Nephritogenic Strains Research Articles

Gross hematuria and congestive heart failure – two sides of the same coin

Poststreptococcal glomerulonephritis (PSGN) is an immune-mediated disease following infection with nephritogenic strains of group A β-hemolytic Streptococcus (GAS), affecting children aged of 2 to 10. We report 2 different presentations of PSGN from “Grigore Alexandrescu” Hospital. Case 1: A 5 years old girl was admitted for gross hematuria. Investigations revealed: anemia, inflammatory syndrome, mild nitrogen retention syndrome, elevated ASO and low levels of serum C3, nephritic-range proteinuria and severe hematuria. she received antibiotic treatment with initial improvement. A relapse occurred in one week, a second course of antibiotic and corticosteroids was necessary. Case 2: A 15-year-old girl was admitted for acute cardiac failure, hypertension and oliguria. Investigations revealed anemia, nitrogen retention, dyslipidemia, inflammatory syndrome, high ASO titers, low serum C3, microscopic hematuria, nephrotic-range proteinuria. She had fluid build-up in both lungs and pericardium. The diagnosis was PSGN and congestive heart failure (volume overload). She received antibiotics, diuretics and ACE inhibitors. PSGN is re-emerging in pediatric practice due to the resurgence of streptococcal infections within children's communities. The clinical presentation might be highly variable, ranging from hematuria to heart failure. Clinicians should be aware and actively consider this diagnosis.

Predictors of rapidly progressive glomerulonephritis in acute poststreptococcal glomerulonephritis.

Acute post-streptococcal glomerulonephritis (APSGN) is an immune-mediated inflammatory respsonse in the kidneys caused by nephritogenic strains of group A β-hemolytic streptococcus (GAS). The present study aimed to present a large patient cohort of APSGN patients to determine the factors that can be used for predicting the prognosis and progression to rapidly progressive glomerulonephritis (RPGN). The study included 153 children with APSGN that were seen between January 2010 and January 2022. Inclusion criteria were age 1-18years and follow-up of ≥ 1years. Patients with a diagnosis that could not be clearly proven clinically or via biopsy and with prior clinical or histological evidence of underlying kidney disease or chronic kidney disease (CKD) were excluded from the study. Mean age was 7.36 ± 2.92years, and 30.7% of the group was female. Among the 153 patients, 19 (12.4%) progressed to RPGN. The complement factor 3 and albumin levels were significantly low in the patients who had RPGN (P = 0.019). Inflammatory parameters, such as C-reactive protein (CRP), platelet-to-lymphocyte ratio, CRP/albumin ratio, and the erythrocyte sedimentation rate level at presentation were significantly higher in the patients with RPGN (P < 0.05). Additionally, there was a significant correlation between nephrotic range proteinuria and the course of RPGN (P = 0.024). We suggest the possibility that RPGN can be predicted in APSGN with clinical and laboratory findings. A higher resolution version of the Graphical abstract is available as Supplementary information.

Острый постстрептококковый гломерулонефрит у детей — реальность и парадоксы. Обзор литературы

Acute post-streptococcal glomerulonephritis (APSGN) is an immune-mediated disease associated with nephritogenic strains of group A beta-hemolytic streptococcus. The epidemiology of APSGN varies in different countries, due to the influence of social, racial, demographic, and climatic conditions. In the modern spectrum of progressive diseases, APSGN occupies a modest place, yielding to other immune glomerulopathies. The prevalence rate has been declining in recent decades due to the decrease in pyoderma, however, it remains endemic to the French Polynesians and Australian Aborigines. The review defines the features of the immunological processes of this disease: nephritogens were identified at the site of the formation of immune complexes (streptococcal plasmin receptor and streptococcal pyrogenic exotoxin B). An assessment of the clinical profile of patients with APSGN (mostly asymptomatic course with a self-limiting (self-limiting) outcome) was carried out. The role of genomic surveillance in tracking potential markers of APSGN is emphasized. Risk factors for the development of kidney damage were identified — hypoalbuminemia, hypocomplementemia, and an increase in inflammatory markers. The paper considers the factors that determine the prognosis in patients, presents the main approaches to treatment (predominantly symptomatic therapy, with the exception of severe and atypical cases of the disease). It is concluded that APSGN remains one of the reasons for the development of AKI in different countries of the world. The article gives recommendations on long-term follow-up of children after APSGN. The purpose is to analyze the prevalence and identify the factors contributing to OPSGN; to determine the specifics of the disease immunological processes of the (immunocomplexity, autoimmunity); to evaluate the clinical profile, diagnostic methods and features of OPSGN treatment; to discuss the possible progression of the disease and whether PSGN is associated with chronic kidney disease (CKD).

