Primary tubercular chorioretinitis: A case report

Abstract

Intraocular tuberculosis often evades diagnosis owing to its nonspecific clinical features and frequent absence of systemic signs. We describe a rare case of primary tubercular chorioretinitis in an immunocompetent woman in her early 20s who presented with acute vision loss, ocular pain, and redness in the left eye. Multimodal imaging demonstrated active inflammation arising within—not at the margin of—pre-existing focal chorioretinal atrophy, accompanied by retinal vasculitis and choroidal hypoperfusion. Systemic workup revealed no extrapulmonary involvement; however, interferon-gamma release assay was strongly positive. Following initiation of standard four-drug antitubercular therapy, adjunctive oral corticosteroids were administered, achieving complete resolution of intraocular inflammation and marked visual recovery, with no recurrence during long-term follow-up. This case highlights intralesional reactivation within chorioretinal atrophy as a distinctive imaging hallmark suggestive of tubercular etiology. Recognition of this pattern may facilitate earlier diagnosis of intraocular tuberculosis, particularly in endemic regions or in patients lacking overt systemic disease. Given the potential for irreversible vision loss, timely initiation of antitubercular therapy—guided by multimodal imaging and immunologic testing—is critical. Our findings underscore the need to consider ocular tuberculosis in the differential diagnosis of posterior uveitis, even in immunocompetent individuals with isolated ocular symptoms, and advocate for heightened awareness of this subtle yet pathognomonic feature to improve diagnostic precision and clinical outcomes.

Introduction

The clinical diagnosis of intraocular tuberculosis (IOTB) remains a formidable challenge owing to its protean manifestations and the frequent absence of systemic involvement. ¹ IOTB can mimic a wide spectrum of uveitic entities and often presents in isolation without evidence of pulmonary or extrapulmonary disease. Although several clinical features, such as broad-based posterior synechiae, retinal vasculitis with or without choroiditis, and serpiginous-like choroiditis (SLC), have been proposed as suggestive findings, none are pathognomonic. Moreover, definitive microbiological confirmation is rarely achievable due to the limited accessibility of ocular tissues for biopsy. ² Consequently, the diagnosis of IOTB typically relies on a composite approach integrating clinical suspicion, supportive immunological testing (particularly interferon-gamma release assays), exclusion of alternative etiologies, and a favorable response to empirical antitubercular therapy. Recent studies have described a distinctive clinical pattern in which active chorioretinitis arises within pre-existing chorioretinal atrophy, a finding reported in a series of patients with posterior uveitis and subsequently associated with tuberculous etiology. ³ This pattern contrasts with that observed in common infectious mimickers such as toxoplasmic retinochoroiditis, where reactivation typically occurs at the margins of pre-existing scars. The underlying mechanism presumably involves reactivation of dormant bacilli within fibrotic or atrophic granulomatous lesions, reflecting a dynamic interplay between persistent mycobacterial antigens and localized host immune responses. Herein, we report a case of unilateral chorioretinitis in a young woman without a history of tuberculosis, in whom active inflammation developed precisely within an area of established chorioretinal atrophy. Despite negative chest imaging and tuberculin skin testing, a strongly positive interferon-gamma release assay (TB-IGRA) and rapid clinical response to standard antitubercular therapy supported the diagnosis. This case not only reinforces the diagnostic value of this emerging imaging feature but also highlights the importance of considering intraocular tuberculosis in cases of so-called idiopathic posterior uveitis, even in the absence of systemic disease, particularly in regions with intermediate tuberculosis endemicity.

