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Invasive cryptococcal rhinitis due to Cryptococcus neoformans var gattii was diagnosed in a castrated, 5-year-old, albino ferret with subcutaneous swelling of the nasal bridge. The diagnosis was based on histology, needle aspirate cytology and positive culture on Sabouraud's dextrose agar and birdseed agar. The ferret was successfully treated using a long course of itraconazole (25 to 33 mg orally once daily with food) subsequent to surgical debulking of the lesion, using sequential cryptococcal antigen titre determinations to guide therapy.

7 of 8 dogs receiving combination drug therapy consisting of flucytosine together with amphotericin B and/or a triazole for cryptococcosis or aspergillosis developed cutaneous or mucocutaneous eruptions during the course of treatment. Lesions resolved in all cases following discontinuation of flucytosine despite continued administration of other antifungals, suggesting the eruption was referable primarily to the flucytosine component of therapy. Lesions developed 13 to 41 days (median 20 days) after commencing flucytosine (105 to 188 mg/kg/day divided and given every 8 h; median dose rate 150 mg/kg/day). The cumulative dose of flucytosine given prior to the first signs of the drug eruption ranged from 1.7 to 6.8 g/kg (median 2.3 g/kg). The eruptions consisted of depigmentation, followed by ulceration, exudation and crust formation. The scrotum was affected in all 4 male dogs, the nasal plane in 6 of 7 cases, while the lips, vulva, external ear canal and integument were involved in a smaller number of cases. There was considerable variation in the severity of lesions, with changes being most marked when flucytosine was continued for several days after lesions first appeared. Some dogs experienced malaise and inappetence in association with the suspected drug eruption. Healing took a variable period, typically in excess of 2 weeks after discontinuing flucytosine, with up to 2 months being required for total resolution of the lesions. All lesions resolved eventually without scarring or permanent loss of pigment.

Examination of the small intestine of pigs with proliferative haemorrhagic enteropathy showed changes consistent with defects in vascular permeability. Early in the disease there were many eosinophils and distension of lacteals and intercellular spaces with proteinaceous material. Later the predominant features were red blood cells and exudate in tissue spaces. This was most severe and extensive at the tips of villi which were covered by a cast of cells and fibrinous exudate. Adenomatous intestinal mucosal cells contained organisms that were free within the apical cytoplasm and were morphologically identical with those seen in the related disease, porcine intestinal adenomatosis. Also these bacteria were seen free in the subepithelial mucosal area, in blood vessels and within membrane-bound vesicles in phagocytic cells in the mucosa and its blood vessels. Mast cells were prominent in some areas as were thrombosed vessels.