A long time has passed since the first Kawasaki disease patient was identified in Japan by Dr. Tomisaku Kawasaki and yet no agreement on its cause and potential agent/s has consistently emerged. Different theories suggested different epidemiological pathways, ranging from a typical infectious disease to different kinds of exacerbated host responses in susceptible children being exposed to one or more noninfectious environmental triggers. Some consensus existed, however, that whatever the trigger was, it enters through the mucosa of the upper respiratory tract. Therefore, assuming that the KD agent is carried by the wind, cases should occur simultaneously in neighboring towns due to the large scale reach of wind patterns and/or propagate fast through infection. The study effectively showed how in cities belonging to the greater Tokyo area on average separated around 30Km, peak incidences of Kawasaki disease occurred simultaneously, that is the same day or one day apart. The epidemiological study showed maximum coherence in the daily variability of Kawasaki patients in cities like Tokyo, Yokohama, Saitama and Chiba. Applying a mathematical model for infectious diseases further confirmed that not even the fastest infectious agent could display on the basis of secondary cases, such a rapid propagation as the one seen for this disease. Therefore, our study discards the action of an infectious agent having to replicate in the host coursing as an infection, and instead favors as the most likely trigger, the role of an idiosyncratic immune response to an environmental particle or toxin.
Article PNAS-USA Number #14-00380 (2014): “Tropospheric winds from northeastern China carry the etiologic agent of Kawasaki disease from its source to Japan” by Xavier Rodó et al.