients, coronary artery complications, incomplete and refractory types occur more frequently in patients with streptococcal or other bacterial/viral infections. Recently, we observed a higher incidence of coronary lesions in KD patients with high anti-streptolysin O (ASO) titer. Therefore, we hypothesized that KD patients diagnosed with concurrent streptococcal infection have poor prognoses, with respect to treatment response and development of coronary artery lesions.Methods A retrospective review was performed in 723 patients with KD who were admitted to 2 major hospitals between June 2010 and September 2017.Results Among 723 patients with KD, 11 initially showed an elevated ASO titer (>320 IU/mL) or elevated follow-up ASO titer after treatment. Of these patients, 5 showed no response to the first intravenous immunoglobulin treatment, 3 had abnormalities of the coronary arteries. This is a significantly higher proportion of patients with a high ASO titer (n=3, 27.3%) than those with a normal ASO titer (n=53 [7.4%], P=0.047). A severe clinical course was seen in 81.8% of patients in the high ASO group versus 14.5% of patients in the normal ASO group.Conclusion It is not certain whether acute streptococcal infection may cause KD, but this study revealed that KD with high ASO titers showed higher rates of severe clinical course. It may be helpful to analyze concurrent streptococcal infection in patients with a severe clinical course.

Cardiac Myosin Epitopes Recognized by Autoantibody in Acute and Convalescent Rheumatic Fever.

Acute rheumatic fever (ARF) is an autoimmune disorder associated with Streptococcus pyogenes infection. A prevailing hypothesis to account for this disease is that epitopes of self-antigens, such as cardiac myosin react to antibodies against S. pyogenes. The goal of our study was to confirm disease epitopes of cardiac myosin, identify immunodominant epitopes and to monitor the epitope response pattern in acute and convalescent rheumatic fever. Enzyme-linked immunosorbant assays were used to determine epitopes immunodominant in acute disease and to track the immune response longitudinally to document any changes in the epitope pattern in convalescent sera. Multiplex fluorescence immunoassay was used to correlate anti-streptolysin O (ASO) and anti-human cardiac myosin antibodies. Disease-specific epitopes in rheumatic fever were identified as S2-1, 4 and 8. Epitopes S2-1, 4, 8 and 9 were found to be immunodominant in acute sera and S2-1, 8, 9, 29 and 30 in the convalescent sera. Frequency analysis showed that 50% of the ARF subjects responded to S2-8. S2-8 responders tended to maintain their epitope pattern throughout the convalescent period, whereas the S2-8 nonresponders tended to spread their responses to other epitopes later in the immune response. There was a significant correlation between anti-cardiac myosin and ASO titers. In addition, S2-8 responders showed elevated ASO titers compared with S2-8 non responders. Our studies confirm the existence of S2-1, 4 and 8 as disease-specific epitopes. We provide evidence that cardiac myosin S2-8 responders remain epitope stable in convalescence, whereas S2-8 nonresponders shift to neoepitopes. Multiplex data indicated a correlation between elevated ASO and anti-human cardiac myosin antibody titers. Mapping of cardiac myosin epitopes recognized in rheumatic fever sera may identify immunophenotypes of rheumatic fever.

Prevalence of rheumatic heart disease in patients with recurrent tonsillitis and elevated anti-streptolysin O titers

IntroductionPatients with elevated anti-streptolysin O (ASO) titers (ASOT) and recurrent tonsillitis episodes are known to be at higher risk for rheumatic heart disease (RHD). However, there is no data regarding prevalence of RHD in this high risk population. In this study, we aimed to screen ambulatory patients with elevated ASOT and recurrent tonsillitis episodes using echocardiography for identification of RHD. We hypothesized that prevalence of RHD is higher in this patient group compared to general population. Methods102 patients (10.33 ± 4.01 years, 50.98% female) who were diagnosed with recurrent tonsillitis and had elevated ASOT were included this study. Echocardiographic evaluation was performed by an experienced cardiologist. ResultsEchocardiographic examination revealed definite RHD in 2/102 (1.96%) patients and borderline RHD in 3/102 (2.94%) patients. ConclusionOur study demonstrates a high prevalence of RHD in patients with recurrent tonsillitis episodes and high ASOT. Screening with echocardiography is beneficial to improve the detection rates of subclinical RHD in such high-risk populations.

