Migration of Baylisascaris procyonis into the vitreous

Diffuse unilateral subacute neuroretinitis (DUSN) is a clinical syndrome first described by Gass and associates in 1978, characterised early by visual loss, vitritis, papillitis, and recurrent crops of grey‐white retinal lesions and later by progressive visual loss, optic atrophy, retinal vessel narrowing, and diffuse retinal pigment epithelial degeneration.¹,²

Baylisascaris procyonis, the common intestinal raccoon roundworm, is believed to cause DUSN and its potential to affect ocular tissue has also been described in animal models.³,⁴,⁵

We describe a case of infection by Baylisascaris procyonis where the larva was found entrapped in the vitreous.

Case report

A 37 year old white man presented for a second opinion. He had experienced flashes and floaters in the left eye for 10 days. He also noted a dramatic decrease in scotopic vision in the left eye. His ocular and medical histories were unremarkable. The patient was a frequent camper.

Examination disclosed uncorrected vision of 20/15 J1+ in the right eye and 20/20 J1+ in the left eye. Relative afferent pupillary defect was present in the left eye. Intraocular pressures, confrontation visual fields and versions were normal, and colour plates were 10/10 in both eyes. Slit lamp examination of the anterior segment was normal. Vitreous cells were present. Dilated ophthalmoscopy revealed an area of fibrosis with protrusion of the larva into the vitreous associated with chorioretinal scarring, retinal pigment epithelium disturbance, and subretinal tracks in the supero‐temporal mid‐periphery (fig 1A). Retinal whitish lesions noted 9 days earlier had disappeared (fig 2). Fluorescein angiography was performed and a progressive increase in fluorescence was observed in the late phases. The image presumed to be the larva was not perfused by the dye or blocked its fluorescence (fig 1B). Complete blood count was normal. Serologies were negative for strongyloidiasis, filariasis and toxocariasis, and were consistent with Baylisascaris procyonis (ELISA 0.772, positive >0.25).

Figure 1 Colour photograph (A) and late phase of the fluorescein angiogram (B) of the supero‐temporal mid‐periphery of the left eye showing an area of fibrosis with protrusion of the larva into the vitreous, associated with chorioretinal scarring, retinal pigment epithelium disturbance, and subretinal tracks. The larva is not perfused by the dye or blocks its fluorescence.

Figure 2 Colour photograph of the left eye acquired 9 days earlier where retinal whitish lesions are seen (A). Lesions had vanished at the time of our examination as is observed in the same area (B).

Diagnosis of DUSN with tracking of the larva into the vitreous caused by Baylisascaris procyonis was made based on the clinical features and positive serology.

Comment

There is a lot of uncertainty regarding the precise aetiology of DUSN, but morphometric, serological and epidemiological findings indicate that Baylisascaris procyonis may be a cause of the disease.⁶

However, Baylisascaris procyonis has so far never been recovered from the retina. In a case report of typical late stage DUSN, where an intact nematode was removed from the subretinal space, morphometric features were compatible with third‐stage Toxocara canis.⁷

No matter the nematode involved, laser photocoagulation of the larva, whenever it is possible to identify it, may lead to visual acuity improvement when it takes place in the early stages of the disease.⁸ Therefore, early diagnosis by prompt location of the larva and its destruction by laser photocoagulation may change the vision threatening prognosis of DUSN. In this case, we were unable to perform the required treatment since the patient did not return for follow up visits.

We are unaware of previous reports about identification of a larva tracking into the vitreous in DUSN patients. This finding may contribute to a better understanding of the larva's cycle in the eye.