Windows on the Fundus: Retinal Changes in Ocular and Systemic Diseases- Glaucoma, Retinal Degeneration, Diabetes Mellitus, Hypertension, Syphilis, and HIV
1. Klara Amangeldievna Rayimova
2. Totawar Shreya Tirupathi
3. Nadimuthu Kiruthika
(1. Lecturer, International Medical Faculty, Osh State University, Osh, Kyrgyz Republic
2. Student, International Medical Faculty, Osh State University, Osh, Kyrgyz Republic
3. Student, International Medical Faculty, Osh State University, Osh, Kyrgyz Republic)
Abstract
The retina is unique among human tissues: it is the only part of the central nervous system — and the only microvascular bed — that can be inspected directly, non-invasively, and in life. The fundus therefore serves simultaneously as the site of primary ocular disease and as a window onto systemic illness, and few skills in medicine reward the clinician as reliably as competent fundoscopy supported by modern imaging. This article reviews the retinal changes of six major disease domains: glaucoma, in which the retinal ganglion cells and their axons die in characteristic patterns now measurable to within microns by optical coherence tomography; the retinal degenerations, dominated by age-related macular degeneration and the inherited dystrophies such as retinitis pigmentosa; diabetic retinopathy, the archetypal microvascular disease and a leading cause of working-age blindness; hypertensive retinopathy, the vascular signature of systemic blood pressure; ocular syphilis, the great mimicker resurgent in the antibiotic era; and the retinal manifestations of HIV infection, from cotton-wool spots to the necrotizing devastation of cytomegalovirus retinitis. For each, the article addresses pathophysiology, clinical and imaging findings, classification, and contemporary management, including the anti-VEGF revolution, advances in OCT and OCT angiography, gene therapy for inherited dystrophies, and the transformative effect of antiretroviral therapy on the infectious retinopathies. The unifying argument is that the retina records the biography of the body's vessels, neurons, and immune defenses — and that the clinician who learns to read it holds a diagnostic instrument of remarkable reach.
Keywords: retina; glaucoma; diabetic retinopathy; hypertensive retinopathy; age-related macular degeneration; retinitis pigmentosa; ocular syphilis; CMV retinitis; HIV
1. Introduction
There is a moment in every medical student's training when the ophthalmoscope first focuses and the fundus swims into view — the orange-red glow, the branching vessels, the pale disc — and with it comes the realization that one is looking at living brain and living blood vessels, the only ones in the body visible without an incision. That anatomical accident has profound clinical consequences. The retina shares embryological origin with the brain and vascular architecture with the kidney and heart; it is supplied by an end-arterial system exquisitely sensitive to hypertension and diabetes; it is defended by a blood–retinal barrier whose failure announces itself as edema and exudate; and its transparency renders visible processes — hemorrhage, ischemia, necrosis, atrophy, neovascularization — that elsewhere in the body can only be inferred. Small wonder that the fundus has been called the mirror of systemic disease, or that the six conditions reviewed here span neurology, metabolism, cardiovascular medicine, and infectious disease while sharing a single stage.
The scope of the problem is vast. Glaucoma is the leading cause of irreversible blindness worldwide, a neurodegeneration of the retinal ganglion cell whose earliest changes are invisible to the patient. Age-related macular degeneration is the leading cause of irreversible central vision loss in the developed world, and the inherited retinal dystrophies, though individually rare, collectively blind tens of thousands and have become the first beachhead of ocular gene therapy. Diabetic retinopathy remains a leading cause of blindness among working-age adults globally, its prevalence tracking the pandemic of type 2 diabetes. Hypertensive retinopathy, long dismissed as a mere signpost, is now understood as an independent marker of cerebrovascular and cardiovascular risk. Syphilis, far from being conquered, has resurged across continents, and its ocular manifestations deceive the unwary. And HIV, though transformed by antiretroviral therapy, still delivers patients with advanced immunosuppression — and with them, cytomegalovirus retinitis — to clinics in every country. Modern imaging has reshaped this landscape: optical coherence tomography (OCT) resolves retinal layers to a few microns, OCT angiography maps flow without dye, ultra-widefield photography captures the periphery, and artificial intelligence now screens diabetic retinopathy autonomously. This article reviews the retinal changes of these six domains in an integrated, clinically oriented manner, with attention to both the classical signs every student must know and the contemporary evidence that guides management in 2025.
