Gastrointestinal granuloma due to Candida albicans in an immunocompetent cat

Duchaussoy, Anne-Claire; Rose, Annie; Talbot, Jessica J.; Barrs, Vanessa R.

Several mechanisms are implicated in the development of C. albicans infection, including an inadequate host immune response (Yan, Yang et al. 2013 ). Induction of the initial mucosal immune responses occurs in the gut associated lymphoid tissue (GALT), within Peyer's patches and mesenteric lymph nodes [11] . Many host cellular pattern recognition receptors (PPARgamma and Dectin-1) have also been identified to interact with C. albicans [12, 13] . Presence of bile acids and an abnormally increased gastric pH may promote C. albicans virulence [14] . Hence chronic gastroenteritis or long term treatment with anti-acids can lead to invasive candidiasis. C albicans itself can delay gastrointestinal ulcer healing by releasing cytokines (IL-1beta and TNF-alpha) which perpetuate ongoing inflammation and promote conditions for gastrointestinal wall invasion and adherence [15] . Altered host/C. albicans interactions could lead to local and systemic infection. In our cat, no underlying disease, gastro-intestinal bacterial overgrowth, chronic inflammation or systemic debilitating diseases were identified. An improvement 6 weeks after the introduction of a hypoallergenic diet (Hills′ Z/d) raises suspicion of a possible inflammatory disorder, which could have been the source of an altered host/C. albicans interaction, although the focal nature of the disease makes this less likely.