Case presentation

The reporting of this case conforms to the Case Report (CARE) guidelines. ⁴ A young woman in her early 20s was admitted to the People’s Hospital of Leshan, Sichuan, China, in late 2021, presenting with a 1-week history of decreased vision, redness, and pain in the left eye. She denied systemic symptoms or prior tuberculosis history. Ophthalmic examination revealed best-corrected visual acuity (BCVA) of 20/20 in the right eye, with intraocular pressure (IOP) of 18 mmHg (1 mmHg ≈ 0.133 kPa) measured using a Topcon non-contact tonometer; the anterior segment and fundus were unremarkable. In the left eye, BCVA was 20/70, and IOP was 14 mmHg. Slit-lamp examination revealed conjunctival injection (+), fine dust-like keratic precipitates (KP) (+), and anterior chamber cells, which were graded as 1+ according to the SUN classification. The pupillary light reflex was brisk, and the lens was clear. Vitreous examination revealed moderate linear opacities (Figure 1). Ultra-widefield fundus photography of the left eye revealed a well-perfused optic disc and a yellow–white, plaque-like lesion, which was approximately 2 disc diameters (DD; 1 DD ≈ 1.5 mm) in size located superonasally, surrounded by pigmentary changes. Segmental, creamy yellow infiltrates of varying lengths were observed along retinal vessels throughout the periphery (Figure 2). Optical coherence tomography (OCT) revealed preserved foveal architecture (Figure 3), mild retinal thickening with indistinct intraretinal layers over the active lesions, and focal atrophy with depression corresponding to the pigmented scar area (Figure 4). Using the Heidelberg Spectralis HRA (Heidelberg Retina Angiograph), imaging of the 55° posterior pole revealed abnormal autofluorescent signals along the vascular arcade inferior to the macula on both (a) infrared reflectance and (b) fundus autofluorescence; however, the area of pigmentary lesion was not captured (Figure 5). Fluorescein angiography combined with indocyanine green angiography revealed hyperfluorescent leakage from retinal lesions, corresponding to choroidal hypoperfusion, and diffuse vascular leakage (Figures 6 to 8). Systemic evaluation, including cranial and thoracoabdominal computed tomography, was unremarkable. Serological tests for syphilis, human immunodeficiency virus, and hepatitis were negative. The tuberculin skin test was negative, whereas the TB-IGRA was strongly positive (1709.01 pg/mL). Based on the characteristic ocular findings and positive TB-IGRA, a diagnosis of tuberculous chorioretinitis was established. The patient was initiated on standard four-drug antitubercular therapy (ATT), comprising isoniazid, rifampicin, ethambutol, and pyrazinamide, in combination with short-term adjunctive oral corticosteroid therapy. Follow-up was conducted at 2 weeks, 6 months, and annually thereafter. At 2 weeks after initiation of therapy, intraocular inflammation had significantly subsided, accompanied by improved BCVA and reduced vitreous haze; oral corticosteroids were subsequently tapered and discontinued. At 6 months, complete resolution of active inflammation was observed with residual chorioretinal scarring, and BCVA recovered to 20/20. Antitubercular therapy was subsequently discontinued, as the patient had achieved sustained clinical remission without evidence of active disease. Long-term follow-up over 4 years revealed no recurrence or new lesions.

Figure 1.

A flat, elevated lesion was observed in the superonasal region of the optic disc (red arrow), accompanied by linear echogenic strands within the vitreous cavity (blue arrow).

Figure 2.

Ultra-widefield fundus imaging demonstrated cord-like vitreous opacities in the posterior pole (blue arrow). A yellow–white, plaque-like lesion measuring approximately 2 disc diameters (1 DD = 1.5 mm) was observed in the superonasal region of the optic disc, with surrounding pigment deposition (green arrow). Segmental changes were observed circumferentially along the retinal vessels, with yellow–white inflammatory exudates adhering to the vessel walls (red arrow).

Figure 3.

Macular optical coherence tomography (OCT) imaging demonstrated signal attenuation in the nasal and superior regions relative to the fovea due to overlying vitreous opacities, resulting in reduced image clarity in these areas. Nevertheless, the foveal architecture remained intact and preserved.

Figure 4.

Optical coherence tomography (OCT) of the lesion. The en face localization image (upper left) delineates the scan trajectory across the lesion, with corresponding serial B-scans (upper right) demonstrating layered structural alterations. The cross-sectional OCT image (bottom) reveals focal retinal thickening at the lesion site, accompanied by disorganization of both the inner and outer retinal layers. A localized excavation involving the retina and the underlying choroid is evident, exhibiting a “scooped-out” appearance, along with choroidal thinning and increased signal transmission into the deeper tissues.

Figure 5.

Multimodal imaging obtained using the Heidelberg Spectralis HRA (Heidelberg Retina Angiograph) with a 55° wide-field lens, centered on the posterior pole. (a) Infrared reflectance (IR) and (b) fundus autofluorescence (FAF) images demonstrate irregular central shadowing obscuring the visual field, consistent with dense vitreous opacities (blue arrow). A corresponding area of increased autofluorescence is observed along the inferior vascular arcade beneath the macula (red arrow). The pigmented lesion was not captured within the scanned field.

Figure 6.

Fluorescein fundus angiography showing marked hyperfluorescent leakage from the active chorioretinal lesion (blue arrow), corresponding to hypoperfusion on indocyanine green angiography (red arrow).

Figure 8.

Fluorescein fundus angiography showed leakage from small retinal vessels and capillaries in the mid-peripheral retina, resulting in a diffuse hyperfluorescent appearance with indistinct margins (green arrow). No corresponding abnormality was observed in the same region on indocyanine green angiography.

