Chapter 130. Streptococcal and Enterococcal Infections (Part 2)

Group A StreptococciLancefields group A consists of a single species, S. pyogenes. As its species name implies, this organism is associated with a variety of suppurative infections. In addition, GAS can trigger the postinfectious syndromes of ARF (which is uniquely associated with S. pyogenes infection; Chap. 315) and PSGN (Chap. 277).Worldwide, GAS infections and their postinfectious sequelae (primarily ARF and rheumatic heart disease) account for an estimated 500,000 deaths per year. Although data are incomplete, the incidence of all forms of GAS infection and that of rheumatic heart disease are thought to be tenfold higher in resourcelimited countries than...
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Chapter 130. Streptococcal and Enterococcal Infections (Part 2) Chapter 130. Streptococcal and Enterococcal Infections (Part 2) Group A Streptococci Lancefields group A consists of a single species, S. pyogenes. As itsspecies name implies, this organism is associated with a variety of suppurativeinfections. In addition, GAS can trigger the postinfectious syndromes of ARF(which is uniquely associated with S. pyogenes infection; Chap. 315) and PSGN(Chap. 277). Worldwide, GAS infections and their postinfectious sequelae (primarilyARF and rheumatic heart disease) account for an estimated 500,000 deaths peryear. Although data are incomplete, the incidence of all forms of GAS infectionand that of rheumatic heart disease are thought to be tenfold higher in resource-limited countries than in developed countries (Fig. 130-1). Figure 130-1 Prevalence of rheumatic heart disease in children 5–14 years old. Thecircles within Australia and New Zealand represent indigenous populations (andalso Pacific Islanders in New Zealand). (From Carapetis et al, 2005, withpermission.) Pathogenesis GAS elaborates a number of cell-surface components and extracellularproducts important in both the pathogenesis of infection and the human immuneresponse. The cell wall contains a carbohydrate antigen that may be released byacid treatment. The reaction of such acid extracts with group A–specific antiserumis the basis for definitive identification of a streptococcal strain as S. pyogenes.The major surface protein of GAS is M protein, which occurs in more than 100antigenically distinct types and is the basis for the serotyping of strains withspecific antisera. The M protein molecules are fibrillar structures anchored in thecell wall of the organism that extend as hairlike projections away from the cellsurface. The amino acid sequence of the distal or amino-terminal portion of the Mprotein molecule is quite variable, accounting for the antigenic variation of thedifferent M types, while more proximal regions of the protein are relativelyconserved. A newer technique for assignment of M type to GAS isolates uses thepolymerase chain reaction to amplify the variable region of the M protein gene.DNA sequence analysis of the amplified gene segment can be compared with anextensive database [developed at the Centers for Disease Control and Prevention(CDC)] for assignment of M type. This method eliminates the need for typingsera, which are available in only a few reference laboratories. The presence of Mprotein on a GAS isolate correlates with its capacity to resist phagocytic killing infresh human blood. This phenomenon appears to be due, at least in part, to thebinding of plasma fibrinogen to M protein molecules on the streptococcal surface,which interferes with complement activation and deposition of opsoniccomplement fragments on the bacterial cell. This resistance to phagocytosis maybe overcome by M protein–specific antibodies; thus individuals with antibodies toa given M type acquired as a result of prior infection are protected againstsubsequent infection with organisms of the same M type but not against that withdifferent M types. GAS also elaborates, to varying degrees, a polysaccharide capsulecomposed of hyaluronic acid. The production of large amounts of capsule bycertain strains lends a characteristic mucoid appearance to the colonies. Thecapsular polysaccharide plays an important role in protecting GAS from ingestionand killing by phagocytes. In contrast to M protein, the hyaluronic acid capsule isa weak immunogen, and antibodies to hyaluronate have not been shown to beimportant in protective immunity. The presumed explanation is the apparentstructural identity between streptococcal hyaluronic acid and the hyaluronic acidof mammalian connective tissues. The capsular polysaccharide may also play arole in GAS colonization of the pharynx by binding to CD44, a hyaluronic acid–binding protein expressed on human pharyngeal epithelial cells. GAS produces a large number of extracellular products that may beimportant in local and systemic toxicity and in the spread of infection throughtissues. These products include streptolysins S and O, toxins that damage cellmembranes and account for the hemolysis produced by the organisms;streptokinase; DNases; protease; and pyrogenic exotoxins A, B, and C. Thepyrogenic exotoxins, previously known as erythrogenic toxins, cause the rash ofscarlet fever. Since the mid-1980s, pyrogenic exotoxin–producing strains of GAShave been linked to unusually severe invasive infections, including necrotizingfasciitis and the streptococcal toxic shock syndrome. Several extracellularproducts stimulate specific antibody responses useful for serodiagnosis of recentstreptococcal infection. Tests for these antibodies are used primarily for detectionof preceding streptococcal infection in cases of suspected ARF or PSGN.