The human fungal pathogen is the major etiological agent of vulvovaginal candidiasis (VVC). Despite this fact, other non- (NAC) species have frequently been reported, as well. Despite their presence in the vaginal environment, little is known about their capacities to elicit immune responses classically associated with -mediated immunopathology, including neutrophil recruitment and proinflammatory cytokine signaling. Therefore, using a combination of and approaches, we undertook a comparative analysis to determine whether a representative panel of NAC species could colonize, induce immunopathological markers, or cause damage at the vaginal mucosa. Using a murine model of VVC, was found to induce robust immunopathology (neutrophils and interleukin 1β [IL-1β]) and elicit mucosal damage. However, all the NAC species tested (including , , , , , and ) induced significantly less damage and neutrophil recruitment than , despite achieving similar early colonization levels. These results largely correlated with a notable lack of ability by the NAC species (including and ) to form hyphae both and Furthermore, both and induced significantly less expression of the gene encoding candidalysin, a key fungal virulence determinant driving VVC immunopathology. In order to determine the relative capacities of these species to elicit inflammasome-dependent IL-1β release, both wild-type and NLRP3 THP-1 cells were challenged While most species tested elicited only modest amounts of IL-1β, challenge with led to significantly elevated levels that were largely NLRP3 dependent. Collectively, our findings demonstrate that although NAC species are increasingly reported as causative agents of VVC, appears to be exceedingly vaginopathogenic, exhibiting robust immunopathology, hypha formation, and candidalysin expression. Thus, this study provides mechanistic insight into why is overwhelmingly the major pathogen reported during VVC.