Abstract 1025 Poster Session IV, Tuesday, 5/4 (poster 135)

The etiology and pathogenesis of Kawasaki Syndrome (KS) remain unknown. Clinical and epidemiologic features are consistent with an infectious cause. Studies of IgA plasma cells in vascular tissue of children with KS suggest an antigen driven immune response to an etiologic agent with a respiratory or GI portal of entry. Cpn is a common cause of community acquired respiratory disease in children and adults. Recent studies have suggested that Cpn may play a role in the development of atherosclerosis. This association has been based on serology and identification of Cpn by culture, PCR, EM or immunostaining in atheromatous tissue. A recent study from Japan found that children with KS were more likely to have anti-Cpn IgM antibody (by microimmunofluorescence-MIF) than controls. However, studies from our laboratory have found a poor correlation between MIF and Cpn culture in children with respiratory infection. To determine any possible relationship between KS and Cpn, paired sera (baseline and 1 yr) from 26 children with KS and single sera from 12 matched controls were examined by MIF and immunoblotting. There were no significant differences in the prevalence of anti-Cpn IgG, IgA or IgM between KS children and controls by MIF, as shown in the table. 61% of KS and 75% of controls were seronegative, 1 each had IgG ≥512, which is felt to indicate acute infection, 1 KS had IgM 16. Over 85% sera from KS and controls reacted with Cpn proteins by immunoblotting, however reactivity to some major proteins differed. There was no significant difference in the reaction to the major outer membrane protein(MOMP)(39-42kD), 6(23%) vs. 2(16.7%). But there was significantly higher reactivity in the KS sera compared to controls to 19-20 kD (69% vs. 8.3%), 64-65 kD (57.7% vs. 16.7%), 68-72 kD (50% vs. 0). The lack of response to the MOMP has also been seen in children with Cpn pneumonia, the MOMP does not appear to be immunodominant in Cpn infection. The 64-65 and 68-72 kD proteins may be heat shock proteins. Chlamydial and human HSP are highly conserved, thus this response may not be specific for Cpn. Serology has limitations in the diagnosis of Cpn infection, most children with + Cpn cultures are MIF negative. Confirmation of an association of Cpn and KS may require identification of the organism in tissue by culture or PCR.

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