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Arrest of endogenous ocular nocardiosis under linezolid therapy

year-long history of systemic lupus erythematosus (SLE) and repeated kidney transplantation for end-stage renal failure was admitted with generalized seizures, pneumonia and multiple cutaneous and mammary abscesses. Scratch biopsies were tested positive for Nocardia. Cranial magnetic resonance imaging (MRI) revealed multiple nodular contrastenhancing lesions in white and grey matter (Fig. 1D). Similar lesions were found in the lung. Within 5 days, she experienced progressive loss of central vision to 1 ⁄ 35 in her right eye, unassociated with other ocular symptoms. Anterior segment examination was inconspicuous, but funduscopy (see Fig. 1A,B) revealed a large yellowish white mass of approximately 6 disc diameters at the posterior pole beneath the inferotemporal vascular arcade. The lesion elevated the neurosensory retina, resulting in an extended serous retinal detachment including the fovea. The peripheral retina was normal. The media were clear without any sign of general ocular inflammation. Based on the clinical and microbiological findings, a subretinal nocardioma was diagnosed. Optical coherence tomography (see Fig. 1G,H) showed a hyper-reflective subretinal focus based on the retinal pigment epithelium (RPE) and extending into the detached, thickened retina, the layers of which were ill defined. Fluorescein angiography (FA) (Fig. 1E) demonstrated early blocking over the serous detachment and late pooling demarcating the solid lesion. Neither indocyanin green angiography (Fig. 1F) nor FA showed intrinsic vessels. Antibiotic therapy was started with cotrimoxazole (sulfamethoxazol plus trimethoprim) 2 · 960 mg ⁄day and linezolid 2 · 600 mg ⁄day orally (anaemia and thrombocytopenia later required a reduced dose of 600 mg four times a day). Immunosuppressive therapy was reduced to oral prednisone and cyclosporine A, pausing mycophenolate mofetile. Subsequently the dimensions of the lesion remained stable. Three months after the initial ophthalmological diagnosis, the lesion became paler and a minor preretinal haemorrhage was visible (Fig. 1C). While the intraocular nocardioma was stable under combination therapy with linezolid and cotrimoxazole, the progression of the lesions in the brain with resulting cerebral oedema required intensification of the therapy to a regimen of linezolid 600 mg ⁄day orally plus ampicillin + sulbactam 3 · 3 g ⁄day intravenously (IV), amikacin 1000 mg q.d. IV and imipenem + cilastatin 4 · 500 mg ⁄day IV, instead of cotrimoxazol that induced a bone marrow suppression. Two years after treatment, the ocular lesion remains stable and inactive. Nocardia is a rare but typically devastating cause of endogenous endophthalmitis. Immunocompromised patients are at particular risk for developing blinding ocular disease. In a recent clinical case series (Ness et al. 2007), infection with Nocardia accounted for 3% of endogenous endophthalmitis. Nocardia spp are ubiquitous aerobic actinomycetae that are commonly found as saprophytes in soil. Nocardiosis causes an acute or chronic suppurative infection with typical abscess formation and spreads mostly to neuroectodermal tissues. Clinically, Nocardia asteroides is the Diagnosis ⁄Therapy in Ophthalmology