INTRODUCTION

Toxoplasma gondii is an obligate intracellular protozoan that infects an estimated one-third of the world’s population. Humans acquire the infection by ingesting tissue cysts in undercooked meat or oocysts shed by cats into soil, water and vegetables, or congenitally through the placenta [1,2]. Seroprevalence is high in many tropical countries; in a population-based survey in Central Java, Indonesia, 62.5% of participants were seropositive, and daily contact with raw meat, unfiltered water and cat density were identified as risk factors [3]. After the acute phase, the parasite persists as tissue cysts in neural and muscular tissue, including the retina, where it may remain clinically silent for years before it reactivates [4,5].

Ocular toxoplasmosis is the most common cause of infectious posterior uveitis worldwide [6]. In a prospective cohort of patients with active uveitis in Jakarta, infection was the most frequent cause of uveitis, and toxoplasmosis was the single most common infectious aetiology, accounting for 19% of cases [7]. Most cases are now thought to result from postnatally acquired rather than congenital infection [8,9]. The typical lesion is a focal necrotizing retinochoroiditis adjacent to a pigmented retinochoroidal scar, accompanied by overlying vitritis [10,11]. Atypical presentations, however, including retinal vasculitis, retinal vascular occlusion, neuroretinitis and marked anterior segment inflammation with raised intraocular pressure (IOP), may mimic viral, tuberculous, syphilitic or non-infectious uveitis and delay the diagnosis [12]. Delay has consequences. Treating presumed non-infectious uveitis with corticosteroids alone can turn a self-limiting lesion into a fulminant, sight-threatening retinochoroiditis [13]. and legal blindness in at least one eye developed in 24% of patients in a large long-term series [14]. We report an 18-year-old man with ocular toxoplasmosis who presented with unilateral hypertensive non-granulomatous panuveitis, retinal vasculitis and a macular retinochoroidal lesion, and who improved without complications after combined antiparasitic and anti-inflammatory treatment. The case is reported in accordance with the CARE guidelines [15].

CASE DESCRIPTION

An 18-year-old man presented with a two-week history of blurred vision, photophobia, eye pain and reduced clarity of vision in the left eye (OS). His symptoms were confined to the left eye. Ophthalmological examination of OS revealed raised IOP together with non-granulomatous inflammation involving the anterior chamber, the vitreous and the retina. Fundus examination showed retinal vasculitis and a round focus of retinochoroiditis at the macula, approximately 1.5 disc diameters in size, with a pigmented central area (Figure 1). Based on the anatomical involvement of the anterior chamber, vitreous and retina, the inflammation was classified as hypertensive non-granulomatous panuveitis according to the Standardization of Uveitis Nomenclature (SUN) criteria. The clinical picture was suggestive of ocular toxoplasmosis.

Figure 1. Color Fundus Photograph of the Left Eye. A round retinochoroidal lesion at the macula shows central pigment clumping surrounded by a yellowish-white border.

Table 1. Macular Optical Coherence Tomography Measurements

Note: OD, right eye; OS, left eye (affected eye).

Serological testing confirmed infection with T. gondii. Macular optical coherence tomography (OCT) was performed in both eyes (Table 1). The central subfield thickness (CST) was 249 µm in the right eye (OD) and 81 µm in OS, the cube volume was 9.8 mm³ and 7.8 mm³, and the cube average thickness was 273 µm and 217 µm, respectively. On the OCT fundus scan through the fovea, the foveal thickness was 255.64 µm in OD and 277.69 µm in OS. The differential diagnosis included acute retinal necrosis and other herpetic retinitis, syphilitic and tuberculous uveitis, and non-infectious causes of retinal vasculitis such as Behçet disease and sarcoidosis. A unilateral focal retinochoroiditis accompanied by intraocular inflammation and positive serology favored ocular toxoplasmosis, which was established as the working diagnosis.

The patient was treated with oral trimethoprim-sulfamethoxazole (co-trimoxazole) as the antiparasitic agent and oral prednisolone to control the posterior segment inflammation. Topical corticosteroids were given for the anterior segment inflammation, and IOP-lowering medication was administered to control the raised IOP. The patient showed significant clinical improvement, and no complications of the disease developed. Because of the risk of recurrence, trimethoprim-sulfamethoxazole was planned to be continued as secondary prophylaxis for one year.

