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INTRODUCTION

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Descriptions of what were likely Streptococcus pyogenes infections are found in the earliest written records of human history. S pyogenes was likely responsible for the apparent scarlet fever epidemic described by Hippocrates in the 5th century BC. The first modern description of streptococcal infection was the demonstration of the organism in patients with erysipelas and wound infection in 1874. The organism was designated Streptococcus pyogenes by Rosenbach in the late 19th century. In the early 1930s, Rebecca Lancefield’s classification of the β-hemolytic strains into characteristic distinct serogroups led to the recognition that serogroup A isolates (S pyogenes) were the strains most commonly responsible for pharyngitis and impetigo/pyoderma. S pyogenes is one of the most important infectious agents encountered in clinical practice causing infections of the upper respiratory tract and skin. S pyogenes also causes a variety of severe systemic infections, including toxic shock syndrome and life-threatening skin and soft tissue infections. Infection with this pathogen is also causally linked to 2 serious nonsuppurative complications, acute rheumatic fever and acute glomerulonephritis.

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PATHOGENESIS AND EPIDEMIOLOGY

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Streptococci are gram-positive cocci that tend to grow as pairs and chains. When cultured on sheep or horse blood agar plates, a characteristic zone of complete hemolysis (β-hemolysis) is observed. S pyogenes (group A streptococci) may be identified either by serologic means or latex agglutination techniques. Additional typing of group A streptococci for epidemiologic purposes is based on variation in the M and T proteins and emm genes (see below). The somatic cellular constituents as well as the extracellular enzymes and toxins responsible of S pyogenes are responsible for many of pathogenic effects observed in vivo. These also are summarized in Table 280-1. The major virulence factor of the organism is the M protein. This protein is anchored to the cell membrane and transverses and penetrates the cell wall. Functionally, the M proteins inhibit phagocytosis, which is a primary virulence mechanism for survival in tissues. Immunity to M protein appears to be a key determinant in protection against infection. In the nonimmune host, M protein mediates its antiphagocytic effect by inhibiting activation of the alternate complement pathway. Genes related to the M protein gene (emm) are called the M gene superfamily and include immunoglobulin-binding proteins. Other streptococcal cell wall antigens are important in the pathogenesis and epidemiologic typing of S pyogenes. Most strains are enveloped in a hyaluronic acid capsule that serves as an accessory virulence factor by inhibiting phagocytosis. Lipoteichoic acid and protein F are cell wall constituents that play roles in the adherence of S pyogenes to fibronectin on the surface of human epithelial cells, an important event in the initiation of the infectious process. Serum opacity factor (OF) is a lipoproteinase associated with M protein that is useful in classifying strains that are not identifiable by M typing.

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Table Graphic Jump Location
Table 280-1Summary of the Molecular Determinants Responsible for ...

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