RESUMO

Two unrelated patients with a family history of rheumatic fever had isolated, acquired chorea. Both index cases, as well as affected family members, had increased expression of the rheumatic B-cell alloantigen D8/17. This test may help differentiate Sydenham chorea from lupus chorea.

Assuntos

RESUMO

Using purified group A streptokinase (SKA) as the antigen, ELISA assays were carried out on the sera of normal unaffected children, acute poststreptococcal glomerulonephritis patients (APSGN) and acute rheumatic fever patients (ARF). The results demonstrate that antibody titers to SKA increase with age in normal children and by age 8 years the vast majority of children have antibodies to SKA. APSGN patients did not demonstrate unique reactivity to SKA when compared to ARF patients either at time of onset of disease or during convalescence. Polyclonal and monoclonal antibodies to SKA which recognize both group A and C streptokinase failed to detect the presence of streptokinase in the biopsy sections obtained from ten well-documented APSGN patients. We conclude that there is no unique reactivity to group A streptokinase in the sera of APSGN patients. Furthermore, we failed to demonstrate the presence of streptokinase in the biopsy specimens of an early case of APSGN patients.

Assuntos

RESUMO

A new, rapid blood test for the detection of B-cell markers in patients with rheumatic fever (RF) was applied to 10 patients with RF, 26 of their family members and 14 normal subjects. Three-hundred microliters of blood was obtained by finger-pricking from each subject and submitted to the immunofluorescence technique using three different antibodies, i.e., D8/17 monoclonal ascites antibody, FIRC-conjugated goat anti-mouse IgM (mu chain specific) and phycoerythrin-conjugated murine anti-HLA-DR antibody. D8/17 lymphocytes (green stain) and B-lymphocytes (red stain) were counted using a double-filter microscope. The percentage of positive cells was 20-64% (average 38.5%) in patients, siblings, fathers and mothers, 4.5% in 12 normal controls and 27.5% in the other 2 controls with a family history of RF. In 90% of the families studied, the patients had the highest percentage of positive cells. We conclude that this rapid test can be used as an aid for RF diagnosis and possibly to detect siblings who are at risk to develop the disease.

Assuntos

RESUMO

Numerous investigators have suspected that there is a genetic predisposition to rheumatic fever (RF). In this context a group of investigators at Rockefeller University have produced a monoclonal antibody that identifies an antigen present in 100% of all RF studied at that center. Using this antibody, labeled D8/17, we studied 47 patients with acute rheumatic fever and rheumatic heart disease. Of these, 39 were not receiving steroids at the of the test and 35 were positive for the marker (89.7%). The highest percentage of positive cells was seen in the probands with 34.6 +/- 13.16%, while unaffected mothers, fathers and siblings gave 24.9, 5.2 and 7.3% respectively. The control group had an average of 7.5% of positive cells. This study and previous ones, performed by the Rockefeller University group in which HLA typing was included, suggest an autosomal recessive mode of inheritance, not associated with the MHC system, for the D8/17 antigen. Rheumatic fever; non-HLA antigen in; genetic predisposition in.

Assuntos

RESUMO

In an attempt to quantify the immuno-histochemical properties of the glomerular basement membrane (GBM), monoclonal antibodies (mAbs) were prepared against heparin sulphate Proteoglycan (HSPG). The HSPG was isolated from bovine glomerulae. Enzyme-linked immuno-sorbent assays (ELISA) and immunoblotting demonstrated that the mAbs reacted with HSPG. Indirect immuno-fluorescence showed that the mAbs stained renal basement membranes (BMs) and BMs in other organs of normal bovine and human tissues in patterns typical of HSPG. Immuno-inhibition studies, and immuno-blotting of heparin lyase digested HSPG, indicated that the mAbs recognizes HSPG core protein. Human kidney biopsies revealed interesting patterns of staining for HSPG. For instance, in kidney biopsies from patients with acute post-streptococcal glomerulonephritis, intact linear staining for HSPG was noted despite abnormal pathological processes shown by widened capillary loops. On the other hand, in membranous and in diffuse proliferative lupus glomerulonephritis, loss of HSPG staining was demonstrated at sites of immuno-deposition of IgG or C3; whereas, increased staining for HSPG was seen in areas of newly formed GBM. Extensive loss of HSPG was seen in areas of glomerular sclerosis and necrosis. In biopsies from patients with minimal change glomerulonephritis and mesangio-proliferative lupus glomerulonephritis, a normal linear GBM distribution of HSPG was noted. The study demonstrates that immunological injury to the HSPG component of the GBM of the kidneys plays an aetiological role in the pathogenesis of proteinuria in man (AU)