Case Report: Coexistence of acute post-streptococcal glomerulonephritis and rheumatic heart disease in a 9 years old girl

Background: Group A-haemolytic streptococcus (GAS), one of the most frequent pathogens in pediatric group causing various diseases, from acute pharyngitis (AP) to severe complication such as acute rheumatic fever (ARF) and acute post-streptococcal glomerulonephritis (APSGN). GAS, round gram positive bacteria typically form pairs or chains, was reported causing 1.78 million cases with 500.000 death due to its severe complication in 2005. Case Illustration: A 9-year-old female patient came to emergency unit (ER) complained swollen face and legs since 5 days ago, accompanied by tea color urine and reduced frequency and volume of micturition. Patient also complained shortness of breath which getting worse since yesterday, easily fatigue and dizziness. Moreover her mother also admitted that her daughter had history of migratory joints pain 3 weeks before admission, with sore throat a month ago. Blood pressure was 110/70 mmHg, Ross score was 8. Physical examination showed puffy face, pretibial edema, heart auscultation we heard pansystolic murmur. Chest radiography showed cardiomegaly and congestive pulmonum while laboratory exam showed ASTO 200, urinalysis showed red color, cloudy clarity, protein 1+, erythrocyte 3+, leukocytes 1+, urinary microscopic examination: 30-40 erythrocytes, 8-12 leukocytes, electrocardiography showed sinus tachycardia, prolonged PR interval, right atrial enlargement, right ventricle hypertrophy with right axis deviation. Patient was diagnosed with APSGN, hypertension grade II and heart failure due to rheumatic heart disease. Summary: APSGN and ARF rarely occur together, the coincidence might be due to streptococci with nephritogenic and rheumatogenic same strains. Early detection and treatment of GAS are crucial to prevent complications.

Clinico-Pathological Correlations of Poststreptococcal Glomerulonephritis

Abstract Postinfectious glomerulonephritis is associated with bacterial, viral, fungal, and parasitic infectious agents and histologically appears most often as acute diffuse endocapillary or proliferative glomerulonephritis secondary infection with: group A streptococcus, streptococcus viridans, staphilococus aureus, diploccocus pneumoniae, Brucella melitensis, Salmonella typhi, Yershinia enterocolitica, Plasmodium falciparum, meningococcus, Mycoplasma, Klebsiella, varicella, variola, mumps. Less commonly, it appears as diffuse crescentic glomerulonephritis and a lot of infectious causes are incriminated like: streptococcus, legionella, varicella, Treponema pallidum or as focal crescentic glomerulonephritis: streptococcus A. It rarely appears as mesangiocapillary glomerulonephritis secondary infection with: streptococcus viridans, hepatitis C virus; diffuse or focal mesangial proliferative glomerulonephritis: hepatitis B virus, salmonella, adenovirus, influenza virus, salmonella; focal segmental, necrotizing and sclerosing glomerulonephritis: bacterial endocarditis; membranous glomerulonephritis: hepatitis B virus, syphilis, filarial, Mycobacterium, plasmodium falciparum; focal proliferative: Mycoplasma; mesangiolytic glomerulonephritis :Echo virus. Poststreptococcal glomerulonephritis (PSGN) is caused by prior infection with specific nephritogenic strains of group A beta-hemolytic streptococcus. The clinical presentation of PSGN varies from asymptomatic, microscopic hematuria to the full-blown acute nephritic syndrome, characterized by red to brown urine, proteinuria (which can reach the nephrotic range), edema, hypertension, and acute kidney injury. The prognosis is generally favorable, especially in children, but in some cases, the long-term prognosis is not benign. Managing a case of PSGN requires cooperation between internists, nephrologists, infectious disease consultants, pharmacists, and nursing staff, functioning as an interprofessional team, to provide excellent care for their patients.