DISCUSSION

This case illustrates ocular toxoplasmosis in a young adult who presented with a florid inflammatory picture of non-granulomatous panuveitis, retinal vasculitis and raised IOP rather than isolated posterior uveitis. Anatomically, the involvement of the anterior chamber, vitreous and retina fulfils the SUN definition of panuveitis, and the inflammation was non-granulomatous in character [16]. The focal retinochoroiditis was the key to the diagnosis, and prompt combined treatment led to a good outcome without complications. T. gondii can rightly be called a silent threat: tissue cysts persist in the retina without causing symptoms and may reactivate years after the original infection, and recurrences develop in most patients who are followed for long enough [17].

The hallmark of ocular toxoplasmosis is a focal necrotizing retinochoroiditis, frequently adjacent to a pigmented scar, with vitreous inflammation that may be dense enough to produce the classic “headlight in the fog” appearance [11]. In an international survey of 192 uveitis specialists, retinochoroiditis adjacent to a pigmented scar accounted for most presentations, but diverse atypical presentations were also reported [18]. Raised IOP is a recognized feature of active disease: in a retrospective series of 61 patients with active retinochoroiditis, 38% had elevated IOP; the rise usually coincided with the inflammatory episode, was transient and responded to medical treatment [12]. Retinal vasculitis is listed among the atypical manifestations of ocular toxoplasmosis and can direct attention towards Behçet disease, tuberculosis, sarcoidosis or viral retinitis [9]. The age of our patient is in keeping with the typical age at presentation; the mean age at first presentation with an active lesion was 29.5 years in a Dutch cohort, and younger patients carry a higher risk of recurrence [17]. The diagnosis is primarily clinical. The SUN Working Group classification criteria require focal or paucifocal necrotizing retinitis together with either a positive polymerase chain reaction (PCR) assay for T. gondii from an intraocular specimen or the characteristic picture of a round or oval retinitis lesion proximal to a hyperpigmented or atrophic chorioretinal scar [19]. A positive serum IgG confirms exposure but, because of the high seroprevalence in the general population, does not by itself prove that a lesion is toxoplasmic, whereas a negative IgG makes the diagnosis unlikely [20]. Intraocular fluid analysis by PCR or calculation of the Goldmann–Witmer coefficient is advised in atypical cases and was used in that setting by 68.8% of the surveyed specialists [18]. In our patient, the diagnosis rested on the clinical picture and serology. Other infectious causes of retinitis and vasculitis, particularly herpetic necrotizing retinitis, syphilis and tuberculosis, should be excluded in such cases, especially in Indonesia, where tuberculosis-associated uveitis is common [7].

OCT helps to document the vitreoretinal interface, the retinal and choroidal changes at the lesion and the course of healing. Active lesions show thickening, disorganization and hyper-reflectivity of the neurosensory retina with a thickened, hyporeflective choroid, accompanied by hyper-reflective vitreous dots and posterior hyaloid thickening, whereas healed lesions show retinal thinning and outer retinal disorganization [21]. In the present case, the lesion involved the macula, and the CST, cube volume and cube average thickness of the affected eye were all lower than in the fellow eye, which is consistent with retinal thinning and disorganization at the site of a healing macular lesion [21]. By contrast, the foveal thickness measured on the fundus scan was slightly greater than in the fellow eye (277.69 vs 255.64 µm). This discordance may reflect the irregular contour of the lesion and errors in automated segmentation, which are considerably more frequent in diseased than in normal eyes [22]. automated macular thickness values in such eyes should therefore be checked on the individual B-scans before they are interpreted. There is no universally accepted treatment regimen. Systematic reviews have not shown that routine antibiotic or corticosteroid treatment improves final visual acuity in immunocompetent patients with acute retinochoroiditis [23,24]. and many lesions are self-limiting. Treatment is nevertheless generally recommended for lesions that threaten the macula or optic disc, large lesions, severe vitritis and immunocompromised patients, and most uveitis specialists treat all non-pregnant patients [18]. Our patient, with a macular lesion, panuveitis, vasculitis and raised IOP, clearly warranted treatment. Oral trimethoprim-sulfamethoxazole is a rational choice because it achieved reductions in lesion size and improvements in visual acuity similar to those of the classic pyrimethamine-sulfadiazine regimen in a randomized trial [25]. no antibiotic regimen has proved superior in meta-analysis [26]. and it is inexpensive, widely available and now the first-line choice of two-thirds of uveitis specialists [18]. Intravitreal clindamycin with dexamethasone is an alternative for patients who cannot take oral drugs [27].