Anterior and Intermediate Uveitis with Retinal Vasculitis: An Unusual Manifestation of Post-Streptococcal Uveitis Syndrome

ABSTRACTPurpose: To report a case of bilateral panuveitis with vasculitis, an unusual manifestation of post-streptococcal uveitis syndrome (PSU).Methods: An 8-year-old patient consulted for bilateral red eye following acute tonsillitis. Exploration revealed bilateral anterior uveitis, vitritis, macular edema, and Frosted Branch Angiitis. Given a clinical suspicion of PSU, blood and serology tests were performed to rule out other causes of vasculitis and retinitis.Results: Serologies came back negative except for highly elevated antistreptolysin-O titers. Topical and oral corticosteroids normalized the patient’s visual acuity and clinical findings within a few weeks. A subsequent anterior-only recurrence was successfully resolved with topical treatment.Conclusions: Although PSU most commonly manifests as anterior uveitis, it may present with involvement of the posterior pole. To achieve a correct diagnosis, clinical suspicion and assessment of antistreptolysin-O titers as well as ruling out other conditions with similar clinical features are the mainstay approaches to diagnosis. Prognosis is generally good.

Acute Poststreptococcal Glomerulonephritis: The Most Common Acute Glomerulonephritis

Acute Poststreptococcal Glomerulonephritis: The Most Common Acute Glomerulonephritis

Uvéites post-streptococciques

The role of streptococcal infections in the development of uveitis remains uncertain. Here we describe a series of patients with suspected poststreptococcal uveitis. Four retrospective cases were collected (two males and two females). All patients had a sore throat or an episode of pyrexia 2 to 10 weeks before the onset of uveitis and elevated antistreptolysin-O titer (ASOT); no other cause of uveitis was found. Uveitis was bilateral in all the cases and recurrent in only one. In two patients, inflammation was limited to the anterior segment. One patient had intermediate uveitis. One patient had posterior uveitis with multiple white-dot lesions as well as macular and optic disc swelling. The two cases with anterior uveitis were treated only topically and the two others received a short course of systemic steroids. No systemic antibiotics were given. These cases suggest that uveitis could be a manifestation of poststreptococcal syndrome and have a good prognosis.

Clinical course of guttate psoriasis: Long‐term follow‐up study

Guttate psoriasis, known to have a better prognosis than other types of psoriasis, shows rapid involution and longer remission, but its clinical course has barely been studied. The aim of this study was to determine the clinical course and to compare the clinical and laboratory features of guttate psoriasis. This is a retrospective study of 26 patients with guttate psoriasis. The patients were divided into two groups; the good one with complete remission and long remission for at least 1 year (group A) and the poor one with incomplete remission and progression into chronic plaque psoriasis (group B). Among 36 patients, 22 patients (61.1%) were group A and 14 patients (38.9%) were group B. In group A, most of the skin lesions disappeared within 8 months. In group B, two patients without proper treatment progressed to plaque psoriasis. The onset age was younger and more frequent upper respiratory infection and high anti-streptolysin O (ASO) titer were found in group A, but family history of psoriasis was more common in group B. Patients had two distingushable clinical courses: rapid involuting course with long-term remission and chronic course without remission. There was a tendency toward younger age of onset with elevated ASO titer in patients with rapid involuting course.

A case of dense deposit disease associated with a group A streptococcal infection without the involvement of C3NeF or complement factor H deficiency

A 14-year-old girl presented with acute glomerulonephritis. Tests revealed hypocomplementemia and elevated Antistreptolysin-O titers, and renal biopsy revealed endocapillary and mesangial proliferative glomerulonephritis with double contours of the glomerular basement membrane (GBM). Despite methylprednisolone pulse therapy and the administration of oral prednisolone, overt proteinuria and hypocomplementemia persisted. A second renal biopsy 6 months later confirmed the initial diagnosis of dense deposit disease (DDD) based on electron-dense deposits in the GBM. C3 nephritic factor (C3NeF) and a deficiency of complement factor H (CFH) were not evident. A nephritis-associated plasmin receptor (NAPlr), nephritogenic group A streptococcal antigen, and the plasmin activity by in situ zymography were been in both the first and second biopsy specimens. The patient received combined immunomodulatory therapy with prednisolone and mizoribine, and the urinary protein decreased to a mild level at 27 months after disease onset. These findings suggest that persistent glomerular NAPlr deposition may be associated with the pathogenesis of DDD in some patients without the involvement of C3NeF or CFH mutation and that DDD patients of this type may respond to immunomodulatory treatment.