A Comprehensive Review Study on Glomerulonephritis Associated With Post-streptococcal Infection.

Post-streptococcal glomerulonephritis (PSGN) is an immune-complex mediated inflammation that used to be considered one of the commonest causes of acute nephritis amongst children. PSGN is characterized by the proliferation of cellular elements called nephritogenic M type as a result of an immunologic mechanism following an infection of the skin (impetigo) or throat (pharyngitis) caused by nephritogenic strains of group A beta-hemolytic streptococci, a gram-positive bacteria that enters the body across pores in the skin or mucus epithelia and is responsible for more than 500,000 deaths annually due to multiple subsequence diseases such as rheumatic heart disease, rheumatic fever, PSGN, and other invasive infections. After the infection, the formation of an immune complex of antigen-antibody and complement system will take place and will deposit in the glomeruli where the injury occurs and leads to inflammation. The manifestations of PSGN can be explained by nephritic syndrome manifestation. PSGN is diagnosed by laboratory tests like microscopy and urinalysis. The imaging studies in PSGN could be used to assess the possible complications of PSGN such as pulmonary congestion and chronic kidney disease. The management of PSGN is symptomatic. If PSGN is not treated, the patient may develop chronic kidney disease. The main way to prevent PSGN is to treat group A streptococcal (GAS) infections by giving good coverage of antibiotic therapy to a patient who has primary GAS infections to prevent the development of the complication.

The development of a community-based public health response to an outbreak of post-streptococcal glomerulonephritis in a First Nations community.

Post-streptococcal glomerulonephritis (PSGN) is a rare immune-mediated condition that typically occurs in children as a result of group A streptococcus (GAS) infection. PSGN is not considered a disease of public health significance, or reportable, in Canada. Higher incidence of PSGN has been described among Indigenous people in Canada. No national or provincial guidance exists to define or manage PSGN outbreaks. To describe an outbreak of seven paediatric cases of PSGN in a remote First Nations community in northwestern Ontario and the development of a community-wide public health response. Following a literature review, an intervention was developed involving screening of all children in the community for facial or peripheral edema or skin sores, and treatment with antibiotics if noted. Case, contact and outbreak definitions were also developed. The purpose of the response was to break the chain of transmission of a possible nephritogenic strain of streptococcus circulating in the community. Relevant demographic, clinical and laboratory data were collected on all cases. Seven paediatric cases of PSGN presented to the community nursing station between September 25 and November 29, 2017. Community-wide screening for skin sores was completed for 95% of the community's children, including 17 household contacts, and as a result, the last of the cases was identified. Nineteen adult household contacts were also screened. Ten paediatric contacts and two adult contacts with skin sores were treated with one dose of intramuscular penicillin, and six paediatric contacts received oral cephalexin. No further cases were identified following the screening. PSGN continues to occur in Indigenous populations worldwide at rates higher than in the overall population. In the absence of mandatory reporting in Canada, the burden of PSGN remains underappreciated and could undermine upstream and downstream public health interventions. Evidence-based public health guidance is required to manage outbreaks in the Canadian context. The community-based response protocol developed to contain the PSGN outbreak in this First Nations community can serve as a model for the management of future PSGN outbreaks.

POS-500 Is IgA nephropathy the chronic form of post streptococcal glomerulonephritis?

Acute post streptococcal glomerulonephritis (APSGN) results from a recent infection caused by nephritogenic strains of group a beta-hemolytic streptococci. On the other hand, there is a strong link between streptococcal tonsillitis and IgA nephropathy.

Poststreptococcal Glomerulonephritis without Hypertension in a Patient with Concealed Skin Lesions

Poststreptococcal Glomerulonephritis (PSGN) is an acute inflammation of renal glomerular parenchyma and is sequelae of pharyngitis or skin infection caused by nephritogenic strains of group A beta-Haemolytic Streptococcus. PSGN is conventionally diagnosed based upon clinical findings and demonstration of recent streptococcal infection by a positive skin/throat culture or serologic tests. Hereby, authors present a case of PSGN in an 18-year-old normotensive male is reported who presented with anasarca. On evaluation, the patient had subnephrotic range proteinuria without haematuria and normal serum creatinine. Concealed healing skin lesions in the gluteal region, suggestive of impetigo were noted and hence, arrived at the diagnosis of PSGN. He was treated with intravenous antibiotics, following which symptoms improved. Young patients with acute presentation of oedema or proteinuria with possible renal cause warrants thorough head to foot examination for unseen skin lesions in otherwise overlooked areas. PSGN responds promptly with early antibiotic therapy.

