Retinal Granuloma Progression After Scleral Buckling in Ocular Toxocariasis: A Case Report

Introduction

Toxocariasis is a common zoonotic parasitic disease caused by nematodes of the genus Toxocara (family Ascarididae), with a higher prevalence in tropical and subtropical regions [1–3]. Human infection typically occurs through the ingestion of food or water contaminated with embryonated eggs of Toxocara canis or Toxocara cati, which are predominantly harbored by domestic and wild canids and felids [4]. Once they are ingested, the eggs hatch within the gastrointestinal tract, producing larvae that escape through the intestinal wall into the circulation, where they circulate throughout the body (systemic spread). This migration can cause 4 distinct clinical manifestations: visceral larva migrans, ocular larva migrans (OLM), neurotoxocariasis, and covert toxocariasis [1,4,5]. Among these, OLM has been identified as among the most reported manifestations in China [6]. However, it is often misdiagnosed because of the similarity of the clinical manifestations to those of other ocular diseases.

Ocular toxocariasis is typically a unilateral condition, classically presenting with peripheral retinal granuloma, posterior pole granuloma, or chronic endophthalmitis [3,5,7]. The most notable manifestation observed is peripheral granulomas in the eye, often accompanied by granulomas at the posterior pole, typically extending from the macular region toward the central retinal periphery and invariably associated with vitritis or occasional occurrence of subretinal bands [8]. Larvae invade the posterior segment of eyes, causing local inflammation which is considered a reaction towards highly immunogenic antigens, and retinal granuloma, a response to larval death; both of these conditions can lead to partial or complete vision loss [5].

Here, we describe a case of atypical ocular toxocariasis that was initially misdiagnosed as chronic rhegmatogenous retinal detachment. The patient subsequently developed postoperative granulomatous proliferation 5 months after surgery. This is an extremely rare reaction, and suggested the presence of ongoing inflammation. This case aims to highlight the challenge of differentiating ocular toxocariasis from chronic rhegmatogenous retinal detachment and to emphasize the importance of managing adjunctive systemic therapy for newly developed postoperative granulomas.

Case Report

A 17-year-old male patient was referred to our hospital, presenting with a 4-month history of progressive vision loss in his right eye. He denied pain, photophobia, redness, and other systemic symptoms such as fever and rash. Four days earlier, he had been diagnosed with chronic rhegmatogenous retinal detachment at a local hospital and was referred to a more advanced facility for further treatment.

At presentation, the best-corrected visual acuity (BCVA) in the right eye was 20/400. The right eye’s intraocular pressure was 7 mmHg. Slit-lamp biomicroscopy revealed 1+ cells in the anterior chamber. Examination by scanning laser ophthalmoscope (SLO) revealed a tractional retinal detachment in the right eye, extending from the 4 to 10 o’clock positions, with multiple fibrous bands beneath the retina (Figure 1A, black arrow). Additionally, a granulomatous tubercle was observed above the temporal peripheral retina, exerting traction on the retina (Figure 1A, blue arrow). Optical coherence tomography verified the existence of a macular retinal detachment in the right eye (Figure 1C, purple arrow), and B-scan ultrasonography demonstrated retinal separation from the eyeball wall (Figure 1E, white arrow). Fundus fluorescein angiography suggested high fluorescence and obvious leakage at the tubercle lesions in the late stage (Figure 2A), along with elevated fluorescence seen in the late stage of the optic disc (Figure 2C). Indocyanine green angiography showed low fluorescence in late-stage tubercle lesions (Figure 2B) and in the optic disc (Figure 2D). No significant abnormalities were observed in the left eye.

Routine laboratory tests, including a complete blood count and urinalysis, were unremarkable. Additional diagnostic evaluations, encompassing a Treponema pallidum hemagglutination assay, assays for human immunodeficiency virus (HIV), hepatitis B surface antigen, and tuberculin test, yielded negative results. Upon further inquiry, we discovered that the patient had a history of pet ownership during his childhood in rural areas, raising suspicion of ocular toxocariasis. Subsequent specialized immunologic testing was performed. The anti-Toxocara IgG diagnostic levels have been suggested as 8.2 U in serum and 1.8 U in intraocular fluid [9]. In addition, the Goldmann-Witmer coefficient (GWC) has been validated as a reliable diagnostic indicator for ocular toxocariasis, particularly in patients presenting with posterior segment lesions or unexplained vitreous inflammation [10,11]. Enzyme-linked immunosorbent assay (ELISA) revealed the levels of IgG anti-Toxocara antibodies in intraocular fluid (5025.99 U; reference range for IgG: <9 U) and serum (38.33 U; reference range for IgG: <9 U). The GWC, calculated as [(Toxocara IgG in intraocular fluid/Total IgG in intraocular fluid)/(Toxocara IgG in serum/Total IgG in serum)], was determined to be 1896.78 (reference range for the GWC: <4).

Based on clinical and diagnostic findings, a diagnosis of intraocular Toxocara infection was confirmed. Given the proliferative change that takes place during retinal detachment, internal-route procedures such as pars plana vitrectomy (PPV) cannot completely eliminate granulomas, which may consequently lead to failure of retinal reattachment. Furthermore, PPV may facilitate the dissemination of residual parasites and amplify the inflammation and proliferation. Therefore, scleral buckling was conducted to resolve tractional retinal detachment, and 532 nm laser photocoagulation was conducted at 100 mW, 200 μm spot, and 0.2 s exposure to seal the suspected peripheral retinal break.

