ABSTRACT
S. pyogenes, also known as the group A streptococcus (GAS), is the most common cause of bacterial pharyngitis. However, the vast majority of cases (about 70%) of pharyngitis are caused by viruses. GAS is a gram-positive, catalase-negative coccus that grows in chains. It grows readily on blood agar incubated at 37°C in the presence of 5% CO2 for 24–48 hours, forming small, gray opalescent colonies surrounded by a large zone of complete hemolysis (β-hemolysis). GAS has a typical gram-positive-type cell wall. M protein which extends from the wall is the most important virulence factor of GAS. There are over 200 types of M protein. GAS has many determinants of pathogenesis that include lipoteichoic acid (pro-inflammatory), adhesins, superantigens (pyrogenic exotoxins), cytotoxins (streptolysin O and S), hydrolytic enzymes and a capsule. GAS is spread person-to-person via respiratory droplets, the hands, and fomites. The bacterium adheres to and invades epithelial cells from where it can extend to subcutaneous tissues and seed the lymphatics and bloodstream. The barrier epithelia, in concert with innate immune factors at these surfaces, are effective barriers to the penetration of GAS. Opsonophagocytosis mediated by the complement cascade, neutrophils and anti-M protein antibodies is central to the clearance of GAS. The virulence of GAS results from its ability to adhere to and invade host cells and to avoid opsonization and phagocytosis by means of capsule, M protein, and C5a peptidase and other determinants of pathogenesis. The hemolysins, streptolysin S and O, are cytotoxins that can lyse erythrocytes, leukocytes, and platelets and likely other host cells. Pyrogenic exotoxins (erythrogenic toxins) are superantigens that result in the release of pro-inflammatory cytokines that mediate shock and organ failure characteristic of streptococcal toxic shock syndrome and give rise to the rash associated with scarlet fever. GAS causes a spectrum of infections ranging from superficial such as pharyngitis and impetigo to invasive such as necrotizing fasciitis and streptococcal toxic shock syndrome. In addition, GAS gives rise to acute rheumatic fever and acute glomerulonephritis that are post-streptococcal forms of immune tissue injury that result from molecular mimicry. Gas is readily identified by gram stain and culture on blood agar as gram-positive, catalase-negative cocci whose colonies are surrounded by a large zone of β-hemolysis. The bacteria are susceptible to bacitracin and are PYR-positive. Rapid tests based on immunologic detection of the Lancefield group A wall carbohydrate antigen are available to directly detect GAS on throat swabs; a negative rapid test must be confirmed by culture. GAS infections are treated with penicillin in patients who are not hypersensitive, otherwise erythromycin or a cephalosporin can be used. Antibiotic treatment of GAS pharyngitis prevents the development of rheumatic fever. Serious soft-tissue infections require drainage and surgical debridement as the first line of therapy. Prophylactic antibiotic therapy is required for several years in individuals who have had rheumatic fever.
