
Transient superficial retinal infiltrates are a recognised feature of Behçet uveitis, but their capacity to mimic infectious retinitis is under-emphasised. We describe the diagnostic pitfalls and multimodal imaging appearances of these infiltrates, and summarise practical clues for distinguishing them from infectious retinitis. Retrospective case series of five patients with Behçet uveitis who developed multiple transient superficial retinal infiltrates between May 2020 and October 2025. Assessments included visual acuity, slit-lamp examination, fundus photography, fluorescein angiography (FFA), optical coherence tomography (OCT), and in selected cases, OCT angiography (OCTA) and indocyanine green angiography (ICGA). Five patients (3 men, 2 women; aged 24–63 years) were included. The infiltrates were unilateral in all five; in one the underlying uveitis was bilateral. They were present at first presentation in three patients and developed during follow-up in two. Three had been misdiagnosed with infectious uveitis and given empirical antimicrobial therapy before referral; the median interval from first presentation to the correct diagnosis was 3.6 months (range 1.4–7.8). Retinal vascular leakage was present in all patients, was diffuse, and showed no spatial correspondence to the infiltrates. OCT showed hyperreflectivity predominantly of the inner retina with a preserved retinal pigment epithelium (RPE). Inflammatory retinal and vitreous deposits were seen in two patients, and OCTA, performed in one, showed capillary non-perfusion corresponding to the affected retina. All infiltrates resolved within days to weeks without chorioretinal scarring, and recurrences were common. Spontaneous regression with concurrent new lesion formation (Case 1) and residual inner-retinal thinning in near periphery (Case 2) were both documented on imaging. Behçet uveitis can present with transient superficial retinal infiltrates that mimic infectious retinitis. Supportive features include inflammatory retinal and vitreous deposits, resolution without chorioretinal scarring, retinal vascular leakage unrelated in distribution to the infiltrates, and inner-retinal hyperreflectivity with a preserved RPE; none excludes infection, and investigation for infectious causes remains necessary. Recurrent transient superficial retinal infiltrates, particularly when accompanied by subtle retinal vascular leakage without a classic diffuse fern-like pattern, should raise suspicion of Behçet uveitis and prompt directed questioning about recurrent oral and genital ulceration.
To report the anatomical and functional outcomes of intravitreal faricimab in two cases of persistent cystoid macular edema (CME) associated with uveitis–glaucoma–hyphema (UGH) syndrome. Two patients with UGH syndrome developed persistent CME refractory to conventional medical treatment. Both patients had a history of three-piece intraocular lens implantation in the sulcus and demonstrated findings suggestive of mechanical iris chafing in the absence of associated retinal vascular pathology. Initial treatment with topical nonsteroidal anti-inflammatory drugs, topical corticosteroids, and periocular corticosteroid injections failed to achieve anatomical resolution of CME. Intravitreal corticosteroid therapy was considered but avoided because of coexisting glaucoma and concerns regarding intraocular pressure elevation. Both patients subsequently received a single intravitreal injection of faricimab, resulting in resolution of CME and improvement in visual acuity, with sustained anatomical stability during follow-up. Intravitreal faricimab demonstrated favorable anatomical and functional outcomes in two patients with refractory CME secondary to UGH syndrome. These findings suggest that faricimab may serve as an alternative treatment strategy in selected cases where conventional therapeutic options are limited.
Periorbital cutaneous anthrax is an exceptionally rare clinical entity that closely mimics periocular necrotizing fasciitis, creating a significant diagnostic challenge. While most reported cases are zoonotic, this report details a 46-year-old male construction worker who developed fulminant periorbital anthrax 48 h after sustaining a soil-contaminated iron rod abrasion, without any known animal contact. He presented with high-grade fever, rapidly progressive periorbital necrosis, and massive non-pitting edema. The initial presentation mimicked necrotizing fasciitis, prompting staged surgical debridement and broad-spectrum antibiotics. Because prior empirical antibiotic therapy rapidly rendered bacterial cultures sterile, early Gram staining provided an important microbiological clue for initiating anthrax-directed therapy. Definitive diagnosis was established via real-time polymerase chain reaction (RT-PCR) confirming Bacillus anthracis through pagA and cap gene amplification. Definitive oculoplastic reconstruction with a full-thickness skin graft, performed 6 months later, successfully corrected the resulting cicatricial ectropion. This case highlights the critical importance of utilizing early Gram stains and molecular diagnostics in culture-negative scenarios to rapidly differentiate toxin-mediated anthrax from polymicrobial necrotizing fasciitis and to establish the appropriate therapeutic and surgical approach.