Familial cases of Henoch‐Schönlein purpura in eight families

Familial cases of Henoch-Schönlein purpura (HSP) have rarely been reported. Familial cases of HSP were reviewed by medical records of 418 children with HSP. Two members developed HSP in eight families. HSP occurred in a mother and her daughter in one family and in siblings, including one pair of twin sisters, in seven other families. Four pairs of patients developed HSP at the same age. Three pairs presented HSP within 1 month of each other and the other pairs presented HSP between 9 months and 5 years. Seven patients had a history of allergic diseases. The clinical courses of 12 patients were reviewed. Upper respiratory tract infection preceded HSP in 10 patients, two of whom had elevated antistreptolysin-O titers. No pairs of patients in a family received the same drugs before the onset of HSP. Abdominal pain was noted in eight patients, arthralgia in six and nephritis in four. Severity of skin lesions, presence of abdominal pain and nephritis, and serum IgA levels at the acute stage varied among family members of HSP. The incidence of HSP in family members of children with HSP seems to be high. Onset at the same age and onset of HSP within 1 month in siblings have not previously been reported. There were no characteristic or similar findings between two patients of the same family. No trigger or genetic factor causing HSP was identified.

An Adult With Acute Poststreptococcal Glomerulonephritis Complicated by Hemolytic Uremic Syndrome and Nephrotic Syndrome

We report the case of a 47-year-old man with the simultaneous occurrence of clinical and laboratory features consistent with acute poststreptococcal glomerulonephritis (APSGN), hemolytic uremic syndrome (HUS), and nephrotic syndrome. Acute nephritic syndrome occurred 3 weeks after having pharyngeal pain and diarrhea. He presented with edema and hypertension on admission. Laboratory evaluation showed hemolytic anemia with fragmentation, thrombocytopenia, elevated lactic dehydrogenase level, low haptoglobin level, low complement C3 level, and elevated antistreptolysin-O titer. Serum creatinine level was 1.22 mg/dL (108 micromol/L), and urinalysis showed marked proteinuria, with protein of 8.7 g/d, and hematuria. The renal biopsy specimen was characteristic of APSGN, but not HUS. Moderate expansion of the mesangial matrix, moderate proliferation of epithelial and endothelial cells, and marked infiltration of neutrophils was seen by means of light microscopy, and many subepithelial humps were seen by means of electron microscopy. Neither fibrin deposition nor evidence of thrombotic microangiopathy was found. Complement C3 deposition along the capillary wall and tubules was seen in an immunofluorescence study. The patient was administered plasma infusion at 320 mL/d and antihypertensive drugs. Serum complement C3 and haptoglobin levels returned to normal within 3 weeks. This is a rare case of the simultaneous occurrence of APSGN, HUS, and nephrotic syndrome.

Henoch‐Schönlein purpura with hypocomplementemia in children

The clinical course and prognosis of Henoch-Schonlein purpura (HSP) associated with hypocomplementemia are not clear. The clinical findings of 10 children with HSP and hypocomplementemia were studied. Purpuric rash in all patients, abdominal pain in five, and arthralgia in nine were noted. The findings in HSP were not different from others with HSP. In eight patients, infection preceded hypocomplementemia. Serum levels of CH50, C3 or C4 were depressed variously. Complement levels returned to normal within 5 weeks in all patients. Antistreptolysin-O (ASO) titer was elevated in all patients and nephritis occurred in eight patients. Six patients had generalized edema and hypertension. Macroscopic hematuria occurred in two patients and heavy proteinuria in five patients. One patient was diagnosed as having poststreptococcal acute glomerulonephritis (PSAGN) combined with HSP nephritis according to renal biopsy findings. In three of eight patients with nephritis, abnormal urinary findings continued for more than 1 year. Hypocomplementemia in children with HSP was transient and was not related to severity of HSP. Incidences of elevated ASO titer and nephritis were high. The nephritis resembled PSAGN during the acute stage and long-term clinical courses varied. These findings suggest PSAGN may be associated with HSP nephritis.

