Abstract
Detailed epidemiologic examination of the distribution of Kawasaki disease (KD) cases could help elucidate the etiology and pathogenesis of this puzzling condition. Location of residence at KD admission was obtained for patients diagnosed in Canada (excluding Quebec) between March 2004 and March 2015. We identified 4,839 patients, 164 of whom (3.4%) developed a coronary artery aneurysm (CAA). A spatiotemporal clustering analysis was performed to determine whether non-random clusters emerged in the distributions of KD and CAA cases. A high-incidence KD cluster occurred in Toronto, ON, between October 2004 and May 2005 (116 cases; relative risk (RR) = 3.43; p < 0.001). A cluster of increased CAA frequency emerged in Mississauga, ON, between April 2004 and September 2005 (17% of KD cases; RR = 4.86). High-incidence clusters also arose in British Columbia (November 2010 to March 2011) and Alberta (January 2010 to November 2012) for KD and CAA, respectively. In an exploratory comparison between the primary KD cluster and reference groups of varying spatial and temporal origin, the main cluster demonstrated higher frequencies of conjunctivitis, oral mucosa changes and treatment with antibiotics, suggesting a possible coincident infectious process. Further spatiotemporal evaluation of KD cases might help understand the probable multifactorial etiology.
Highlights
Kawasaki disease (KD) is an acute, mucocutaneous illness of unknown etiology[1]
We explored the spatiotemporal distribution of both KD cases and coronary artery aneurysm (CAA) complications in Canada between March 2004 and March 2015, with the goal of identifying non-random clusters that might help explain the association between occurrence and infectious and/ or environmental phenomena
The vast majority of KD and CAA cases occurred in children less than 5 years of age
Summary
Kawasaki disease (KD) is an acute, mucocutaneous illness of unknown etiology[1]. First reported in 19672, KD primarily affects children younger than 5 years of age and is indicated by a constellation of clinical signs including vasculitis, which can lead to arterial complications[3], namely coronary artery aneurysms (CAA)[4]. Given uncertainty regarding the etiology and specific treatment, efforts are ongoing to elucidate the genetic, environmental and infectious causes of KD and the optimal strategies to prevent complications[7,8,9]. While the genetic susceptibility for KD within certain population groups is well-documented, with the observation of consistently-higher incidence rates amongst those of East Asian descent[10], the possible environmental and infectious causes remain unclear. The documented seasonality of KD11 and its frequent co-occurrence with infection[12,13] has led many to conclude that KD is associated with an environmental and/or infectious trigger inciting an extreme inflammatory response in genetically-susceptible children[14]. We explored the spatiotemporal distribution of both KD cases and CAA complications in Canada between March 2004 and March 2015, with the goal of identifying non-random clusters that might help explain the association between occurrence and infectious and/ or environmental phenomena
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