Type-Specific Streptococcal Antibodies in Pyodermal Nephritis (original) (raw)
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emm Typing and Validation of Provisional M Types for Group A Streptococci
Emerging Infectious Diseases, 1999
The Lancefield M-typing system, a typical serologic system based on antigen-antibody reactions, is dependent on the preparation of type-specific antisera and extraction of a protein identified as M protein on the surface of group A streptococci (GAS) (1). The antisera against the M-protein antigens are produced with whole-cell streptococcal vaccines used to immunize rabbits. Acceptable antisera contain specific-precipitin antibodies and type-specific antibodies that must enhance the phagocytosis of the strain used to immunize the rabbit (2,3). The precipitin antibodies are made specific by absorption of the serum with streptococcal cells to remove the carbohydrate group antibodies and any crossreactive precipitin antibody to heterologous M-type strains. Each rabbit antiserum is tested for reaction with antigens of all known M types. Approximately half of GAS strains produce an apoproteinase, an enzyme that causes mammalian serum to increase in opacity. This reaction is called the serum opacity factor reaction, and the responsible enzyme is referred to as opacity factor (OF). The OF enzymes are OF type-specific because each M type that produces OF can induce type-specific OF antibodies that can be used in OF inhibition tests (3,4). Preparation of the OF antisera and specific details of the OF tests are described elsewhere (3,4). Some laboratories have used OF typing to predict M types in epidemiologic investigations. Even though it is not uniformly agreed that OF typing antisera results should be reported as M or provisional M-typing results, anti-OF antisera in many situations predict the M type in a typespecific manner. For reporting purposes, if
Kidney International, 2005
Is the nephritogenic antigen in post-streptococcal glomerulonephritis pyrogenic exotoxin B (SPE B) or GAPDH? Background. Acute glomerulonephritis can follow infection by group A streptococci. An immune-complex pathogenesis is accepted, but the causative antigen(s) is still controversial. In recent years, 2 streptococcal antigens, the cationic cysteine proteinase exotoxin B (SPE B) and the plasmin receptor, a glyceraldehyde phosphate dehydrogenase (Plr, GAPDH) have attracted attention because: (1) they were localized in glomeruli in patients with acute post-streptococcal glomerulonephritis (APSGN); and (2) serum antibody to these antigens was associated with nephritogenic streptococcal infections. To date, putative nephritogens were always tested independently. Here, the relevance of SPE B and GAPDH was evaluated in the same renal biopsies and serum samples of welldefined APSGN patients. Methods. Renal biopsies (17 patients) and serum samples (53 patients) with APSGN and appropriate controls were examined. Immunofluorescent staining of frozen sections was performed using specific antibodies to SPE B and GAPDH. Serum antibodies were investigated by both enzyme-linked immunosorbent assay (ELISA) and Western blot methodology. Results. Glomerular deposits of SPE B were demonstrated in 12/17 APSGN biopsies, and 2 cases were borderline; circulating antibodies were found in all instances (53/53 patients). Glomerular deposition of GAPDH was detected in 1/17 biopsies, and 2 cases were borderline; circulating antibodies were found in 5/47 patients. In 31 control biopsies, only weak staining for each antigen was found in 2 cases. Conclusion. In this study, glomerular deposits of and antibody response to zymogen/SPE B are more consistently present in APSGN than deposits and antibody response to GAPDH. Zymogen/SPE B is likely to be the major antigen involved in the pathogenesis of most cases of APSGN.