Assuntos

RESUMO

Acute rheumatic fever (ARF) has the characteristics of an autoimmune disease, triggered by cross-reactive antigens shared by the group A streptococcus and a variety of tissues including the heart, endothelium, and basal ganglia. Using two parameters of cellular reactivity, migration inhibition and blastogenic transformation, ARF patients from Trinidad show significant lymphocyte reactivity to streptococcal antigens, particularly those from an ARF associated streptococcal strain. This reactivity, studied over a 2-year period, peaked at 1 to 6 months after the acute onset and remained significantly elevated for at least 2 years. The reactivity is directed mainly toward a nonionic detergent extractable material in the cell membrane. These studies suggest a possible streptococcal strain specificity in ARF and demonstrate persistent sensitization, which explains the increased susceptibility to recurrences in the 2 years following the acute episode.

Assuntos

RESUMO

The group G streptococcus has generally not been considered a prominent pathogen. In a 1982 study of the colonization rate by beta-haemolytic streptococci in apparently healthy children, age 5-11 years, 25 of 69 isolates belonged to group G. This surprisingly high rate of group G colonization (14.3%) led to a retrospective study of school surveys in 1967 which showed that the colonization rate with this organism was 2.3% (range 1.3-3.5%). A review of bacitracin-sensitive streptococcal isolates from hospital admissions of patients with acute glomerulonephritis (AGN), rheumatic fever, and their siblings, between January 1967 and July 1980, was conducted. Of 1063 bacitracin-sensitive isolates, 63 were group G, and 52 of these were isolated from AGN patients and their siblings, i.e. 7 from skin lesions of AGN patients, 40 from the throats of siblings and only 5 from the skins of the siblings. The other 11 group G isolates were from rheumatic-fever patients and their siblings. Thus, the group G colonization rate fluctuates in the population. The isolation of only group G streptococci from skin lesions of patients with AGN suggests a possible association between group G streptococcal pyoderma and acute post-streptococcal glomerulonephritis.

Assuntos

RESUMO

During January to March, 1982, the throats of 175 apparently healthy school children, age range 5 - 11 years, were swabbed and examined for the presence of beta-haemolytic streptococci as a prerequisite to the determination of the immune response to streptococcal antigens in normal children.j There were 68 isolates comprising 39 belonging to Group A, 1 to Group B, 4 to Group C and 24 to Group G. This high rate of Group G colonisation was surprising. Subsequent examination of past record showed that of 114 throat swabs of apparently healthy school children taken in 1967, 36 yield streptococcal isolates of which 4 belonged to Group G. Of 199 cultures from skin lesions, 166 yielded streptococcal isolates of which 4 belonged to Group G but 2 of which were of mixed culture with Group A. These observations led to a review of cases of post streptococcal sequelae, acute rheumatic fever (ARF) and acute glomerulonephrotos (AGN) which occurred at the General Hospital, San Fernando, between January 1976 and July 1980 during which time all bacitracin positive streptococcal isolates from patients with post streptococcal sequelae were sent to the Public Health Laboratory, Colindale, England for grouping and typing. Of 1,073 isolates, 958 belonged to Group A, 18 to Group B, 19 to Group C, 5 to Group D and 63 to Group G. Of the 63 Group G isolates, one was isolated from the throat of a patient with ARF and 8 from siblings of ARF patients. More interestingly, there were 7 Group G isolates from skin lesions on patients with AGN and 47 from siblings of AGN patients. Though Group G streptococci have been associated with pharyngitis, neonatal sepsis and suspected gonococcal infections, this is the first report of a possible Group G associated post streptococcal acute glomerulonephritis (AU)

Assuntos

Assuntos

RESUMO

Acute poststreptococcal glomerulonephritis (APSGN) is likely the result of immune complex mechanisms. The current theories in search of the streptococcal antigen responsible for the initiation of the disease are reviewed. The finding of an extracellular protein unique to streptococci isolated from patients with APSGN and its possible role in the pathogenesis of this disease is presented.

Assuntos

RESUMO

A prospective, triple-blind study was undertaken to determine whether antiheart antibody or a rise in titer to a virus occurred in patients after intrapericardial surgery and, if so, whether either was related to clinical evidence of the postpericardiotomy syndrome. In 257 patients, AHA in high titer appeared in 62 (24%), all of whom had the syndrome. None of the 102 patients with no AHA had the syndrome. In 137 subjects, a rise in titer to one or more viral agents occurred in 21 of 31 (68%) of those with AHA and PPS. This study suggests that an immunologic response and viral illness are related to PPS.

Assuntos