Etiopathogenetic, Morphological, Diagnostic and Therapeutic Aspects of Acute Glomerulonephritis: Current Status

The review provides up-to-date information on the etiological factors and pathogenic mechanisms of development, morphological changes, clinical and laboratory manifestations of acute glomerulonephritis, as well as therapeutic possibilities for its treatment. The review provides up-to-date information on the etiological factors and pathogenetic mechanisms of development, morphological changes, clinical and laboratory manifestations of acute glomerulonephritis, as well as therapeutic possibilities for its treatment. The epidemiological issues of acute post-streptococcal glomerulonephritis are presented, indicating the characteristics of the effects of nephritogenic strains of Streptococcal infection. The immunopathological reactions of the body in acute glomerulonephritis to the causative agent of the disease and its antigens with the development of an imbalance of subpopulations of T-lymphocytes, the nephritogenic potential of streptococcal proteins, a marker of active proliferation of mesangiocytes, C3 and C4 fractions of complement, and also the renin-angiotensin-aldosterone system are shown. The article emphasizes that the informational content of serological tests in acute glomerulonephritis increases while assessing the C3 and C4 fractions of serum complement. The pathological effects of angiotensin II and aldosterone on the renal tissue with the chronization of acute glomerulonephritis, the development of nephrotic proteinuria and a rapid decrease in renal function are presented. The data of a direct correlation between the severity of histological changes and the clinical manifestations of acute glomerulonephritis, possibly the prognosis, are shown. Presented are modern data on the assessment of the main clinical manifestations of acute glomerulonephritis (urinary syndrome, edema syndrome and arterial hypertension). When discussing the treatment of acute glomerulonephritis, the controversial issues of the use of antibiotic therapy, preventive tonsillectomy are noted. The literature data on the treatment options for edematous syndrome and arterial hypertension using thiazide and loop diuretics, calcium antagonists, beta-blockers, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers are presented. The issues of immunosuppressive therapy using glucorticoids, as well as prognostic criteria for acute glomerulonephritis are discussed.

An Unusual and Missed case of Streptococcal Pharyngitis Presenting as Membranoproliferative Glomerulonephritis; case Report

Streptococcal pharyngitis is common in the pediatric age group. Although its treatment is simply achieved by administration of a single dose of benzathine penicillin, oral penicillin for 10 days, or azithromycin for 5 days, it has serious complications such as rheumatic fever (RF) and chorea if left untreated. Treatment of pharyngitis does not prevent glomerulonephritis but prevents the spread of streptococci that can cause an epidemic in glomerulonephritis if they are of the nephritogenic strain. Post Streptococcal Glomerulonephritis (PSGN) is common in school age children and usually has a benign course as more than 95 percent of the cases recover the acute phase and less than 5 percent progress in their course to Rapidly Progressive Glomerulonephritis (RPGN) and ultimately about one percent develop End Stage Renal Failure (ESRF). Herein, we present a 12-year-old male with a history of untreated streptococcal pharyngitis who first came to our clinic with a history of arthralgia and arthritis, fatigue, hematuria, petechia, purpura, elevated levels of Blood Urea Nitrogen (BUN) and Creatinine (Cr), and low grade fever. Echocardiography revealed endocarditis which was treated. However, renal failure required renal replacement therapy (RRT), and massive proteinuria needed renal biopsy which revealed membrano proliferative glomerulonephritis (MPGN). Keywords: Streptococcal Infections; Membranoproliferative; Glomerulonephritis; Pharyngitis; Renal failure.