Group A streptococcal antigen in the glomeruli of children with henoch-schönlein nephritis
American Journal of Kidney Diseases, 2003
Background: Although the pathogenesis of Henoch-Schö nlein nephritis (HSN) remains unclear, there is substantial evidence that it is an immune complex-mediated disease. HSN is preceded by upper-respiratory tract infection in 30% to 50% of patients, but there is no evidence that group A streptococcal (GAS) infection has a pathogenetic role in this disease. Recently, nephritis-associated plasmin receptor (NAPlr), a GAS antigen, was found primarily in the glomerular mesangium of patients with early-stage acute poststreptococcal glomerulonephritis. Methods: To determine the possible role of NAPlr in HSN, expression of the receptor was determined in glomeruli using fluorescein isothiocyanate-labeled rabbit polyclonal anti-NAPIr antibody, and serum antistreptolysin O (ASO) titers were measured in children with HSN. Results: Ten of 33 patients (30%) with HSN showed segmental or global mesangial staining with NAPlr antibody, whereas only 4 of 120 patients (3%) with other renal diseases were positive (P < 0.001, Fisher's exact test). Patients with HSN also showed significantly greater ASO titers than patients with other renal diseases (P ؍ 0.03, Mann-Whitney U test). Serum ASO titers were significantly greater in patients with HSN with than without glomerular NAPlr antigen (P ؍ 0.03, Mann-Whitney U test). Conclusion: These findings suggest that the deposition of NAPlr in the mesangium, induced by GAS infection, may have a role in the pathogenesis of HSN in some patients.
Upsala Journal of Medical Sciences, 2005
We studied history, renal histopathology and microbiology of an epidemic of acute glomerulonephritis associated with throat infections and uncommon culture results in four neighbour families. A 40-year-old man (index patient) was referred to a university hospital for dialysis and kidney biopsy due to a suspected acute glomerulonephritis. An acute tonsillitis had preceded the condition. Penicillin treatment had been started four days before the discovery of renal failure. Throat swabs were positive for-hemolytic streptococci, group C (GCS). GCS were also found in throat cultures from his wife and two of their children. The bacteria were typed as Streptococcus constellatus. A third child had S. constellatus expressing Lancefield antigen group G. A neighbour and two of his children fell ill the following week with renal involvement. Throat swabs from both these children were positive for S. constellatus. His third child had erythema multiforme and S. constellatus in the throat while a fourth child hadhemolytic streptococci group A; Streptococcus pyogenes. Kidney biopsies on the index patient and his neighbour showed an acute diffuse prolipherative glomerulonephritis compatible with acute post-streptococcal nephritis and microbiological analysis of renal tissue revealed in both cases S. pyogenes and S. constellatus. The
Post-streptococcal acute glomerulonephritis in Chile—20 years of experience
Pediatric Nephrology, 2004
In order to characterize the epidemiological and clinical picture of post-streptococcal acute glomerulonephritis (PSAGN), a prospective study was designed to investigate all admissions to a general hospital of a local health service in Chile. The protocol included the investigation of previous streptococcal infections (SI), clinical symptoms and signs, socioeconomic situation (SES), throat and skin swabs for the isolation of group A beta-hemolytic streptococci, sequential determination of serum antistreptolysin O (ASO) titer, anti-DNAase B antibodies, and C3. During the 20 years studied, 926 cases were admitted (56% males). Incidence showed an endemic period (EP) 1980–1983, an epidemic outbreak (EO) 1984–1989, and a late period (LP) 1990–1999, with a rate per 100,000 inhabitants of 6.2, 13.2, and 1.7, respectively. The clinical picture was similar in the three periods. SES was homogeneous, with 80% of the population in low and middle-low categories. The average size of the family was 6.9 compared with 4.8 in the general population. Pyoderma was more frequent than pharyngeal infection, and more so during the EO. The isolation rate of group A beta-hemolytic streptococci from the pharynx was 20% compared with 60% from skin swabs. During EP, the most prevalent serotypes were T14-M0 and T1-M1 from the pharynx and TImp19-M0 from the skin. During EO, T14-M0 was more prevalent (30%). M or T classification was possible in EP and EO in 80%–85% of all strains isolated from the two locations. Significant titers for ASO and anti-DNAase B were found on admission: 55% and 75%, respectively. Both tests allowed identification of 100% of previous SI. In conclusion, the incidence of PSAGN had an uneven trend during the observed period. EO was mainly due to skin infection and a predominance of one serotype, T14-MO, was observed. After the EO, the yearly rate gradually decreased from 13.2 in 1988 to 0.0 in 1999, a rate similar to that of industrialized nations.