Subretinal abscess as an initial presentation of systemic nocardiosis

Background

A subretinal abscess is a sign of severe and vision-threatening endogenous endophthalmitis. It can be due to bacterial emboli from the liver, lungs, urinary tract or endocardium.1 Common organisms for endogenous endophthalmitis include Gram-positive Staphylococcus aureus and Streptococcus, followed by Gram-negative species; however, a subretinal abscess is still a rare presentation and may suggest other infectious aetiologies.2–4

Nocardiosis is a rare and devastating multisystem disease categorised as an opportunistic infection due to its tendency to infect immunocompromised patients, such as those infected with HIV, organ transplant recipients and those on chemotherapy or long-term immunosuppression. With the widespread use and advent of newer immunosuppressants, the rate of opportunistic infections like nocardiosis is on the rise.5

Our case report emphasises the importance of recognising early signs of systemic infection in the eye. Herein, we report a case of endogenous spread of Nocardia infection with initial presentation as a subretinal abscess.

Case presentation

A 50-year-old middle-aged man presented to the eye clinic with complaints of right eye redness, watering and pain that was associated with headache and gradually decreasing vision for 10 days prior to presentation.

On examination, he was found to have bilaterally round, reactive pupils with no relative afferent pupillary defect. The best-corrected visual acuity in the right eye was 20/100 and in the left eye was 20/25. The intraocular pressure was 12 mm Hg in the right and 16 mm Hg in the left eye. The anterior chamber examination revealed occasional cells in the right eye. The fundus examination of the right eye revealed a large, approximately 20 disc diameter, superonasal, elevated subretinal white-yellow mass, and a few pale-coloured, raised, satellite lesions, as well as multiple vitreous opacities (figure 1). The left fundus examination was within normal limits.

On further direct questioning, it was revealed that the patient had been experiencing low-grade fever and non-productive cough for 1 month. He had previously been in good health 6 months ago when he developed numbness in his feet for 10 days prior to the diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP), which ascended to involve numbness in his upper extremities. There was no associated backache or urinary incontinence. His nerve conduction studies confirmed acute sensorimotor axonal neuropathy of demyelinating type, and he received plasmapheresis. Following five cycles of intravenous immunoglobulin, he was advised to continue prednisolone 50 mg/day on a tapering schedule, as well as azathioprine 100 mg/day, which was later increased to 150 mg/day. He continued his medicines with significant improvement in CIDP symptoms until he developed the presenting ocular complaints after 6 months of immunosuppressive treatment.

Investigations

Complete blood count revealed normal white cell count (7.7×10³/µL) but with a differential of high neutrophils (89%) and low lymphocytes (6.2%). Erythrocyte Sedimentation Rate (ESR) and C-Reactive Protein (CRP) were high at 85 mm/first hour and 19.5 mg/dL, respectively, along with low calcium (8.5 mg/dL) and low vitamin D (20.1 ng/mL). Differential diagnoses were ruled out by negative HIV serology and tuberculosis interferon-gamma release assays (IGRA), as well as normal toxoplasmosis IgG and IgM levels. Fundus photography (figure 1) and optical coherence tomography (figure 2) were performed for ophthalmic evaluation. A provisional diagnosis of a subretinal abscess, likely of an infectious origin and highly suspicious for nocardiosis, was made and the patient was advised to get a CT scan of the chest, considering his concurrent symptoms of fever and cough. The CT scan revealed randomly distributed nodular soft tissue densities in bilateral lung fields, some of which showed cavitation (figure 3). Similarly, an MRI of the brain with contrast was done to evaluate intracranial spread, which revealed multiple ring-enhancing lesions suggestive of disseminated cerebral abscesses (figure 4) and subretinal fluid collection in the nasal half of the right eye (figure 5).

To confirm the diagnosis blood cultures, bronchoalveolar lavage (BAL) and vitreous tap were done, which revealed the growth of Nocardia species in blood and BAL.

Differential diagnosis

On fundus examination we suspected an abscess, granuloma or a metastatic tumour. Tuberculous granuloma was ruled out by clinical evaluation and negative IGRA, whereas sarcoidosis was ruled out by normal serum ACE levels. There was no history suggestive of cancer. Other causes of an abscess such as S. aureus and fungus were considered but ruled out as well.

Treatment

The patient was initially given intravitreal amikacin (0.4 mg/0.1 mL), vancomycin (1 mg/0.1 mL) and amphotericin (5 μg/0.1 mL) in an attempt to cover a broad spectrum of micro-organisms that may cause a subretinal abscess.

Meanwhile, culture samples of blood, BAL and vitreous were sent. Blood cultures revealed the growth of Nocardia species, sensitive to amikacin, linezolid and trimethoprim/sulfamethoxazole (TMP/SMX). His immunosuppression was gradually tapered, then put on hold. The patient was kept on intravenous amikacin 750 mg/day and imipenem 2 g/day for 1 week, which was later switched to an oral combination of TMP/SMX and linezolid according to sensitivity reports.

Outcome and follow-up

Follow-up revealed no improvement in right eye visual acuity; however, there was funduscopic evidence of a regressing and visually flatter appearance of the large superonasal lesion in the right eye (figures 6 and 7). Unfortunately, despite aggressive therapy, the patient had a rupture of the abscess along with vitritis for which a debulking vitrectomy was done 1 month after the initial presentation. Fortunately, his left eye vision remained stable. The lesions in his brain and chest resolved with treatment. After completing 7 months of TMP/SMX, we stopped the antibiotics due to no systemic signs of infection. However, the patient had raised ESR (36 mm/first hour) in the eighth month and in the eleventh month (55 and 53 mm/first hour). The patient was still clinically stable with no signs of active infection in the body or eye, so it was decided to continue to observe him on a 3 monthly follow-up.

During this time his symptoms of CIDP remained stable, and neurology decided not to resume immunosuppressant therapy unless absolutely necessary. One year after the presentation he continues to do well without any signs of recurrence of the infection or CIDP.