Acute Poststreptococcal Glomerulonephritis: The Most Common Acute Glomerulonephritis

Acute Poststreptococcal Glomerulonephritis: The Most Common Acute Glomerulonephritis

Acute Post-Streptococcal Glomerulonephritis in Children – A Review

Acute post-streptococcal glomerulonephritis (APSGN) is characterized by abrupt onset of hematuria, edema, hypertension, oliguria and impaired renal function following streptococcal group A â hemolytic streptococcal throat and skin infection. There is a declining incidence of APSGN worldwide, particularly in industrialized nations because of easier and earlier access to competent medical treatment of streptococcal infections and the widespread use of fluorination of water since virulence factors in streptococcus pyogens are reduced with fluoride exposure. But in the underdeveloped world, global burden of APSGN continues to be significant with lower estimate of 9.3 to 9.8 cases per 1,00,000 population per year to higher estimates as high as three times these values. Furthermore, clusters of cases are more frequently reported in poor communities in industrialized countries while epidemics of more than 100 cases are reported in the middle ranger countries with mean annual health expenditure per capita of about 550 US dollars. APSGN typically follows 1to2 weeks after pharyngeal infection and 2 to 4 weeks after skin infection by nephritogenic strains of group A â hemolytic streptococcus in a range of 5 – 15 years of age. Subclinical cases are 4 – 10 times higher than symptomatic patients. The acute phase generally resolves within 4-8 weeks but microscopic hematuria may persist for 1-2 yr after the initial presentation. Acute complications of symptomatic patients are hypertensive heart failure, encephalopathy and retinopathy. There can be acute renal failure and rarely rapidly progressive ( crescentic) glomerulonephritis, hyperkalemia, hyperphosphatemia, hypocalcemia and acidosis. Treatment is directed towards reduction of hypertension, but prompt address of complications are essential to avoid immediate mortality. Heart failure is treated with diuretic and anti-hypertensive, digoxin is ineffective. Hypertensive encephalopathy is treated by I.V phenobarbitone for convulsion, supportive measures for unconsciousness and blood pressure control. Acute renal failure is managed by supportive measures, rarely requires dialysis. Short and long term prognosis is excellent, with1% mortality during acute stage and 1% ending up with chronic kidney disease, but in higher age group abnormal urinalysis are present in higher number of patients. DOI: http://dx.doi.org/10.3329/bjch.v38i1.20025 Bangladesh J Child Health 2014; VOL 38 (1) : 32-39

Scabies: A Review of Diagnosis and Management Based on Mite Biology

Scabies is a contagious parasitic dermatitis that is a significant cause of morbidity, especially outside of the United States. Scabies is diagnosed most often by correlating clinical suspicion with the identification of a burrow. Although scabies should be on the differential for any patient who presents with a pruritic dermatosis, clinicians must consider a wide range of diagnostic possibilities. This approach will help make scabies simultaneously less over- and underdiagnosed by clinicians in the community. Atypical or otherwise complex presentations may necessitate the use of more definitive diagnostic modalities, such as microscopic examination of KOH prepared skin scrapings, high-resolution digital photography, dermoscopy, or biopsy. Scabies therapy involves making the correct diagnosis, recognizing the correct clinical context to guide treatment of contacts and fomites, choosing the most effective medication, understanding how to use the agent properly, and following a rational basis for when to use and reuse that agent. Although the development of new therapeutic agents is always welcome, tried and true treatments are still effective today. Permethrin is the gold standard therapy, with malathion being an excellent topical alternative. Ivermectin is an effective oral alternative that is especially useful in crusted scabies, patients who are bed ridden, and in institutional outbreaks. Despite the availability of effective therapeutics, treatment failures still occur, mostly secondary to application error (ie, failure to treat the face and scalp or close contacts, failure to reapply medication) or failure to decontaminate fomites. Because increasing resistance to scabies treatments may be on the horizon, we propose that standard of care for scabies treatment should involve routine treatment of the scalp and face and re-treating patients at day 4 on the basis of the scabies life cycle to ensure more efficient mite eradication. Practitioners should attempt to treat all close contacts simultaneously with the source patient. To eradicate mites, all fomites should be placed in a dryer for 10 minutes on a high setting, furniture and carpets vacuumed, and nonlaunderables isolated for a minimum of 2 days, or, for those who wish to be rigorous, 3 weeks.