Figure 7.

Fluorescein fundus angiography demonstrating vessel wall staining and leakage involving the major retinal vessels in the mid-peripheral retina (green arrow), consistent with retinal vasculitis. No corresponding abnormality was observed in the same region on indocyanine green angiography.

Discussion

In recent years, the global incidence of TB has demonstrated a resurgence, partly attributable to the widespread use of antimicrobial agents and immunosuppressive therapies. The prevalence of intraocular TB (IOTB) varies markedly by region, ranging from 0.2%–2.7% in low-incidence areas (e.g. United States, Europe, and Japan) to 5.6%–10.5% in high-burden countries such as India. ⁵ Although nationwide epidemiologic data on IOTB in China are lacking, reports from tertiary referral centers indicate that IOTB accounts for approximately 3%–10% of uveitis cases, particularly among patients with posterior or panuveitis. Notably, China is currently classified as a low- to intermediate-burden country, with an estimated TB incidence of 49 per 100,000 population in 2024. ⁶ IOTB typically results from hematogenous dissemination from a primary focus. However, in rare instances, it may arise as a primary infection following epithelial injury, independent of systemic disease. Clinically, it most commonly manifests as retinal vasculitis, retinal vasculitis with choroiditis, or multifocal choroiditis; these features are attributable to the choroid’s dense vascular network and sluggish blood flow, which facilitate the deposition of tuberculin antigens and immune complexes.^2,7 The clinical entity of tuberculous chorioretinitis was first described by Graefe and Leber in 1868. Nevertheless, its diagnosis remains challenging because of the inaccessibility of choroidal tissue for biopsy, low microbiological yield, and frequent absence of concurrent systemic TB. Consequently, it is often misdiagnosed as intraocular malignancy or “idiopathic” choroiditis. ⁸ In clinical practice, diagnosis frequently relies on a constellation of characteristic fundus findings, supportive ancillary testing, and a favorable response to empirical ATT,^9,10 thereby underscoring the inherent diagnostic uncertainty that defines this condition.^1,11 Chauhan et al. ¹² highlighted the rarity and atypical presentation of extrapulmonary tuberculosis presenting as chorioretinitis and emphasized the need to raise awareness and improve diagnostic capacity for ocular tuberculosis in resource-limited settings. Current international diagnostic criteria for tuberculous chorioretinitis include the following: ¹³ (a) acute or subacute anterior or posterior uveitis occurring in young or middle-aged adults, with posterior involvement typically characterized by large, confluent peripapillary or juxtapapillary lesions demonstrating a migratory pattern; (b) radiographic findings suggestive of tuberculosis on chest imaging or microbiological confirmation of Mycobacterium tuberculosis; (c) positive immunologic testing, such as IGRA; (d) a positive purified protein derivative (PPD) skin test; and (e) a favorable clinical response to antitubercular therapy (ATT).

In the present case, a young woman presented with unilateral ocular inflammation characterized by features of both anterior and posterior uveitis, including subacute anterior chamber reaction, vitreous opacities, and plaque-like yellow–white fundus lesions with perivascular infiltrates. These findings are consistent with choroiditis accompanied by retinal vasculitis. Although systemic evaluation revealed no evidence of extrapulmonary tuberculosis and only the IGRA was positive, the diagnosis was supported by a robust clinical response to standard four-drug ATT. This case underscores that in patients presenting with unexplained chorioretinitis, occult intraocular tuberculosis should be considered even in the absence of systemic manifestations. Notably, ocular tuberculosis often occurs in the setting of latent infection and may represent an underrecognized cause of the so-called idiopathic uveitis, particularly in regions with limited diagnostic resources. ¹⁴ White dot syndromes were considered in the differential diagnosis; however, the presence of marked anterior chamber inflammation, dense vitreous haze, and a solitary pigmented lesion with associated retinal vasculitis, together with noncharacteristic multimodal imaging findings, made this diagnosis unlikely. From a diagnostic perspective, toxoplasmic chorioretinitis remains an important differential consideration given its overlapping presentation with focal white retinal lesions and pigmentary scarring. Serpiginous choroiditis (SC) and tubercular SLC are also frequently invoked in the differential diagnosis of posterior uveitis with chorioretinal lesions; however, their clinicopathologic profiles are distinct and should not be used interchangeably. SC is a bilateral, recurrent, and presumably immune-mediated entity characterized by contiguous, centrifugal spread from the peripapillary region, resulting in geographic chorioretinal atrophy.^15,16 In contrast, SLC, most often associated with M. tuberculosis, typically demonstrates a multifocal or placoid configuration, frequently accompanied by more pronounced intraocular inflammation and a less stereotyped pattern of progression.^17,18 In the present case, the phenotype diverges from both entities. The lesion was solitary, well circumscribed, and nonprogressive, lacking the hallmark serpiginous extension or lesion confluence observed in SC as well as the multifocality and inflammatory burden more typical of SLC. The coexistence of retinal vasculitis further supports an infectious chorioretinal process rather than a primary serpiginous spectrum disorder. These distinctions are not merely semantic but diagnostically consequential, as misclassification may obscure the underlying etiology and lead to suboptimal therapeutic strategies. Accordingly, our findings are more consistent with focal tuberculous chorioretinitis, highlighting the need for careful phenotypic discrimination within the spectrum of tuberculous ocular disease.