Faricimab (Vabysmo™, Roche/Genentech, Basel, Switzerland) is a humanized, bispecific monoclonal antibody which binds and inhibits both angiopoietin-2 and all vascular endothelial growth factor (VEGF)-A isoforms. It has been approved for the treatment of neovascular age-related macular degeneration, diabetic macular oedema, and retinal vein occlusion. Given that faricimab-associated intraocular inflammation is increasingly documented in recent large cohorts [1–6], the primary novelty of this report lies in the detailed serial photographic documentation of the morphological evolution and complete resolution of the granulomatous keratic precipitates over a 5-month follow-up period. A retrospective chart review was conducted to extract clinical data, multimodal imaging, and serial slit-lamp photographs of a patient who developed intraocular inflammation following faricimab therapy. The Standardization of Uveitis Nomenclature (SUN) criteria and the Naranjo Probability Scale were applied to grade the inflammation and assess the likelihood of the adverse drug reaction, respectively. Ten days after her seventh faricimab injection, the patient presented with vision loss, mild eye pain, increased intraocular pressure, mutton-fat keratic precipitates, and unilateral granulomatous anterior and intermediate uveitis. The condition was successfully managed with topical corticosteroids and hypotensive eye drops, leading to complete clinical resolution. The adverse drug reaction was considered probable; however, aqueous humor viral testing was not performed, leaving viral etiology as an unexcluded alternative diagnosis. This observation contributes to the understanding of faricimab’s real-world safety profile. While it highlights a potential risk of delayed-onset intraocular inflammation, infectious etiologies must be strictly evaluated before definitively attributing such events to the drug, emphasizing the need for ongoing monitoring and research.
Pediatric sinusitis-associated orbital subperiosteal abscess (SPA) can threaten vision and sometimes prompts urgent orbital drainage, but the clinical and radiologic factors associated with this management decision remain incompletely defined. This retrospective cohort study included consecutive patients younger than 18 years admitted to a tertiary referral eye hospital in Tehran, Iran, with computed tomography (CT)-confirmed orbital SPA secondary to sinusitis during four autumn-winter seasons from 2022 to 2026. SPA volume was calculated on admission CT images using an ellipsoid approximation formula. The primary outcome was orbital abscess drainage during the index hospitalization, representing the treatment performed rather than an independently adjudicated need for surgery. Group comparisons, multivariable logistic regression, sensitivity analyses, and exploratory receiver operating characteristic (ROC) analysis were performed. The study included 112 patients; 78 (69.6
To describe the spectrum, clinical course, and outcomes of ocular inflammatory adverse events linked to immune checkpoint inhibitors (ICIs) in a Singapore cohort. This retrospective cohort examined six patients who developed ocular symptoms after ICI treatment, including ipilimumab-nivolumab and pembrolizumab. We analyzed clinical features, symptom onset timing, diagnoses, treatments, and outcomes. Six Chinese Singaporean patients (2 men, 4 women; aged 52–72 years) presented with eye redness, pain, and blurred vision 2–14 days after ICI doses. Symptoms arose after the first dose in one patient and after the second to tenth doses in the others. Diagnoses included anterior uveitis (n = 3; two granulomatous) and granulomatous panuveitis (n = 3), with initial best-corrected visual acuity from 20/25 to 20/100. All received topical and/or systemic corticosteroids without needing to stop ICIs. One patient had anterior uveitis recurrence 3 months later, with both episodes resolving using topical steroids. Two panuveitis cases progressed to sunset-glow fundus; another showed bilateral choroidal granulomas on angiography without visible clinical signs. Final visual acuity ranged from 20/20 to 20/50, with no significant long-term morbidity over 8–72 months of follow-up. Ocular inflammatory adverse events from ICIs in this Singapore cohort showed a predominantly granulomatous spectrum with favorable corticosteroid responses, enabling ICI continuation. Multimodal imaging highlighted choroidal granulomas and sunset-glow fundus evolution. Early recognition and multidisciplinary care preserved vision across diverse Asian patients without oncologic compromise.