Glomerulonefrite aguda após infecção de vias aéreas superiores ou pele: análise descritiva de 82 pacientes entre 14 e 64 anos de idade

Acute glomerulonephritis (AGN) after infection of the upper airways or skin is a kidney disease usually caused by streptococcal nephritogenic strains and may present with sudden onset of gross hematuria, hypertension, edema and, occasionally, acute renal failure, is common in childhood and little incident in adults and younger individuals. To analyze, in a descriptive way, data from the initial presentation of GNA after infection of the upper airways or skin in patients over 14 years of age, with emphasis on its epidemiological and clinical aspects. We reviewed the clinical data of 82 patients treated at our department during the period 1972-2001, divided into three groups: group 1, with individuals between 14 and 20 years (n = 52), group 2, between 21 and 30 years (n = 19) and group 3, aged ≥; 31 years (n = 11). There was a predominance of the table among younger patients (group 1), male and white, mostly preceded by infection of the skin, appearing most commonly on lower extremity edema and/or face. In some cases, even with nephrotic syndrome, and hypertension, especially in adults over 30 years (group 3), being the least frequent finding of gross hematuria, and rarely, acute renal failure. Our findings underscore the importance of studying the AGN after infection of the upper airways or skin in younger individuals and adults, seeking to better characterize its clinical, mainly because it is a group of patients where the disease is less incident.

M Protein Gene ( emm Type) Analysis of Group A Beta-Hemolytic Streptococci from Ethiopia Reveals Unique Patterns

The genetic diversity of group A streptococcal (GAS) isolates obtained in 1990 from Ethiopian children with various streptococcal diseases was studied by using emm gene sequence analysis. A total of 217 GAS isolates were included: 155 and 62 isolates from throat and skin, respectively. A total of 78 different emm/st types were detected among the 217 isolates. Of these, 166 (76.5%) belonged to 52 validated reference emm types, 26 (11.9%) belonged to 16 already recognized sequence types (st types) and 25 (11.5%) belonged to 10 undocumented new sequence types. Resistance to tetracycline (148 of 217) was not correlated to emm type. Isolation rate of the classical rheumatogenic and nephritogenic strains was low from cases of acute rheumatic fever (ARF) and acute glomerulonephritis (AGN), respectively. Instead, the recently discovered st types were overrepresented among isolates from patients with ARF (3 of 7) and AGN (9 of 16) (P < 0.01) compared to isolates from subjects with tonsillitis and from healthy carriers (10 of 57 and 16 of 90, respectively). In contrast to rheumatogenic strains from the temperate regions, more than half of the isolates from ARF (four of seven) carried the genetic marker for skin preference, emm pattern D, although most of them (six of seven) were isolated from throat. Of 57 tonsillitis-associated isolates, 16 (28%) belonged to emm pattern D compared to <1% in temperate regions. As in other reports emm patterns A to C were strongly associated with throat, whereas emm pattern D did not correlate to skin. This first large-scale emm typing report from Africa has demonstrated a heterogeneous GAS population and contrasting nature of GAS epidemiology in the region.

Glomerulonephritis associated with acute pneumococcal pneumonia: a case report

Streptococcus pyogenes is the most common cause of post-infectious glomerulonephritis. There have been isolated case reports of nephritis following infections with Streptococcus pneumoniae. We report here the case of a 6-year-old white female who presented with blood culture-confirmed pneumococcal pneumonia associated with glomerulonephritis. Her acute renal failure improved over several days, and renal function was normal by 8 weeks post-hospitalization. This case serves to reinforce the concept that other organisms besides Streptococcus pyogenes can trigger a similar post-infectious glomerulonephritis and should be considered in the differential diagnosis of any child who presents with acute glomerulonephritis and respiratory findings. Additionally, pneumococcus group 7 may be a nephritogenic strain and requires further investigation.

Molecular genetic analysis of a group A Streptococcus operon encoding serum opacity factor and a novel fibronectin-binding protein, SfbX.

