Candida albicans is a common diploid, polymorphic fungal organism that often colonises mucosal surfaces in healthy human adults without incidence of disease. however, impairment of host defence mechanisms owing to underlying immune deficiencies, hiv infection, prolonged chemotherapy, major surgery or immunosuppressant treatments can predispose individuals to infections ranging from mucocutaneous forms of candidiasis, to systemic infections such as candidaemia and invasive candidiasis (enoch et al., 2006; netea et al., 2008). candida has thus risen to be the fourth most common form of bloodstream infections in the usa over the past three decades (wisplinghoff et al., 2004). such systemic infections exhibit an associated mortality rate estimated at >30% in the usa, at >25% in the uk and at >35% in mainland europe; of the reported deaths, roughly 30-50% are directly attributable to candidaemia. c. albicans is responsible for the vast majority of life-threatening disseminated infections (up to 80%) and, indeed, is the most common fungal pathogen in humans (edmond et al., 1999; kibbler et al., 2003; gudlaugsson et al., 2003; wisplinghoff et al., 2004; tortorano et al., 2006). considering the above, it is highly desirable to develop a relevant model system with which to study the host-pathogen interactions taking place during a infection. ideally, this would be one that combines predictive power with genetic tractability, one that is easy to manipulate, and also, one that is available in large numbers. although mammalian models offer much, they are time consuming, expensive and labour intensive (ashman et al., 1996; navarro-garcia et al., 2001; maccallum et al., 2009) (for a review, see de repentigny, 2004). furthermore, typical sample sizes are too small for in-depth statistical analysis or modelling of lifetime data; this therefore precludes predictions concerning the outcome of an infection. with the realisation that innate immune responses constitute the prototypical host defence that is conserved in metazoans came the usage of genetically tractable invertebrate model systems, such as caenorhabditis elegans and drosophila melanogaster , as more practical alternatives for analysing fungal pathogenesis (for a review, see mylonakis et al., 2007). although c. elegans has been used very successfully for high-throughput screening of antifungal compounds (tampakakis et al., 2008; okoli et al., 2009), the nematode innate immune system was seen to be quite different to that of mammals and insects (for a review, see irazogui et al., 2010), and this therefore raises issues concerning its suitability as a model system for dissecting the mammalian host defence response. by contrast, studies with d. melanogaster have revealed extensive conservation between the mechanisms of mammalian and insect innate immunity (for a review, see lemaitre and hoffmann, 2007); however, is yet to be fully exploited as a model system for analysing infection. indeed, the limited studies available were performed using immune- deficient flies (alarco et al., 2004; chamilos et al., 2006; chamilos