2. Methods
This article was prepared as a narrative review informed by a structured survey of the peer-reviewed literature and international clinical guidelines. PubMed, Scopus, and Google Scholar were searched through November 2025 using combinations of the terms "glaucoma," "retinal nerve fiber layer," "diabetic retinopathy," "anti-VEGF," "hypertensive retinopathy," "age-related macular degeneration," "retinitis pigmentosa," "ocular syphilis," "CMV retinitis," and "HIV retinopathy." Priority was assigned to landmark randomized trials (Early Treatment Diabetic Retinopathy Study, DRCR Retina Network protocols, PANORAMA, CLARITY, AREDS/AREDS2), preferred practice patterns and society guidelines (American Academy of Ophthalmology, CDC STI Treatment Guidelines), and recent systematic reviews and meta-analyses. Foundational studies were retained where they defined classifications or established enduring principles. All synthesis, clinical framing, and interpretation are original to this article; quantitative findings are attributed to their primary sources.
3. Results
3.1 Glaucoma: the neurodegeneration written in the nerve fiber layer
Glaucoma is, in essence, a retinal disease whose victim is a single cell type: the retinal ganglion cell, whose axons form the retinal nerve fiber layer (RNFL), converge at the optic disc, and constitute the optic nerve. The defining funduscopic changes are therefore those of progressive neuroaxonal loss. The neuroretinal rim of the optic disc thins in a characteristic sequence — inferior and superior poles first, reflecting the vulnerability of the arcuate axon bundles — producing the enlargement and vertical elongation of the optic cup, an increasing cup-to-disc ratio, rim notching, splinter (Drance) hemorrhages at the disc margin, peripapillary atrophy, and, in advanced disease, the deep excavation of "bean-pot" cupping with nasal displacement of vessels. Within the retina, RNFL defects appear as dark, wedge-shaped slits radiating from the disc, best seen with red-free light; diffuse thinning may precede focal defects. These structural changes obey a crucial temporal rule: they precede detectable visual field loss, and histological studies suggest that a substantial proportion of ganglion cells may be lost before standard perimetry flags abnormality — the rationale for structure-based early diagnosis.
Optical coherence tomography has transformed this examination from an art into a measurement. Modern spectral-domain OCT quantifies the peripapillary RNFL and the macular ganglion cell–inner plexiform layer (GCIPL) with micrometer precision, comparing them against normative databases; systematic review of longitudinal data places the age-related decline of the GCIPL at roughly −0.24 μm per year, against which glaucomatous progression stands out as abnormally fast (Vilares-Morgado et al., 2025). The macular ganglion cell analysis is particularly valuable because over half of macular retinal thickness is ganglion cell–derived and because macular involvement in glaucoma is more common, and more threatening to central vision, than once believed. OCT angiography adds a vascular dimension, demonstrating reduced peripapillary and macular vessel density that correlates with disease severity. It bears emphasis that these retinal changes occur across the glaucoma spectrum — primary open-angle, normal-tension, and secondary glaucomas alike — because intraocular pressure is a risk factor, not the definition; the disease is the optic neuropathy, and its signature is written in the RNFL. Management aims to slow ganglion cell loss through pressure reduction (drops, laser trabeculoplasty, and increasingly minimally invasive glaucoma surgery), with neuroprotection remaining an unmet frontier. The clinical pearl endures: chronic glaucoma is asymptomatic until late, the field loss respects the horizontal meridian, and by the time a patient notices, the disease is far advanced — hence screening by disc examination and, increasingly, by OCT.
