While the incidence of many diseases has declined in developed countries, regions of the world with low income and poor infrastructure continue to suffer a high burden of Streptococcus pyogenes (group A streptococci) diseases with millions of deaths yearly (Carapetis, Steer, Mulholland, & Weber, 2005). The majority of these deaths follow the development of rheumatic heart disease (RHD), which remains a concern in both developed and developing countries. In more affluent countries, the prevalence of RHD is much lower; the majority of S. pyogenes-associated deaths are attributed to the clinical manifestations associated with invasive disease.
Our general understanding of the epidemiology of group A streptococci and their related diseases remains relatively poor in comparison to other infectious diseases. Many countries with established infectious disease surveillance programs undertake relatively little surveillance of diseases caused by S. pyogenes and other pyogenic streptococci. However, this has improved over the years with many countries establishing the presence of invasive group A streptococcal infections as a statutory notifiable disease. To fully understand the epidemiology of these diseases in terms of how they disseminate, the host and strain characteristics of importance to onward transmission, disease severity, and both inter- and intraspecies competition for ecological niches, researchers would need to undertake comprehensive investigations that follow a large cohort of individuals for a substantial period of time. Understanding these factors would also allow for the development of effective prevention strategies. The size and severity of the burden of S. pyogenes disease highlights the importance of epidemiologic surveillance to detect changes in disease distribution in various populations.
Since the early 1980s, there have been some remarkable changes in the worldwide epidemiology of group A streptococcal infections, particularly in the reporting of invasive group A streptococcal infections. Outbreaks of infection of both suppurative and non-suppurative S. pyogenes sequelae were frequently reported in the 1980s and 1990s (Efstratiou, 2000). The increase in the incidence of invasive S. pyogenes infections has frequently been associated with specific clones, which raises the possibility that the rise of particularly virulent clones was responsible for this re-emergence—in particular, the MT1 clone which is dominant among invasive S. pyogenes isolates in most developed countries (Luca-Harari, et al., 2009; O'Loughlin, et al., 2007). The incidence of invasive S. pyogenes infection varies by time and geographic region, which presumably reflects a population’s susceptibility to particular strains, but also the natural variation in the predominant types (O'Brien, et al., 2002). Variation in the type distribution may also lead to fluctuations in the severity of infections and in overall mortality rates.
S. pyogenes infections may be observed in persons of any age, although the prevalence of infection is higher in children, presumably because of the combination of multiple exposures (in schools or nurseries, for example) and host immunity. The prevalence of pharyngeal infection is highest in children older than three years and has been described as a ‘hazard’ in school-aged children (Martin, Green, Barbadora, & Wald, 2004). Disease in neonates is uncommon, which may reflect a protective, transplacentally-acquired immunity.
For this chapter, we will focus upon the epidemiology of S. pyogenes infection, with emphasis on the novel molecular genomics approaches that are being applied to global epidemiology, as well as the prevention, control, and management of these devastating diseases.
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