Drug-induced retinal vasculitis (DIRV), a complex diagnostic entity, masquerades as infectious or primary autoimmune diseases. Delineating them is a daunting task. This update aims to consolidate clinical evidence focussing on characteristic “vascular signatures” using advanced multimodal imaging tools. Type III (immune complex-mediated) and Type IV (T-cell-mediated) hypersensitivity pathways were involved in diverse range of drugs causing DRIV. The critical therapeutic strategies are highlighted to prevent permanent ischemic damage. Advances in the recent metagenomic markers are added to aid the clinician from a practical standpoint to aid in preventive and personalised ophthalmic care.
To report a case of Purtscher-like retinopathy (PLR) associated with macular edema in a young person with systemic lupus erythematosus (SLE) whose vision was restored with a systemic corticosteroid regimen and to highlight the rare and vision-threatening complication of SLE. Case report. A 27-year-old female without significant ophthalmological history who had stopped taking azathioprine and methylprednisolone for her SLE presented with sudden painless unilateral vision loss (best-corrected visual acuity [BCVA] RE: 1 m CF, LE: 20/20). Fundus examination revealed bilateral Purtscher-flecken and cotton wool spots, while optical coherence tomography (OCT) identified intra- and subretinal fluid representing macular edema with paracentral acute middle maculopathy (PAMM) on the right eye. The findings led to PLR diagnosis, and the patient received IV methylprednisolone with tapering. Five months after initial encounter, the patient’s vision recovered (BCVA RE: 20/30, LE: 20/20) and OCT showed resolution of the pathology. While PLR is rarely found in people with SLE, it should be considered as a differential diagnosis in people with SLE presenting with sudden vision loss due to the condition being easy to diagnose clinically and its prompt treatment using corticosteroids may restore the vision loss and resolve the retinal pathology.
To determine the period prevalence of new or recurrent ocular inflammation, including corneal allograft rejection, occurring within 30 days after COVID-19 vaccination. This retrospective cohort study was conducted at a tertiary referral eye center. A systematic random sample of 4,638 patient charts (50
To describe the longitudinal clinical and multimodal imaging findings of a patient with progressive subretinal fibrosis and uveitis (SFU) syndrome. Case report. An 85-year-old woman with a history of cardiomyopathy, systemic hypertension, hyperlipidemia and hypothyroidism presented with a 5-day history of acute bilateral visual decline. At baseline, best-corrected Snellen visual acuity was 20/80 OD and 20/400 OS. Fundus examination revealed multifocal chorioretinal lesions with fibrotic subretinal changes and vitreous inflammation. Fundus autofluorescence demonstrated scattered areas of hypoautofluorescence with hyperautofluorescent borders, and fluorescein angiography revealed window defects with late staining but no leakage. Spectral-domain optical coherence tomography (SD-OCT) showed diffuse retinal pigment epithelium (RPE)-Bruch’s membrane (BrM) splitting and overlying fuzzy subretinal hyperreflective material (SHRM). Primary vitreoretinal lymphoma and multifocal choroiditis were initially suspected; however, systemic and uveitis work-up was negative. The patient’s advanced age was atypical for new-onset SFU and further contributed to diagnostic uncertainty. Despite oral corticosteroid treatment and intravitreal dexamethasone implants OU, the disease progressed relentlessly, leading to widespread subretinal fibrosis and chorioretinal atrophy, and severe visual decline (20/100 OD, counting fingers OS at 12 months). SFU is a rare, aggressive, and underrecognized immune-mediated uveitic syndrome that can masquerade as neoplastic or inflammatory chorioretinopathies. This atypical late-onset case expands the known age spectrum of the disease and highlights the importance of considering SFU in rapidly progressive chorioretinal fibrosis in older adults. OCT biomarkers – particularly RPE–BrM splitting and fuzzy SHRM – may signal early SFU, emphasizing timely recognition and immunomodulatory therapy to prevent vision loss.