Concurrently, topical levofloxacin (4 times a day for 3 weeks), 1% prednisolone acetate (4 times a day for 3 weeks), and bovine basic fibroblast growth factor (4 times a day for 3 weeks) were prescribed. Five months postoperatively, the BCVA in the right eye improved to 20/100. Subretinal fluid was completely absorbed (Figure 1D, purple arrow), and the retina was reattached (Figure 1F, white arrow). Postoperative SLO examination revealed absorbed fibrous bands (Figure 1B, black arrow), but the pre-retinal granulomatous tubercle had increased (Figure 1B, blue arrow) and new thick granulomas had developed above the temporal peripheral retina (Figure 1B, green arrow). Meanwhile, the white dot-shaped lesion had become larger (Figure 1B, red arrow), accompanied by moderate vitritis (Figure 1F, orange arrow). Consequently, oral prednisone (0.5–1 mg/kg/day with slow taper) and albendazole (400 mg twice a day for 2 weeks) were initiated. The vitreous inflammation was subsequently controlled, and no further granuloma formation was observed.

Discussion

Toxocariasis is a neglected parasitic infection, primarily affecting children and adolescents [1,12]. A meta-analysis by Rostami et al reported a global Toxocara seroprevalence of 19% (95% CI: 16.6–21.4%) [13]. A number of risk factors are indicated, such as male sex, rural residence, younger age, close contact with dogs, cats, or contaminated soil, and consumption of raw or undercooked meat or of untreated water [13,14]. In the present case, the patient lived in a rural area and had a history of cat ownership. In the area, routine deworming practices were likely absent.

Accurate diagnosis relies on ophthalmic examination results, imaging modalities, serological testing, and molecular assays [15]. Chronic rhegmatogenous retinal detachment, by contrast, is more common among younger individuals and is characterized by peripheral or inferior retinal breaks, thin and atrophic detached retina, and the presence of subretinal fibrotic strands [16]. In the present case, the patient initially presented with sub-retinal fibrous strands and pre-retinal fibrous nodules, without obvious vitritis, which was easily confused with chronic rhegmatogenous retinal detachment, and the typical granulomatous proliferation of ocular toxocariasis was not manifested until 5 months after retinal reattachment. This case serves to illustrate why early serologic evaluation is essential for diagnosis when this illness is clinically suspected. In this case, a significantly high GWC of 1896.78 pointed convincingly to the existence of intraocular Toxocara infection.

Ocular toxocariasis can be managed with medical management or surgical intervention, depending on the intraocular inflammation and associated comorbidity [15]. In contrast to previous reports in which PPV was adopted as the primary surgical intervention, scleral buckling was performed during the initial management in the present case.

Some postoperative recurrences have been reported. Lin et al documented a case of recurrent vitreous opacification within 3 weeks following surgery, which was attributed to the incomplete excision of proliferative membranes containing Toxocara larvae during the initial PPV [17]. Fonseca et al similarly reported delayed development of a secondary macular granuloma 1 year after treatment with combined systemic albendazole and corticosteroids, suggesting possible larval reactivation or migration [18]. In contrast, granulomatous progression in our case occurred at 5 months. We suspect this delay may be related to the use of scleral buckling rather than PPV, which likely minimized opportunities for retinal injuries and larval displacement. The progressive granuloma observed suggests that the postoperative inflammation may not only depend on the surgical procedure but also reflect persistent intraocular antigenic stimulation or unrecognized larval migration, consistent with findings by Ahn et al, who reported continuous or intermittent larval movement in 16.1% of individuals with ocular toxocariasis [19].

Considering that our patient presented with only tractional retinal detachment preoperatively, without obvious vitreous inflammation, oral corticosteroids were not administered during the perioperative period due to the lack of definitive inflammatory manifestation. Moreover, according to the literature, ocular toxocariasis is primarily characterized by a proliferative immune response of the host to larval antigens rather than the presence of viable worms [5]. Therefore, we did not prescribe systemic anti-parasitic therapy either preoperatively or perioperatively. Five months after the operation, the patient developed progressive granuloma and vitreous inflammation. We reviewed the literature again and then suspected active parasitic infection or disease recurrence. In accordance with the suggestions in the literature, systemic corticosteroids combined with albendazole were initiated, resulting in successful control of the vitritis and prevention of further granuloma progression. This outcome was consistent with previous studies in which corticosteroids and albendazole were efficient in managing ocular toxocariasis, especially in the case of active or recurrent inflammation [15,19–21].

This case underscores the potential for ocular toxocariasis presenting with subretinal proliferative fibrous bands to masquerade as chronic rhegmatogenous retinal detachment, emphasizing the imperative for clinicians to distinguish them. To some extent, scleral buckling may be more effective than PPV in the reattachment of retinal detachment caused by ocular toxocariasis and can delay the occurrence of postoperative inflammation.

Conclusions

This case highlights that ocular toxocariasis can masquerade as chronic rhegmatogenous retinal detachment and may demonstrate delayed granulomatous progression even after successful scleral buckling. Anatomical reattachment alone does not exclude ongoing immunologic activity. Because clinical manifestations may be nonspecific, serologic testing – including assessment of the GWC – is essential for accurate diagnosis. While scleral buckling may be prioritized to address proliferative retinal changes, persistent or recurrent inflammation warrants timely adjunctive systemic anti-inflammatory and antiparasitic therapy. Prolonged follow-up is critical to detect recurrence early and to optimize long-term visual outcomes.