<span class="paragraphSection"><div class="boxTitle">Abstract</div><div class="boxTitle">Background.</div>Invasive group A <span style="font-style:italic;">Streptococcus</span> (iGAS) disease caused by type <span style="font-style:italic;">emm89</span> strains has been increasing worldwide, driven by the emergence of an epidemic clonal variant (clade 3 <span style="font-style:italic;">emm89</span>). The clinical characteristics of patients with <span style="font-style:italic;">emm89</span> iGAS disease, and in particular with clade 3 <span style="font-style:italic;">emm89</span> iGAS disease, are poorly described.<div class="boxTitle">Methods.</div>We used population-based iGAS surveillance data collected in metropolitan Toronto, Ontario, Canada during the period 2000–2014. We sequenced the genomes of 105 <span style="font-style:italic;">emm89</span> isolates representing all <span style="font-style:italic;">emm89</span> iGAS disease cases in the area during the period and 138 temporally matched <span style="font-style:italic;">emm89</span> iGAS isolates collected elsewhere in Ontario.<div class="boxTitle">Results.</div>Clades 1 and 2 and clade O, a newly discovered <span style="font-style:italic;">emm89</span> genetic variant, caused most cases of <span style="font-style:italic;">emm89</span> iGAS disease in metropolitan Toronto before 2008. After rapid emergence of new clade 3, previously circulating clades were purged from the population and the incidence of <span style="font-style:italic;">emm89</span> iGAS disease significantly increased from 0.14 per 100000 in 2000–2007 to 0.22 per 100000 in 2008–2014. Overall, <span style="font-style:italic;">emm89</span> organisms caused significantly more arthritis but less necrotizing fasciitis than strains of the more common type <span style="font-style:italic;">emm1</span>. Other clinical presentations were soft tissue and severe respiratory tract infections. Clinical outcomes did not differ significantly between <span style="font-style:italic;">emm89</span> clades overall. However, clade 3 <span style="font-style:italic;">emm89</span> iGAS disease was more common in youth and middle-aged individuals.<div class="boxTitle">Conclusions.</div>The rapid shift in <span style="font-style:italic;">emm89</span> iGAS strain genetics in metropolitan Toronto has resulted in a significant increase in the incidence of <span style="font-style:italic;">emm89</span> iGAS disease, with noticeably higher rates of clade 3 disease in younger patients.</span>
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