3.2 Retinal degenerative changes: age-related macular degeneration and the inherited dystrophies
The retinal degenerations share a final common pathway — photoreceptor and retinal pigment epithelium (RPE) death — but arrive there by very different roads. Age-related macular degeneration (AMD) is the prototype of acquired degeneration. Its early and intermediate stages are marked by drusen, the yellowish extracellular deposits of lipid and protein accumulating between the RPE and Bruch's membrane, accompanied by RPE pigmentary change; drusen size, number, and confluence, along with pigmentary abnormalities, stratify progression risk in the AREDS simplified severity scale. Late disease bifurcates into two forms. Geographic atrophy, the "dry" end stage, is the slow, inexorable centrifugal loss of RPE and photoreceptors that engulfs the fovea and with it reading and face recognition. Neovascular (wet) AMD arises when choroidal vessels breach Bruch's membrane, producing the dramatic fundus of subretinal and intraretinal fluid, hemorrhage, lipid exudate, and eventually disciform scarring; OCT renders these changes with precision and now guides treatment. Therapy divides along the same line. Wet AMD has been revolutionized by intravitreal anti-VEGF agents — ranibizumab, aflibercept, and the longer-acting faricimab and high-dose aflibercept 8 mg, plus the port-delivery system — which have converted a blinding disease into a chronic, manageable one at the cost of indefinite injections. Dry AMD long had no therapy; the AREDS and AREDS2 trials established antioxidant–zinc supplementation for intermediate disease, and 2023 brought the first drugs for geographic atrophy — the complement inhibitors pegcetacoplan and avacincaptad pegol — which slow atrophy growth modestly and mark the beginning of a pharmacological era for dry AMD.
The inherited retinal dystrophies are the genetic counterpart, with retinitis pigmentosa (RP) as the exemplar. RP begins with degeneration of rods, and its classic fundus triad is unforgettable: bone-spicule pigmentary retinopathy in the mid-periphery, attenuated "thread-like" retinal arterioles, and waxy pallor of the optic disc. The clinical course mirrors the rod-first pathology — night blindness (nyctalopia) in youth, progressive constriction of the visual field to tunnel vision, and late involvement of central acuity — while the electroretinogram documents the failing photoreceptor responses and the gene panels increasingly supply a molecular diagnosis from among more than 90 implicated genes. Management has shifted from resignation to cautious optimism: voretigene neparvovec, the first approved ocular gene therapy, restores functional vision in RPE65-associated dystrophy; retinal prostheses, optogenetics, stem-cell approaches, and CRISPR-based editing are in trials; and supportive measures — vitamin A palmitate in selected patients, protection from light and smoking, low-vision rehabilitation, and genetic counseling — retain their place. The broader lesson of the degenerations is that the retina, once thought irreplaceable, has become a proving ground for gene and cell therapy precisely because it is accessible, small, and enclosed.
3.3 Diabetes mellitus: the archetypal microangiopathy
Diabetic retinopathy is the disease for which the phrase "the eye as a window" might have been coined. Chronic hyperglycemia damages the retinal microvasculature through sorbitol accumulation, advanced glycation end-products, oxidative stress, and protein kinase C activation, with pericyte loss as the earliest histological event; the consequence is a progressive failure of vascular integrity that the fundus records stage by stage. Nonproliferative diabetic retinopathy (NPDR) is graded by its lesions: microaneurysms, the first clinically visible sign, appearing as tiny red dots; dot-and-blot and flame-shaped hemorrhages; hard exudates of leaked lipid; cotton-wool spots of nerve fiber layer infarction; venous beading and loops; and intraretinal microvascular abnormalities (IRMA), the shunt vessels of worsening ischemia. The ETDRS-derived severity scale and its simplified "4-2-1" clinical rule — severe hemorrhages in four quadrants, venous beading in two, or IRMA in one — identify severe NPDR and the threshold of danger. Proliferative diabetic retinopathy (PDR) begins when ischemia-driven VEGF tips the retina into neovascularization: fragile new vessels on the disc (NVD) or elsewhere (NVE) that bleed into the vitreous, contract into fibrovascular membranes, and produce the twin catastrophes of vitreous hemorrhage and tractional retinal detachment; anteriorly, rubeosis iridis can seal the angle into neovascular glaucoma. Diabetic macular edema — thickening from leaky microvasculature that may arise at any stage — is the most common cause of visual loss in diabetes, diagnosed and quantified by OCT and classified by center involvement.
