Streptococcus

About: Streptococcus is a research topic. Over the lifetime, 2145 publications have been published within this topic receiving 61790 citations.

Pathogenesis of Group A Streptococcal Infections

Abstract: Group A streptococci are model extracellular gram-positive pathogens responsible for pharyngitis, impetigo, rheumatic fever, and acute glomerulonephritis. A resurgence of invasive streptococcal diseases and rheumatic fever has appeared in outbreaks over the past 10 years, with a predominant M1 serotype as well as others identified with the outbreaks. emm (M protein) gene sequencing has changed serotyping, and new virulence genes and new virulence regulatory networks have been defined. The emm gene superfamily has expanded to include antiphagocytic molecules and immunoglobulin-binding proteins with common structural features. At least nine superantigens have been characterized, all of which may contribute to toxic streptococcal syndrome. An emerging theme is the dichotomy between skin and throat strains in their epidemiology and genetic makeup. Eleven adhesins have been reported, and surface plasmin-binding proteins have been defined. The strong resistance of the group A streptococcus to phagocytosis is related to factor H and fibrinogen binding by M protein and to disarming complement component C5a by the C5a peptidase. Molecular mimicry appears to play a role in autoimmune mechanisms involved in rheumatic fever, while nephritis strain-associated proteins may lead to immune-mediated acute glomerulonephritis. Vaccine strategies have focused on recombinant M protein and C5a peptidase vaccines, and mucosal vaccine delivery systems are under investigation.

Pathogenesis of group A streptococcal infections.

Abstract: Group A Streptococcus (GAS; Streptococcus pyogenes) is a human pathogen which causes significant morbidity and mortality globally. GAS typically infects the throat and skin of the host, causing mild infections such as pharyngitis and impetigo, in addition to life threatening conditions including necrotizing fasciitis, streptococcal toxic shock syndrome (STSS), and bacteremia. Repeated infection with GAS may result in the non-suppurative sequelae, acute rheumatic fever, and acute glomerulonephritis. GAS remains sensitive to the antibiotic penicillin which can be administered as a means to treat infection or as prophylaxis. However, issues with patient compliance and a growing concern over the possible emergence of resistant GAS strains may limit the usefulness of antibiotics in the future. A vaccine capable of preventing GAS infection may be the only effective way to control and eliminate GAS infection and disease.

Invasive Group A Streptococcus Infections

Abstract: The late 1980s have witnessed the emergence of severe group A streptococcus (GAS) infection; shock, bacteremia, and acute respiratory distress syndrome are common features, and death has been associated with this infection in 30% of patients. Such infections have now been described in all parts of the United States, Europe, and Australia and have occurred predominantly in otherwise healthy adolescents and adults. The characteristic clinical and laboratory features of the streptococcal toxic shock syndrome include deep-seated infection associated with shock and multiorgan failure. Strains of GAS isolated from patients with invasive disease have been predominantly M types 1 and 3, which produce pyrogenic exotoxin A or B or both. In this report, the clinical and demographic features of streptococcal bacteremia, myositis, and necrotizing fasciitis will be presented and compared with those of streptococcal toxic shock syndrome. Current concepts of the pathogenesis of invasive streptococcal infection will also be presented in terms of the interaction between virulence factors of GAS and host defense mechanisms. Finally, new concepts for future treatment of serious streptococcal infections will be proposed.

Disease Manifestations and Pathogenic Mechanisms of Group A Streptococcus

Abstract: Streptococcus pyogenes, also known as group A Streptococcus (GAS), causes mild human infections such as pharyngitis and impetigo and serious infections such as necrotizing fasciitis and streptococcal toxic shock syndrome. Furthermore, repeated GAS infections may trigger autoimmune diseases, including acute poststreptococcal glomerulonephritis, acute rheumatic fever, and rheumatic heart disease. Combined, these diseases account for over half a million deaths per year globally. Genomic and molecular analyses have now characterized a large number of GAS virulence determinants, many of which exhibit overlap and redundancy in the processes of adhesion and colonization, innate immune resistance, and the capacity to facilitate tissue barrier degradation and spread within the human host. This improved understanding of the contribution of individual virulence determinants to the disease process has led to the formulation of models of GAS disease progression, which may lead to better treatment and intervention strategies. While GAS remains sensitive to all penicillins and cephalosporins, rising resistance to other antibiotics used in disease treatment is an increasing worldwide concern. Several GAS vaccine formulations that elicit protective immunity in animal models have shown promise in nonhuman primate and early-stage human trials. The development of a safe and efficacious commercial human vaccine for the prophylaxis of GAS disease remains a high priority.

Defining the Group A Streptococcal Toxic Shock Syndrome: Rationale and Consensus Definition

Abstract: GROUP A streptococcus (Streptococcus pyogenes) may cause a variety of illnesses ranging from very common, usually clinically mild conditions such as pharyngitis and impetigo to less common severe infections including septicemia and pneumonia. In 1987, Cone et al1described two patients with severe group A streptococcal infections having clinical features similar to the staphylococcal toxic shock syndrome. This syndrome, designated the "streptococcal toxic shock—like syndrome" or the "toxic streptococcal syndrome,"2was further characterized by Stevens et al3in a series of 20 patients. Most patients included in this series were less than 50 years old and otherwise healthy. All had invasive group A streptococcal infections characterized by signs including shock, multi—organ system involvement, and rapidly progressive, destructive soft-tissue infection (necrotizing fasciitis). The case-fatality rate was 30% even though most patients received appropriate antimicrobial therapy, supportive care, and, where necessary, surgical debridement. Ten available isolates were serotyped and