First report of Candida palmioleophila endogenous endophthalmitis

Abstract

Endogenous fungal endophthalmitis (EFE) by Candida palmioleophila (Cp) has to our knowledge not previously been reported. Ocular candidiasis complicates candidaemia at a rate of approximately 2–26% (Ullmann et al. 2012). The majority of cases are chorioretinitis whilst EFE is less common (Ullmann et al. 2012). Symptoms of EFE are reduced vision, pain and photophobia, and findings are conjunctival hyperaemia, infiltrates in the choroid, retina or vitreous (Osthoff et al. 2006). Cp can be misdiagnosed as C. famata or C. guilliermondii (Sugita et al. 1999; Jensen & Arendrup 2011). In contrast to those species, Cp is susceptible to echinocandins but highly fluconazole resistant. A 51-year-old man with acute myeloid leukaemia was admitted with acute Pneumococcus pneumonia. The patient complained of blurred vision and floaters in the left eye (LE). Ophthalmoscopy revealed multiple preretinal haemorrhages progressing to LE vitritis and multiple new preretinal haemorrhages and creamy white infiltrates bilaterally 1 week later (Fig. 1). Peripheral blood cultures yielded Candida initially identified as C. guilliermondii. Intravenous fluconazole (200 mg BID) was initiated. Susceptibility pattern (Etest) was as follows: amphotericin B, voriconazole, caspofungin susceptible and fluconazole intermediate. At the reference laboratory, the isolate was re-identified as Cp with the following EUCAST MICs (mg/L): fluconazole MIC>16 (R), itraconazole 0.125 (S), voriconazole 0.25 (S according to the CLSI breakpoints, R according to the EUCAST breakpoints), posaconazole 0.03 (S), caspofungin 1 (S) and Etest MIC: amphotericin B 0.047 (S). Due to insufficient clinical effect and the new susceptibility results, treatment was 4 weeks later changed to amphotericin B (50 mg QD) for 3 weeks, then combined with 5-flucytosine (2500 mg QID) intravenously for 3 weeks and finally changed to oral voriconazole (200 mg BID) for 4 weeks. Increased inflammation and white choroidal infiltrates developed in both eyes. Vitrectomy with intravitreal injection of amphotericin B was performed in both eyes, which resulted in gradual improvement (Fig. 1). A vitreous sample on day 58 was microscopy and culture negative. At 3-year follow-up, there was no sign of recurrence, and visual acuity was 6/6 in RE and 6/9 in LE. Cp is intrinsically highly resistant to fluconazole and shows moderately reduced susceptibility to voriconazole, which may compromise efficacy unless high exposure can be achieved (Jensen & Arendrup 2011). Although Cp is echinocandin susceptible, echinocandins are less attractive for EFE due to the poor penetration across the blood–brain barrier. Therefore, initial combination therapy of intravitrous amphotericine B, intravenous flucytosine and intravitreal installation of amphotericin B deoxycholate potentially followed by voriconazole if therapeutic drug monitoring ensures significant drug levels currently appears as the optimal treatment of EFE by Cp (Barza 1998). Optimal and timely management of EFE necessitate a close collaboration between a laboratory with mycological expertise and a skilled ophthalmologist (Jensen & Arendrup 2011).