The group A Streptococcus (GAS) sof gene encodes the serum opacity factor protein, which is capable of opacifying mammalian sera and binding at least two host proteins, fibronectin and fibrinogen. The sof gene exists in approximately 50% of clinical isolates, and there is a classical association of so-called nephritogenic strains with the opacity factor-positive phenotype. In both a type emm49 strain and a type emm12 strain, the sequences upstream of the 5' end of sof and downstream of the putative terminator were determined to be nearly identical to a region in the M type 1 genome approximately 10 kb upstream of the emm1 gene. This close genetic linkage is likely reflected in the strict correlation of opacity factor phenotype with specific emm genotypes. A new fibronectin-binding protein gene, sfbX, was discovered immediately downstream of sof in emm12 and emm49 strains and in several other sof-positive strains. The sof and sfbX genes were found to be expressed on the same transcription unit, which was correlated with the putative promoter and rho-independant terminator sequences that flank these two genes. The sfbX genes from different emm types are predicted to encode approximately 650-residue surface-bound proteins sharing 89 to 92% sequence identity. SfbX residues approximately 1 to 480 are not highly similar to those of other known proteins, with the closest match being the Staphylococcus aureus coagulase protein. The remaining portions of these proteins (residues 481 to 650) contain four putative fibronectin-binding repeats highly similar to those of other streptococcal fibronectin-binding proteins and a potential LP(X)SG cell wall anchor motif. Targeted in-frame allelic-exchange mutagenesis, complementation, and heterologous-expression studies found that serum opacification is encoded by sof alone and that sfbX encodes a fibronectin-binding function. A recombinant SfbX protein was found to bind immobilized fibronectin and to partially inhibit GAS adherence to fibronectin. The sfbX gene was found to be present only in sof-positive strains, and together these genes could influence the spectrum of tissues colonized by sof-positive GAS.

Poststreptococcal glomerulonephritis

Poststreptococcal glomerulonephritis is a nonsuppurative sequela of streptococcal infection that occasionally complicates pregnancy. Although group A beta-hemolytic streptococci are responsible for the majority of cases, multiple groups of streptococci can cause postinfectious glomerulonephritis. Infection of the skin or pharynx with streptococci typically precedes kidney involvement by 6 days to 2 weeks. The risk of developing acute nephritis after streptococcal infection ranges from 1–15%. This disorder usually affects children, and is more frequent in males. Poststreptococcal glomerulonephritis is considered an immune complex disease because interactions between antigen–antibody complexes and the complement system result in glomerular injury. Patients present with a wide range of complaints including hematuria, edema, malaise, lethargy, nausea, fever, weakness, anorexia, cough, and dyspnea. The most common exam findings include hypertension, edema, and hematuria. The differential diagnosis includes multisystem disease, other primary glomerular diseases, nonstreptococcal postinfectious glomerulonephritis, and urinary tract infection. The diagnosis is confirmed by the detection of antistreptococcal antibodies, and renal biopsy showing hypercellularity and proliferation. Treatment is supportive, and renal function tends to improve rapidly. Antibiotics are indicated if the patient is concurrently infected. Penicillin is the drug of choice, but erythromycin can be used in the penicillin-allergic patient. Immunity is lifelong, but recurrences may develop after infection with a different nephritogenic strain. If signs of irreversible kidney damage are present, the disease is considered chronic. Presentation in pregnancy may be confused with preeclampsia as hypertension, edema, and proteinuria are presenting signs in both entities. Poststreptococcal glomerulonephritis may lead to preterm delivery but typically has a successful outcome.

Allele substitution of the streptokinase gene reduces the nephritogenic capacity of group A streptococcal strain NZ131.

To investigate the role of allelic variants of streptokinase in the pathogenesis of acute poststreptococcal glomerulonephritis (APSGN), site-specific integration plasmids were constructed, which contained either the non-nephritis-associated streptokinase gene (skc5) from the group C streptococcal strain Streptococcus equisimilis H46A or the nephritis-associated streptokinase gene (ska1) from the group A streptococcal nephritogenic strain NZ131. The plasmids were introduced by electroporation and homologous recombination into the chromosome of an isogenic derivative of strain NZ131, in which the streptokinase gene had been deleted and which had thereby lost its nephritogenic capacity in a mouse model of APSGN. The introduction of a non-nephritis-associated allelic variant of streptokinase did not rescue the nephritogenic capacity of the strain. The mutant and the wild-type strains produced equivalent amounts of streptokinase. Complementation of the ska deletion derivative with the original ska allele reconstituted the nephritogenicity of wild-type NZ131. The findings support the hypothesis that the role of streptokinase in the pathogenesis of APSGN is related to the allelic variant of the protein.