However, a key distinguishing feature is that toxoplasmic reactivation typically occurs at the margins of pre-existing scars, reflecting the reactivation of dormant cysts. ¹⁹ In contrast, our case demonstrated active inflammation arising within a pre-existing chorioretinal atrophic lesion, suggesting a distinct pathogenic mechanism. ²⁰ This pattern may reflect the immunopathological features of M. tuberculosis infection. Following infection, dendritic cells activate CD4⁺ and CD8⁺ T cells, which in turn stimulate infected macrophages. The bacillus can evade lysosomal degradation, resulting in persistent infection and chronic antigenic stimulation. This promotes the aggregation of immune cells into granulomas, where a dynamic balance is maintained between bacterial containment and survival. Over time, these granulomas may undergo fibrosis or calcification, forming chorioretinal atrophic scars. Reactivation of dormant bacilli within these lesions may disrupt local immune equilibrium, leading to recurrent inflammation precisely within areas of prior atrophy. Emerging evidence, particularly from studies by Basu et al., ²¹ further supports a unifying disease spectrum in intraocular tuberculosis, wherein retinal vasculitis and chorioretinal lesions represent interconnected manifestations rather than distinct entities. Retinal vasculitis is typically characterized by perivascular inflammation, vascular sheathing, and occlusive changes and is frequently associated with adjacent chorioretinal atrophic patches that likely represent healed granulomatous inflammation. The observation that such lesions often localize along retinal vessels has led to the concept of “subvascular lesions,” suggesting a spatial and pathogenic continuum between choroidal and retinal involvement. ²² In this context, the coexistence of retinal vasculitis and chorioretinal atrophy in our case may reflect both prior and ongoing host–pathogen interactions. The presence of active inflammation within a pre-existing atrophic lesion further supports the concept that these scars may serve as reservoirs for latent infection, with the potential for intralesional reactivation. Collectively, these findings support a unified pathogenic framework in which chorioretinal atrophy represents the sequela of healed granulomatous inflammation, while subsequent intralesional reactivation and associated retinal vasculitis reflect dynamic and evolving host–pathogen interactions along a continuous spectrum of intraocular tuberculosis.

Standard management of tuberculous chorioretinitis is based on systemic ATT, administered in accordance with the principles of early initiation, combination therapy, appropriate dosing, regular adherence, and a full treatment course, all of which are essential to prevent irreversible vision loss and limit disease transmission. ²³ During treatment, patients were closely monitored for ethambutol-induced optic neuropathy, with regular assessment of visual acuity, color vision, and optic nerve function; no evidence of drug-related toxicity was observed throughout follow-up. Adjunctive corticosteroids are commonly used to control intraocular inflammation in tubercular choroiditis; however, they should be used only in conjunction with appropriate antitubercular therapy to prevent disease exacerbation or reactivation. ²⁴ The role of immunosuppressive agents remains controversial and is generally reserved for refractory or recurrent cases, particularly in SLC, under adequate antimicrobial coverage. ²⁵ This study has several limitations. As a single case report, the findings may not be generalizable. In addition, microbiological confirmation was lacking, and the diagnosis was based on clinical and immunological evidence, supported by the response to therapy.

Conclusion

Intraocular tuberculosis remains a significant diagnostic challenge owing to its ability to mimic a broad spectrum of more common intraocular inflammatory conditions, particularly uveitis, thereby predisposing to misdiagnosis and delayed treatment. Our findings highlight that active inflammation arising within pre-existing chorioretinal atrophy may represent a distinctive and clinically relevant imaging feature of tubercular chorioretinitis. Recognition of this intralesional reactivation pattern may serve as a clinically actionable imaging biomarker, facilitating earlier diagnosis and more accurate differentiation from its mimickers in real-world clinical practice.