Sir,

Case report

A 65-year-old man presented to eye casualty with a 2-month history of bilateral gradual loss of vision. The patient denied any other ocular or systemic symptoms. He had no past ocular history. His past medical history revealed a left total hip replacement 3 years ago, which was complicated with a multiresistant Staphylococcus aureus (MRSA) infection, which, due to multidrug resistance, had been treated with long-term linezolid 600 mg b.d. for 1 year. This antibiotic had been stopped 1 week before review by the ophthalmology team.

On examination, his visual acuities were counting fingers bilaterally. Ishihara test detected a loss in bilateral colour vision, scoring 2/15 and 1/15 in the right and left eye, respectively. His pupillary responses were normal. Anterior segment examination was unremarkable and dilated fundoscopy revealed no evidence of optic atrophy or oedema.

Normal blood tests results included Hb (14.2 g/dl), WBC (8.1 × 109/l), platelets (365 × 109/l), and vitamin 12B (482 μg/l). Syphilis antibodies and mitochondrial studies were also negative.

Abnormal blood tests included a low folate level (2.7 μg/l) and hence the patient was commenced on folic acid supplements.

Visual-evoked potential (VEP) of the left eye showed a prolonged latency of 128.7 and diminished amplitude of 3.13 uV. The right eye VEP also showed a prolonged latency of 125.1 ms with diminished amplitude of 2.39 uV (Figure 1) (normal amplitude values for laboratory: 4–20 uV).

Figure 1
figure 1

First VEP.

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An MRI scan of his brain and orbits was performed and detected no abnormality.

Visual field test showed a right superior scotoma and a left superior arcuate scotoma.

Over the next 4 months, his visual acuities gradually improved to 6/6 in the right eye and 6/9 in the left. This patient still however had abnormal VEP studies showing prolonged latencies and diminished amplitudes bilaterally (Figure 2) (right eye: latency 133.2 ms, amplitude 3.34 uV; left eye: latency 124.8 ms, amplitude 2.53 uV).

Figure 2
figure 2

Second VEP.

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Fifteen months after his initial presentation, his visual acuities had returned to 6/5 and 6/6 in his right and left eye, respectively. Dyschromatopsia and visual field defects remained stable and nonprogressive (Figures 3 and 4). After treatment with folic acid supplements his folate levels had risen to within normal limits (4.3 μg/l). VEP studies at this time had returned to normal (Figure 5). The patient reported no further symptoms.

Figure 3
figure 3

Right eye (last visual field test).

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Figure 4
figure 4

Left eye (last visual field test).

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Figure 5
figure 5

Third (last) VEP.

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Comment

Toxic optic neuropathy is typically a progressive bilateral symmetrical painless visual loss, which may cause a central or centralcaecal scotoma. There is currently no specific treatment for this disorder; however, early detection and prompt management may ameliorate and even prevent severe visual loss.1

Our case demonstrates the progressive loss of vision, which returns to normal following the cessation of the causative agent. The loss of vision was accompanied by low folate levels, persistent dyschromatopsia, and severely affected VEPs. His visual field defects are not of a typical optic neuropathy picture; however, no other cause for the defects has been discovered.

Linezolid is a synthetic antibacterial agent that belongs to a new class of antimicrobials. According to this, drugs data information leaflet, neuropathy (peripheral and optic) has been reported with use longer than the recommended duration of 28 days.2

There is a growing body of evidence that shows long-term linezolid use is associated with severe peripheral and optic neuropathy. In most cases, the optic neuropathy resolved with drug cessation, leaving a residual deficit in central visual acuity.3, 4, 5, 6, 7, 8 The mechanism of toxicity remains unclear although previous reports of linezolid associated optic neuropathies suggest mitochondrial dysfunction as the most possible cause of neurotoxicity. In particular, low folate levels subsequently cause elevated plasma homocysteine, which can lead to inhibition of neuronal mitochondrial function.9, 10, 11

Given the high profile of MRSA infections, the use of such antimicrobial agents may be used increasingly in an attempt to control persistent infections. We therefore feel that this case should be brought to the attention of the ophthalmic community so that they are aware of its possible ophthalmic toxicity.