![]() ![]() In some regions of the world, GAS resistance to antibiotics such as macrolides, clindamycin, and lincosamide has become an increasing concern ( 25, – 28, 30), and epidemiological vigilance is required to ensure that treatment matches the antibiotic sensitivity profile of circulating GAS strains. GAS remains exquisitely and universally sensitive to penicillin, while antibiotics such as cephalosporins, macrolides, and clindamycin are also used clinically ( 27, – 29). Treatment regimens for GAS infections naturally center on the use of appropriate antibiotics. However, in the last 50 years, there have been widespread reports of significant outbreaks of ARF ( 15, 16), APSGN ( 17, 18), GAS invasive disease ( 14, 19, – 21), puerperal sepsis ( 22, – 24), and scarlet fever ( 25, 26). Several studies had noted a reduction in GAS disease burden in industrialized countries in the mid-20th century ( 11, – 14). Global disease burden figures reported by the World Health Organization (WHO) rank GAS as the ninth leading infectious cause of human mortality, with the majority of deaths being attributable to invasive infections and RHD, primarily in nonindustrialized countries ( 5, 10). In addition, GAS infection can trigger serious postinfectious immune-mediated disorders, including acute poststreptococcal glomerulonephritis (APSGN), acute rheumatic fever (ARF), and rheumatic heart disease (RHD) ( 5, – 9). GAS causes a diverse range of human infections, both benign and serious, which include pharyngitis, impetigo, cellulitis, scarlet fever, puerperal sepsis, bacteremia, pneumonia, streptococcal toxic shock syndrome (STSS), necrotizing fasciitis, and endocarditis. ![]() Over 100 years later, a safe and effective commercial vaccine against Streptococcus pyogenes (group A Streptococcus ) is still not licensed for human use ( 2, – 4). One 24-year-old male subject, presenting with endocarditis and a history of scarlatina and acute rheumatic fever, received 16 doses of vaccine over a 3-month period, prepared from streptococci isolated from the subject's own blood, yet died 7 days after the final dose ( 1). In 1909, Meakins reported serotype-specific immunity stimulated by experimental vaccination of humans against streptococci. The development of a safe and efficacious commercial human vaccine for the prophylaxis of GAS disease remains a high priority. Several GAS vaccine formulations that elicit protective immunity in animal models have shown promise in nonhuman primate and early-stage human trials. While GAS remains sensitive to all penicillins and cephalosporins, rising resistance to other antibiotics used in disease treatment is an increasing worldwide concern. 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. 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. Combined, these diseases account for over half a million deaths per year globally. Furthermore, repeated GAS infections may trigger autoimmune diseases, including acute poststreptococcal glomerulonephritis, acute rheumatic fever, and rheumatic heart disease. ![]() 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. ![]()
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