Isolated endogenous endophthalmitis secondary to Nocardia spp in an immunocompetent adult

Nocardia spp cause opportunist pulmonary, cerebral or soft‐tissue infections and exogenous endophthalmitis. Endogenous endophthalmitis is rare, occurring as the result of haematogenous dissemination, and in association with underlying immunodeficiency. We present the case of a patient with endogenous nocardial endophthalmitis, diagnosed by histopathological characteristics on subretinal biopsy, in an immunocompetent host with no evidence of extraocular infection.

A 49‐year‐old man presented with a 9‐day history of worsening vision and ophthalmic pain. A left‐sided choroidal mass was visualised on funduscopy. The patient refused admission and returned 3 days later with retinal detachment and no perception of light in his left eye. No history of ocular trauma or surgery was seen. He had injected intravenous drugs 6 years ago, but was taking no regular drugs.

Investigations included an unremarkable blood film, immunoglobulins and complement, and negative HIV antibody. Hepatitis C antibody and RNA were positive. No other foci were found on chest x ray, echocardiogram or abdominal ultrasound. A computed tomography scan showed left‐sided proptosis and preseptal periorbital soft‐tissue swelling, with extension through the posterior margin of the globe.

Microscopy of the vitreal fluid showed a few leucocytes, but culture showed no growth. A subretinal fine‐needle aspiration was carried out; haematoxylin and eosin staining showed a purulent aspirate containing proteinaceous material admixed with apoptotic and viable neutrophils. No granulomatous inflammation was identified. Grocott stain showed distinctive colonies (fig 1) of non‐mycelial, beaded, filamentous organisms, branching at about 90°. They tested weakly Gram positive, weakly acid fast, positive on Wade–Fite stain and negative for periodic acid‐Schiff. In the context of the distinct morphology and tinctorial stain characteristics, features were those of Nocardia spp. Prolonged culture showed no growth.

Figure 1 Distinctive colonies on Grocott stain.

Intravenous trimethoprim–sulphamethoxazole was started, but the patient absconded after 3 days and could not be located. He presented again after 4 months, with resolution of systemic symptoms and ophthalmic pain. Visual acuity was unchanged. A computed tomography scan showed reduction in size of the left globe and resolution of preseptal soft‐tissue swelling. It was decided not to start antibiotics again. No evidence of recurrence is seen in 6 months.

Nocardial endophthalmitis usually occurs after ocular trauma or surgery.¹ Endogenous endophthalmitis, although rare, is associated with haematogenous dissemination from pulmonary or cerebral foci, and occurs in patients with underlying malignancy, HIV infection, immunosuppressive chemotherapy or prolonged corticosteroid treatment.²,³ Only one case was previously reported of endogenous nocardial endophthalmitis, without extraocular infection, in an immunocompetent patient.⁴ A potentially immunosuppressive role, however, of hepatitis C infection is a matter for speculation.

Nocardia spp have distinctive histopathological features, such as beading, branching at 90°, absent sulphur granules, weak acid‐fast nature and positive Wade–Fite stain, which differentiate them from Actinomyces spp. Although Nocardia spp have been isolated from vitreal samples, the role of subretinal biopsy in establishing an early diagnosis has been highlighted.²,⁵ This should be considered promptly in worsening endophthalmitis of unknown aetiology.

Finally, the outcome of this case despite minimal antibiotics is a point for discussion. Owing to the typical chronic course of infection, 6–12 months of trimethoprim–sulphamethoxazole is recommended.⁵ Previous reports describe a poor prognosis with ocular nocardial infection, which often resulted in enucleation and death from extraocular foci.²,³ Earlier reports have suggested that the mortality for localised pulmonary nocardiosis in previously healthy patients may be lower.⁴ Our findings may support a similar pattern in localised ocular infection.