dublinienis isolates (r = 0.452; P = 0.046). However, the difference in the effect elicited by nystatin on CSH did not have a positive relationship with the clampdown of adhesion to BEC (r = 0.127; P = 0.584)

and GT formation (r = 0.106; P = 0.658). C. dubliniensis is now well recognised as an opportunistic emerging pathogen associated with oral Doxorubicin mouse candidosis. Particular attention has been paid to studying candidal adhesion to BECs of the oral mucosa, as it is intimately associated with all forms of oral candidosis.[8, 9] In addition, GT, which marks the onset of hyphal growth, is a phenotypic characteristic associated with candidal adhesion. One reason for the pathogenic nature of C. dubliniensis may be its ability to transform from the blastospore or yeast phase to the mycelial or hyphal phase.[26] For instance, candidal hyphae are thigmotrophic Pirfenidone in nature and traverse along surface irregularities both in vivo and in vitro, thus helping in the

retention of the organism in hostile habitats such as the oral cavity.[12] In addition, the sheer physical size of the hyphal element poses a problem for the host phagocytic response.[11] Apart from the aforementioned biological phenotypic traits, the relative CSH of Candida is considered a non-biological physical force of critical importance pertaining to candidal adhesion. For instance, new Hazen and Hazen [27] have demonstrated that hydrophobic Candida are more virulent than their hydrophilic counterparts. Shibl et al., [28] and Ramadan et al., [29] have shown that the reduction in CSH following limited exposure to antimicrobials promoted increased ingestion of microbes by polymorphonuclear leukocyte (PMNL), thus increasing the susceptibility of the organisms to the killing effect of PMNL. Hydrophobic cells also exhibited greater adherence to epithelial cells and extracellular matrix proteins and decreased susceptibility to phagocytic killing.[30] In addition, it has been stated that

enhanced virulence of hydrophobic cells over hydrophilic cells may be due to the potential of hydrophobic cells to bind to various organs following clearance from the bloodstream.[30] Furthermore, to these adhesion-related traits, another form of measuring Candida virulence is with the PAFE, which measures the growth recovery capacity after a limited exposure to antifungal agents, where more virulent and resistant organisms will have low PAFE, whereas a susceptible and less virulent organism will have higher PAFEs.[18-20, 31] The PAFE, suppression of adhesion to BEC and almost complete abrogation of GT production by limited exposure to the polyene antifungal agent may be related to the mechanism of action of nystatin on the Candida cell wall. Polyenes bind to the sterol components in the cell wall of Candida and make it more permeable.