Ocular toxoplasmosis is the most common cause of posterior uveitis worldwide and a major cause of visual impairment. Previous studies suggest that the disease may follow a more aggressive clinical course in patients from Latin America; however, direct comparative evidence between geographic populations remains limited. This study aimed to characterize the clinical, serological, and imaging features of a multiethnic cohort of patients with ocular toxoplasmosis and to assess differences according to geographic origin. A retrospective chart review was performed including 144 patients diagnosed with ocular toxoplasmosis at a tertiary referral center in Barcelona, Spain. Clinical characteristics, recurrence patterns, visual outcomes, and serological findings were analyzed. Outcomes were compared between Latin American (n = 73) and European (n = 71) patients. Latin American origin (OR 8.21; p < 0.001) and older age at disease onset (OR 1.04; p = 0.009) were independently associated with atypical disease presentation. Latin American origin (β = +0.20 LogMAR; p = 0.02), congenital disease (β = +0.52 LogMAR; p < 0.001), and retinal zone I involvement (β = +0.57 LogMAR; p < 0.001) were independently associated with worse visual acuity outcomes. Latin American origin (OR 4.85; p = 0.002) and longer time since disease onset (OR 1.05; p = 0.04) were independently associated with multiple recurrences, whereas congenital disease (OR 0.03; p = 0.01) was associated with lower recurrence risk. Serum IgG levels were significantly higher in Latin American patients (p = 0.002), who also more frequently required systemic corticosteroids along with antiparasitic treatment. Patients of Latin American origin showed a higher prevalence of atypical disease, increased recurrence rates, and poorer visual outcomes compared with European patients. These findings support the hypothesis of a more severe disease phenotype in this population and highlight the importance of closer monitoring and individualized management strategies in patients at higher risk of severe ocular toxoplasmosis.
PURPOSE:To describe the clinical features and outcomes of cytomegalovirus retinitis (CMVR) presenting after intravitreal fluocinolone acetonide (FAc) implantation. METHODS:Single centre, retrospective observational case series involving three patients who developed CMVR several months after FAc implantation at the uveitis department at Moorfields Eye Hospital, London, UK. Clinical history, immune status, ocular findings, imaging, and management were reviewed. RESULTS:The first patient with pulmonary sarcoidosis and no systemic treatment presented 14 months post-implant with granular retinitis and severe occlusive retinal vasculitis. He developed renal toxicity to valganciclovir, necessitating intravitreal foscarnet and FAc implant removal. The second patient with presumed ocular sarcoidosis on multiple immunosuppressive agents developed fulminant necrotising CMVR eight months after FAc implantation and responded well to systemic valganciclovir with adjunctive intravitreal foscarnet therapy. The third patient, an elderly man with previous CMV retinitis in the context of follicular lymphoma, experienced reactivation at the margin of an old scar several months after FAc implantation and was stabilised with intravenous and intravitreal foscarnet. Although two patients had bilateral implants, the retinitis remained unilateral. Across cases, presentations ranged from granular retinitis with vasculitis to fulminant necrosis and late reactivation. CONCLUSION:Delayed-onset CMVR can occur in eyes treated with FAc implants, particularly in immunosuppressed patients. Recognition of atypical presentations, early PCR testing and timely antiviral therapy are essential to preserve vision.