A Study of Membranoproliferative Glomerulonephritis in Iran

The aim of this study was to review the morphologic patterns of membranoproliferative glomerulonephritis (MPGN) in 100 Iranian patients using light microscopy (LM) and electron microscopy (EM), and to compare the treatment and outcome in 13 patients with two biopsies. A retrospective study of 713 kidney biopsies of Iranian patients received between 1981 to 1994 was carried out. Of the 713 kidney biopsies, MPGN (n=106) and membranous glomerulopathy (n=112) made up the highest numbers of cases. Among 100 MPGN patients, 55 (55%) were MPGN type I, 10 were type II (10%), and 35 type III (35%). Eighty-three (83%) had nephrotic proteinuria, 39 (39%) had hematuria, and 52 (52%) were hypertensive. Complement levels were estimated in 58, with low C3 in 10. The glomerular involvement was irregular, with focal hypercellularity in 47 patients (47%), widely patent capillaries in 50 (50%), arteriosclerosis in 48 (48%), and with hyaline change in 25 (25%). Follow-up data (22-130 months) was available in 61 (61%) patients: 6 (10%) died after 14-56 months, 27 (44%) were on maintenance hemodialysis for 15-110 months, and three received transplants. Thirteen patients had detailed follow-up and a second biopsy after 24-120 months. All 13 presented with edema and nephrotic range proteinuria, with hematuria and hypertension in five and azotemia in four. Seven of the 13 patients received initial steroids, followed by antiplatelet or antihypertensive drugs. Four (type III) patients received antiplatelet and antihypertension drugs, and two (type III) received only antihypertensive drugs. In the first biopsy, glomerular changes by light microscopy were non-uniform in 7 of 10 (70%) type III MPGN cases. Vascular changes were absent or mild in 11, and moderate in two. In the second biopsies, 10 showed decrease in cellularity, with many open capillaries, persistence of deposits by EM in all, and progression of vascular sclerosis in eight, and tubulointerstitial changes in 10. Among the 13, six were clinically stable, another six received dialysis followed by transplant in three, and one had relapses with episodes of cryoglobulinemia. Three patients died. There is a high incidence of MPGN in Iranian patients, with a substantial number of type III MPGN cases. Second biopsies showed decreased cellularity, but increase in chronic tubulointerstitial and vascular cases. Steroids did not appear to benefit the outcome in types I and III MPGN patients compared to patients who received antihypertensive and antiplatelet treatment without steroids.

Does endomyocardial biopsy aid in the diagnosis of active rheumatic carditis?

Carditis is the only component of rheumatic fever that leads to permanent disability. The diagnosis of carditis is presently made by using composite clinical criteria based on the revised Jones' criteria. Since myocardial involvement is an important component of rheumatic carditis, right ventricular endomyocardial biopsies were performed in 54 patients with clinical acute rheumatic fever and quiescent rheumatic heart disease to evaluate the role of biopsy for the diagnosis of rheumatic carditis. In 11 of the 54 patients, clinical consensus was certain about rheumatic fever and carditis based on the revised Jones' criteria (group 1). Histomorphological abnormalities in these patients were scarce. The diagnostic features of rheumatic myocarditis including Aschoff nodules or histiocytic aggregates were encountered in 3 patients (27%). Lymphocytic infiltration was sparse. A majority of patients demonstrated myocyte degeneration, interstitial degeneration, or occasional interstitial mononuclear cell infiltration, but since these histopathological lesions may occur in other conditions also, they were considered nondiagnostic. In 33 of the 54 patients with preexisting rheumatic heart disease, the diagnosis of carditis was suspected based on varied clinical presentations. Since previous cardiac findings were not available in these patients, the clinical diagnosis of carditis could not be made without equivocation (group 2). Twenty-three patients presented with unexplained acute onset of congestive heart failure and evidence of recent streptococcal infection (group 2A). While 13 of them had one or more other major manifestations, 10 patients had only minor manifestations. Mimetic carditis was suspected in the remaining 10 of 33 patients based on carditis having occurred in previous episodes of rheumatic fever (group 2B). The endomyocardial biopsy provided confirmatory evidence of rheumatic myocarditis in 9 patients of group 2A but in none of the 10 patients with suspected mimetic carditis. Nondiagnostic myocyte or interstitial alterations were frequently observed in group 2. Ten of the 54 patients had no clinical evidence of active carditis (group 3). No histological alterations diagnostic of rheumatic carditis were noted in these patients. Twenty-two follow-up biopsies were performed in the first 10 consecutive patients. Diagnostic histiocytic aggregates or Aschoff nodules were observed in initial biopsies in 4 of 10 patients, and nonspecific myocyte or interstitial alterations were observed in 9. All patients with diagnostic changes in initial biopsy demonstrated fibrohistiocytic nodules in 6- or 12-week biopsy samples. Nondiagnostic alterations, similar to those seen in acute cases, were present in 5 of 8 patients at 6 weeks, 5 of 8 patients at 12 weeks, and 3 of the 6 patients at 24 weeks despite the presumed adequate immunosuppressive therapy. No complications related to biopsy were encountered. The present study highlights the low frequency of diagnostic features in the biopsy specimens of patients with definite clinical rheumatic carditis. Although such alterations are not observed in patients with chronic rheumatic heart disease, endomyocardial biopsy does not appear to provide additional diagnostic information where clinical consensus is certain about diagnosis of rheumatic carditis. Our study, however, substantiates the concept of carditis underlying unexplained congestive heart failure of acute onset in patients with preexisting rheumatic heart disease and elevated antistreptolysin-O titers.

