To the Editor, Unlike with acute forms of leukaemia, fungal infections are rare in chronic lymphocytic leukaemia (CLL). Most previous reports have been on patients with prolonged neutropenia or after allogeneic stem cell transplantation (SCT). We would like to document a patient with CLL who had a fungal infection at unusual sites as a result of combination therapy with alemtuzumab (Campath-1H) and methyl prednisolone. This patient was neither neutropenic nor had he received SCT. A 65-year-old man was on treatment with alemtuzumab, methyl prednisolone and ciclosporin for relapsed CLL and autoimmune haemolytic anaemia. He had a neutrophil count of 2.7 9 10/L with normal serum levels of immunoglobulins and was hence not on prophylactic antimicrobials. He presented with acute onset of pain in his right eye and developed a partial loss of vision in his right temporal field over the next 24 h in the absence of fever or raised inflammatory markers. He was referred to a tertiary care centre for ophthalmological evaluation and management. Examination of the right eye revealed pan-uveitis with a vitreous abscess (Fig. 1). A vitreous biopsy showed infection by Aspergillus fumigatus. MRI scan of the brain revealed a 4 mm ring-enhancing lesion in the cortex of the left frontal lobe, consistent with cerebral aspergillosis (Fig. 2). Toxoplasma serology was negative. A highresolution CT scan of his chest was normal. He was treated with oral voriconazole and intravitreal amphotericin instillations complicated by vitreal haemorrhage due to thrombocytopenia. Both the fungal infection and the haemorrhage improved over the next 6 weeks and his vision cleared gradually. A repeat MRI scan of his brain showed complete resolution of the lesion. The combination of alemtuzumab and high-dose methyl prednisolone (CamPred) is now increasingly being used to treat patients with CLL refractory to purine analogues and those with deletions of the TP53 gene [1–3]. Alemtuzumab, a humanised anti-CD52 monoclonal antibody, targets both B and T lymphocytes in addition to monocytes, macrophages and a subset of antigen-presenting dendritic cells. It thus significantly impairs the immunological surveillance mechanisms against infections. Whilst on this heavily immunosuppressive regimen, a high index of suspicion against viral reactivations and fungal