Acanthamoeba keratitis (AK) is a sight-threatening corneal infection that may initially lack typical epithelial or perineural findings and mimic other infectious or inflammatory anterior segment disorders. Endotheliitis-like presentations of AK with stromal edema, keratic precipitates, Descemet membrane folds, and anterior chamber inflammation have been reported, but progression to severe stromal necrosis with spontaneous sloughing of necrotic corneal tissue is rarely documented. A 48-year-old contact lens wearer presented with right eye pain, redness, and decreased vision. Initial examination at a local clinic revealed anterior chamber inflammation without epithelial defects, radial keratoneuritis, or a ring infiltrate, and topical betamethasone was started before referral. At referral (0 weeks; 12 days after symptom onset), slit-lamp examination revealed diffuse stromal edema, fine keratic precipitates, Descemet membrane folds, and anterior chamber inflammation, closely mimicking viral corneal endotheliitis. Aqueous humor polymerase chain reaction for human herpesviruses 1–8 was negative. Because viral endotheliitis or noninfectious anterior uveitis was considered, topical corticosteroids and systemic prednisolone were administered (initially 30 mg/day and was gradually tapered). During follow-up, the clinical appearance evolved toward AK, and anti-infective therapy was revised. Corneal scraping was performed, but direct microscopy and bacterial and fungal cultures were negative. PCR testing of a corneal scraping specimen for Acanthamoeba, bacteria, and fungi was negative. Despite treatment, stromal necrosis progressed to severe corneal melting. At 34 weeks after referral, necrotic corneal tissue spontaneously sloughed as a sequestrum and was submitted for pathological evaluation. Hematoxylin and eosin and periodic acid-Schiff staining revealed necrotic corneal stromal tissue with inflammatory cell infiltration and multiple double-walled cystic structures consistent with Acanthamoeba cysts, confirming AK. This case illustrates a diagnostically challenging form of AK that initially mimicked corneal endotheliitis, yielded negative scraping-based microbiological tests, and was ultimately confirmed by histopathologic examination of spontaneously sloughed necrotic stromal tissue. Severe AK rarely manifests as necrotic stromal sequestration and spontaneous sloughing, in addition to the more commonly recognized destructive outcomes such as corneal thinning, perforation, or keratoplasty-requiring disease. Repeated diagnostic reassessment is important in contact lens wearers with atypical endotheliitis-like keratitis, particularly when the disease progresses despite antiviral or anti-inflammatory therapy.
Abstract Background Fungal keratitis is a sight-threatening condition that accounts for approximately 30–40% of keratitis cases in developing countries. Its management remains challenging despite the availability of various antifungal agents, highlighting the potential role of targeted drug delivery in recalcitrant cases. Purpose To evaluate the efficacy of corneal intrastromal voriconazole (ISV) injection in the management of fungal keratitis unresponsive to conventional antifungal therapy. Methods This prospective interventional case series included 21 eyes of 21 patients with smear-positive fungal keratitis that failed to respond to at least two weeks of topical antifungal therapy. All patients underwent detailed ophthalmological examination and ulcer assessment using anterior segment optical coherence tomography (AS-OCT). Intrastromal voriconazole (50 µg/0.1 mL) was administered circumferentially around the ulcer. Treatment response was evaluated through serial follow-up, including assessment of ulcer size, infiltrate extent, hypopyon level, presence of satellite lesions, and best-corrected visual acuity (BCVA). Results The mean age of the patients was 57.19 ± 6.74 years, with a predominance of males (76.2%). Most patients were from rural areas (76.2%) and had a history of vegetative trauma (71.4%). The mean ulcer size was 4.64 ± 0.95 mm, and the mean infiltrate size was 6.43 ± 1.29 mm. Hypopyon was present in 57.1% of cases, and the mean ulcer depth measured by AS-OCT was 257.14 ± 68.12 μm. Aspergillus was the most isolated organism (52.4%). BCVA improved significantly from 2.71 ± 0.46 LogMAR at baseline to 1.34 ± 0.68 at 3 months (P < 0.001). Complete resolution was achieved in 19 patients (90.5%). Fourteen patients (66.7%) responded to a single injection, while five (23.8%) and two (9.5%) required two and three injections, respectively. Most cases (84.2%) resolved within 2–4 weeks. Two patients (9.5%) showed disease progression and required therapeutic penetrating keratoplasty and were excluded from the final analysis. Conclusion Intrastromal voriconazole injection appears to be an effective adjunctive treatment for recalcitrant fungal keratitis, improving clinical outcomes and potentially reducing the need for therapeutic or tectonic keratoplasty.
