The virulence and adhesive properties of 50 isolates of Candida albicans serotypes A and B collected over 6 years from 48 paediatric burn patients were examined to provide more detailed information about candidal pathogenesis in burn patients and to examine the relevance of the commonly used epithelial cell adhesion assay for determining fungal virulence. The isolates represented a fair distribution of serotypes (29 isolates were serotype A and 21 isolates were serotype B) and a total of 28 serotype-biotype combinations were found; 32% of the serotype-biotype combinations appeared only once, while 44% of the isolates showed similar biotype tests for two of three digits. Adhesion of the isolates to plastic and to buccal epithelial cells (BECs) was examined and compared after growth in a chemically defined medium. There were significant differences in the adhesion of individual isolates to plastic or BECs, but no correlation was found between biotype and adhesiveness. Serotype B isolates were found to be more adhesive to BECs (p<0.05) but not to plastic. There was no apparent correlation between candidal adhesiveness and site of isolation from these patients (autografts, blood, faeces, throat swabs, tracheal aspirates, wounds and intravenous catheters), although isolates from catheters were generally less adhesive to epithelial cells. Virulence in a systemic infection mouse model revealed that there were significant differences in virulence between isolates, but no correlation was found between virulence and the biotype, serotype or site of isolation. Similarly, no correlation was found between virulence and adhesiveness or cell-surface hydrophobicity. These results suggest that, although variations in adhesiveness between isolates of C. albicans can be detected in an epithelial cell adhesion assay, such tests may not be useful as reliable predictors of virulence. These data also suggest that candidal pathogenesis is the result of a multifactorial process whereby, in some instances, adhesion may play only a transient role in infection.
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