Corticosteroids are used to limit the tissue damage caused by the inflammatory response, which in this patient included panuveitis, vasculitis and raised IOP. They were given systemically by 97.4% of surveyed specialists, although no randomized trial has established their benefit, optimal dose or timing [28]. They should always be given under antiparasitic cover: corticosteroid monotherapy in misdiagnosed patients has led to fulminant retinochoroiditis, retinal detachment and poor final vision [13]. and corticosteroids given without antiparasitic drugs were a risk factor for visual loss in a large cohort [14]. Topical corticosteroids control the anterior segment inflammation, and IOP-lowering drugs are usually sufficient because the IOP rise is generally transient [12]. Recurrence is the main long-term threat. Recurrences developed in 79% of patients followed for more than five years in a Dutch series [14]. the risk is highest in the first year after an active episode (26%) [29]. and younger patients are more likely to have a recurrence [17]. Intermittent trimethoprim-sulfamethoxazole reduces this risk. One tablet every 3 days reduced recurrences from 23.8% to 6.6% over 20 months [30]. and one tablet every 2 days for 12 months prevented all recurrences in the first year compared with 12.8% in the placebo group [31]. with a benefit that persisted over six years of follow-up [32]. These trials enrolled patients with recurrent disease, so the evidence after a first episode is less direct; however, the high early risk supports prophylaxis during the first year after an active lesion [29]. The one-year course planned for our patient is consistent with this evidence and with current practice, in which most specialists prescribe prophylaxis to selected patients [18]. Adherence, blood counts and renal function should be monitored during this period.

This report has limitations. The diagnosis was based on clinical features and serology rather than on intraocular fluid analysis, the automated and line-scan OCT measurements of the affected eye were discordant, and the follow-up reported here does not yet cover the full year of prophylaxis. Because the lesion involved the macula, a recognized risk factor for permanent visual loss [14], long-term follow-up of central visual function is required. Nevertheless, the case offers a practical lesson: in a young patient with unilateral hypertensive panuveitis and retinal vasculitis, a careful search for a focal retinochoroidal lesion and an adjacent scar should precede any decision to start corticosteroids, and antiparasitic therapy should be started before or together with them.

CONCLUSION

Ocular toxoplasmosis may present in young adults as hypertensive non-granulomatous panuveitis with retinal vasculitis, a picture that can mimic other infectious and non-infectious uveitides. Recognizing the macular retinochoroiditis, supported by serology, allowed prompt treatment with oral trimethoprim-sulfamethoxazole, oral prednisolone, topical corticosteroids and IOP-lowering therapy, which resulted in significant improvement without complications. Early diagnosis is essential to prevent visual impairment, and intermittent trimethoprim-sulfamethoxazole prophylaxis for one year may reduce the risk of recurrence, which is highest in the first year after an active episode.

DECLARATIONS

None

CONSENT FOR PUBLICATION

The Authors agree to be published in the Journal of Society Medicine.

FUNDING

None

COMPETING INTERESTS

The authors declare no conflicts of interest in this case report.

AUTHORS’ CONTRIBUTIONS

N.S.S and M.R were both responsible for the clinical management of the patient, data collection, literature review, drafting of the original manuscript, and critical review and editing of the manuscript. Both authors read and approved the final version of the manuscript and agree to be accountable for all aspects of the work.

ACKNOWLEDGMENTS

This case was presented as an e-poster at the 50th Annual Scientific Meeting (PIT) and 17th National Congress (KONAS) of the Indonesian Ophthalmologists Association (PERDAMI), Bandung, Indonesia, 3–7 September 2025.

REFERENCE