To describe an atypical late-onset presentation of Vogt–Koyanagi–Harada (VKH) disease initially interpreted as autoimmune glial fibrillary acidic protein astrocytopathy (GFAP-A) in association with an ovarian teratoma. A 59-year-old woman presented with bilateral optic disc edema, visual field defects, and headache following a flu-like illness. Comprehensive ophthalmologic, neurologic, and systemic evaluation was performed, including multimodal ocular imaging, cerebrospinal fluid (CSF) analysis with antibody testing, and neuroimaging. Clinical course and response to corticosteroid therapy were assessed longitudinally. Initial findings, including CSF anti-GFAP positivity, lymphocytic pleocytosis, white matter lesions, and an ovarian teratoma, supported a diagnosis of GFAP-A. However, sequential multimodal imaging revealed diffuse, steroid-responsive choroidal inflammation with choroidal thickening, folds, mild subretinal fluid, hypocyanescent dark dots on indocyanine green angiography, fluorescein angiography pinpoints, and bilateral hot discs. Granulomatous anterior uveitis and subsequent choroidal depigmentation further supported VKH. Bilateral sensorineural hearing loss was also consistent with this diagnosis. The longitudinal ocular phenotype proved more consistent with VKH than with primary astrocytopathy-related optic neuropathy. Late-onset VKH may present predominantly with optic disc edema and central nervous system involvement, closely mimicking inflammatory neurologic disease. Recognition of subtle choroidal inflammation and integration of longitudinal multimodal imaging are essential to avoid misdiagnosis and guide appropriate immunosuppressive management.
To describe ultrawide-field fluorescein angiographic features of extensive retinal capillary non-perfusion in eyes with intraocular cytomegalovirus infection. Retrospective, single-centre observational study. Five patients (six eyes) with intraocular CMV infection were included (mean age 62 years; range 15–84). All eyes showed widespread retinal haemorrhages without features of classical oedematous/haemorrhagic necrotising cytomegalovirus retinitis. In eyes with retinitis, the lesions showed a granular phenotype.Three eyes presented with hypertensive uveitis and raised intraocular pressure without neovascularisation. Ultrawide-field fluorescein angiography demonstrated extensive capillary non-perfusion involving both arterioles and venules, reflecting a predominantly occlusive vasculopathy. Vitreous haemorrhage occurred in three eyes, and one progressed to phthisis bulbi despite virological control. Predisposing factors included haematological malignancy, severe malnutrition, local corticosteroid implantation, diabetes with preceding shingles, and systemic immunomodulatory therapy. All the patients received systemic and intravitreal anti viral treatment and were additionally treated for the raised intraocular pressure and respective complications secondary to retinal ischemia. Intraocular cytomegalovirus infection in non-human-immunodeficiency-virus patients may present as hypertensive uveitis with an occlusive pan-retinal vasculopathy, with or without retinitis, best recognised on ultrawide-field fluorescein angiography. Antiviral therapy and laser may achieve initial control but are insufficient alone; long-term monitoring and patient counselling are essential to address recurrent haemorrhage and neovascular glaucoma.
Endophthalmitis caused by Nocardia brasiliensis is extremely rare and typically affects immunocompromised individuals, frequently leading to severe vision loss due to diagnostic delays. We report a case of N. brasiliensis endophthalmitis in an older man without prior history of systemic immunosuppression but with newly identified diabetes mellitus, characterized by an indolent initial course followed by fulminant progression. A 67-year-old man without known systemic immunosuppression presented with a two-month history of recurrent right-eye pain and redness, followed by rapid vision loss and a hypopyon. Aqueous humor analysis and metagenomic sequencing identified N. brasiliensis. Despite intravitreal amikacin, systemic antimicrobial therapy, and subsequent pars plana vitrectomy with silicone oil tamponade, intraocular inflammation advanced, resulting in worsening corneal opacification, irreversible structural damage, and a final best-corrected visual acuity of light perception. N. brasiliensis endophthalmitis may progress rapidly and result in severe, irreversible ocular damage, even in patients without overt systemic immunodeficiency. Early microbiologic identification and prompt, targeted antimicrobial therapy combined with timely surgical intervention are critical, although visual outcomes may remain poor in advanced cases.
