Abstract 111

Kawasaki disease (KD) is a paediatric inflammatory disease and is the most common cause of acquired heart disease in children in developed countries. The cause of KD is unknown but epidemiological data indicate that it is most likely to be an infectious agent. The clinical features of KD are consistent with either bacterial or fungal infection rather than a virus, as KD is associated with an intense inflammatory process. It has been suggested that the oral and respiratory mucosa are the primary site of infection as the initial infection in KD patients is likely to be in the mucosal surfaces of the respiratory track with prominent lymphadenopathy and oral mucous membrane inflammation. This study examines whether the agent causing KD induces disease through production of novel toxins, or inflammation inducing antigens in the supernatants of cultured bacteria isolated from KD patients and healthy controls. Throat swabs were collected from children with KD (n=14), other diseases (n=10) and healthy children (n=8), and were inoculated into growth medium, incubated and then centrifuged. The supernatants were collected and toxicity was measured by microscopic observation as well as by resazurin dye reduction of cells after growth in the presence of the KD or control supernatant. An effect of the toxins in activating inflammation was also tested by the addition of the supernatants to healthy donor peripheral blood mononuclear cells (PBMCs) and measurement of interleukin 6 production by Enzyme linked immune assay (ELISA). There was no significant difference in the reduction of cells after growth between control and KD supernatants. No difference in the production of IL-6 was observed between the three groups. Further analysis and larger sample size are required to establish whether novel toxins are present in cultured supernatants of KD patients.