Infection of group A streptococcus and antibody response to extracellular antigens.

A study demonstrating the relationship between pharyngeal infection of group A streptococci and the antibody response was performed. Group A streptococci were recovered from 44 (9.4%) of 466 children, of which 41 strains were typable by T-protein. Fifty-five percent of 41 children from whom group A streptococci were recovered showed a significant rise in anti-streptolysin O (ASO) titers in sera. In children from whom group A streptococci were recovered and with elevated ASO titers, titers of antideoxyribonuclease B (ADNase B) were significantly higher than those who were negative for group A streptococci and also showed elevated or normal titers for ASO. Patients with acute rheumatic fever demonstrated elevated titers of both ASO and ADNase B. These findings suggest that a combination of ASO and ADNase B titers should be applied to diagnose the streptococcal infections. Antinicotinamideadenine dinucleotidase showed a low level of titers in children who had group A streptococci in their throat and exhibited elevated titers in streptococcal antibodies, and also in patients with acute rheumatic fever.

Comparison of Two Slide Tests for Detection of Group A Streptococcal Antibodies

Screening sera for streptococcal antibodies is a useful clinical procedure when recent streptococcal infection requires verification. Presently there are two test kits available that detect five (or more) of the antibodies that may be present. These two screening tests were compared using antistreptolysin O (ASO) and antideoxyribonuclease B (ADB) titers as the reference for true streptococcal infection. All four procedures were performed on 69 sera collected from a pediatric population. Both screening tests were found to be sensitive, specific, economical, and easy to perform; however, both were more sensitive to elevated ASO titers than to elevated ADB titers. In certain clinical situations, therefore, antibody titrations may be necessary to document completely recent streptococcal infection.

Latex antistreptolysin O test as a tube dilution procedure.

Recently, several investigators reported on the usefulness of a latex antistreptolysin O (ASO) test as a screening procedure for the detection of elevated ASO titers. The present report deals with applications of a variant of this technic to the quantitation of ASO titers in serum. One hundred fourteen serum specimens were analyzed for ASO activity by this tube dilution technic and by two standard hemolytic methods, the Todd method and the International Unit procedure. The results with all three assays were comparable.

RHEUMATIC FEVER UNDER 3 YEARS OF AGE

Ten definite cases of rheumatic fever occurring under 3 years of age are reported. These represent 0.5% of all initial attacks of rheumatic fever in children 16 years old or less admitted to our hospital between 1939 and 1966. Thus, rheumatic fever in the first few years of life is rare but not nonexistent. Our youngest patient was 19 months old. The predominant manifestations of the disease in the first few years of life were carditis and congestive heart failure, and all but one of the patients had significant mitral regurgitation. Polyarthritis was also a common feature. Elevated antistreptolysin-O titers were demonstrated in all cases in which the test was performed. Therefore, evidence of a preceding streptococcal infection is important in considering this diagnosis, even in children under 3 years of age. The differentiation of rheumatic fever from congenital heart disease, viral myocarditis, and rheumatoid arthritis is dicussed. In our experience, the prognosis for the infant with rheumatic carditis has improved since the introduction of penicillin and corticosteroids.