Abstract Background Endophthalmitis is a severe intraocular infection associated with potentially devastating visual outcomes. Shinella , a Gram-negative bacillus commonly found in water and soil, has never been reported as a cause of human disease. Case presentation A 49-year-old female farmer presented with a 7-day history of vision loss, ocular irritation, and ophthalmalgia in her right eye. She had been previously misdiagnosed and treated with high-dose systemic corticosteroids at another institution. She underwent emergent pars plana vitrectomy. Vitreous samples were analyzed using conventional culture and metagenomic next-generation sequencing (mNGS), which identified Shinella species as the predominant pathogen. Intravitreal amikacin and systemic ceftazidime were initiated on postoperative day 3 after culture confirmed Gram-negative bacilli. Two weeks of targeted antibiotic therapy resulted in complete resolution of intraocular inflammation and near-full visual recovery. Conclusion To our knowledge, this is the first reported case of intraocular infection caused by Shinella species. This case highlights Shinella as a potential ocular pathogen and demonstrates the utility of pars plana vitrectomy combined with mNGS for diagnosing atypical intraocular infections.
Abstract Purpose To describe two consecutive postoperative endophthalmitis clusters—one caused by non-tuberculous mycobacteria (NTM) and the other by Pseudomonas aeruginosa —linked to a defective autoclave sterilization process in a single tertiary eye hospital in India. Methods This retrospective study reviewed 25 cases of postoperative endophthalmitis between April and August 2024. The first cluster included 21 eyes infected with NTM, while the second involved 4 eyes infected with P. aeruginosa . Clinical data, microbiological findings, management strategies, and outcomes were analyzed. Environmental cultures and sterilization protocols were also reviewed to identify the source of contamination. Results The first cluster presented insidiously, with symptoms appearing on average 40.4 ± 7.3 days postoperatively. Cultures revealed Mycobacterium abscessus , M. fortuitum , or M. brisbaneii in 18 of 21 eyes. All patients underwent pars plana vitrectomy with intravitreal vancomycin, ceftazidime, and dexamethasone, followed by oral linezolid. Visual recovery was favorable in most cases (20/21 eyes), with only one progressing to phthisis. The second cluster, occurring shortly thereafter, involved four cases of acute postoperative endophthalmitis caused by P. aeruginosa . Three eyes recovered useful vision, while one developed phthisis. Investigation revealed a defective autoclaving protocol as the common source of infection. Conclusions These consecutive clusters highlight how minor deviations in sterilization protocols, compounded by high ambient humidity, can precipitate catastrophic outbreaks. Prompt identification, aggressive treatment, and reinforcement of sterilization standards prevented recurrence and resulted in excellent outcomes.
BACKGROUND:H1N1 influenza and Mycoplasma are common causes of pneumonia, but ocular symptoms after infection are rare. We report a case of bilateral decreased vision, exudative retinal detachment and high intraocular pressure secondary to H1N1 influenza and mycoplasma infection. CASE PRESENTATION:A 7-year-old male presented with decreased vision in his right eye and was found to have exudative retinal detachment and high intraocular pressure secondary to combined infection of H1N1 influenza and mycoplasma. The boy was previously diagnosed with X-linked congenital retinoschisis (XLRS) at age 3. After anti-viral and anti-mycoplasma treatments, the exudative retinal detachment resolved, and the intraocular pressure was under control. CONCLUSIONS:This case highlights the possibility of exudative retinal detachment secondary to H1N1 influenza and mycoplasma, especially in patients with short axial length.