Management has been transformed twice. The first transformation was systemic and laser-based: the DCCT and UKPDS proved that glycemic control prevents and slows retinopathy, blood pressure and lipid control add further protection, and panretinal photocoagulation (PRP) reduced severe visual loss in PDR by some 60% in the Diabetic Retinopathy Study. The second transformation is pharmacological: intravitreal anti-VEGF therapy is now first-line for center-involved diabetic macular edema and has proven capable of treating PDR itself — DRCR Protocol S showed ranibizumab noninferior to PRP with less visual field loss and less macular edema over five years, while PANORAMA and DRCR Protocol W demonstrated that aflibercept reduces progression and the onset of vision-threatening complications even in nonproliferative disease, albeit without short-term visual benefit in eyes still seeing well (Bahr and Bakri, 2023; American Academy of Ophthalmology, 2024). The AAO Preferred Practice Pattern (2024) now frames anti-VEGF as effective across PDR and DME while retaining PRP as a durable option — notably for patients unlikely to maintain the punishing follow-up of injection regimens — and pars plana vitrectomy for non-clearing hemorrhage and tractional detachment, increasingly with preoperative anti-VEGF to ease surgery. Newer agents extend durability: faricimab (dual VEGF/Ang-2 inhibition) and high-dose aflibercept stretch intervals, and biosimilars promise access. Screening remains the quiet hero — annual or risk-based fundus examination, increasingly by validated AI systems — because retinopathy is treatable precisely when it is asymptomatic, and pregnancy, with its acceleration of retinopathy, mandates intensified surveillance.
3.4 Hypertension: the retina as a gauge of vascular damage
Hypertensive retinopathy is the visible record of the eye's confrontation with elevated blood pressure, evolving through a sequence of stages that the classical classifications codified. The Keith–Wagener–Barker system, dating to 1939, grades the fundus from grade I (mild generalized and focal arteriolar narrowing, the increased tortuosity and "silver wiring" of sclerotic arterioles) through grade II (more marked narrowing with arteriovenous nicking, where the thickened arteriole compresses the venule at crossings), grade III (the addition of hemorrhages, cotton-wool spots, and hard exudates — sometimes a macular star of lipid), to grade IV (all of the foregoing plus optic disc edema, the signature of malignant hypertension). Later schemas by Scheie and, more recently, simplified three-category systems proposed for prognostic use reflect the same physiology: an early vasoconstrictive phase, a sclerotic phase of arteriolosclerosis, an exudative phase of blood–retinal barrier breakdown, and a malignant phase of disc edema signaling failure of cerebral autoregulation as well. The individual signs each carry meaning — cotton-wool spots are axoplasmic stasis from precapillary arteriolar occlusion; AV nicking betrays the shared adventitial sheath at crossings; the macular star reflects lipid precipitated along Henle's fibers — and the modern literature treats retinopathy not merely as a staging curiosity but as an independent predictor of stroke, cardiovascular events, and cognitive decline, with retinal vascular caliber changes measurable even before hypertension is diagnosed. Management is the management of hypertension itself: fundoscopic regression follows pressure control, but grade IV disease — hypertensive emergency with disc edema — demands urgent, controlled blood pressure reduction, and any fundus showing hemorrhages or exudates in a "known hypertensive" should prompt a harder look at adherence, targets, and end-organ damage elsewhere.
3.5 Syphilis: the great mimicker at the fundus
Ocular syphilis has earned back the epithet its parent disease has long carried. Syphilis is resurging globally, and the eye is involved at any stage — primary through tertiary — with posterior uveitis and panuveitis the most common presentations and with a particular predilection for patients co-infected with HIV. Its retinal manifestations are protean, which is precisely the point. The classic picture is acute syphilitic posterior placoid chorioretinitis: large, yellowish, placoid lesions at the level of the RPE in the macula or mid-periphery, whose autofluorescence and OCT signatures (disruption of the ellipsoid zone and RPE nodularity) are now well characterized. Equally common are a superficial retinal precipitate–studded vitritis, retinal vasculitis with perivascular sheathing, necrotizing retinitis that mimics herpetic disease, papillitis and neuroretinitis, and the late atrophic, pigmentary retinopathy that resembles retinitis pigmentosa — complete with bone spicules and a waxy disc — in congenital and long-standing acquired disease. Chorioretinitis with a "ground-glass" retinal appearance and serous detachments adds to the repertoire. The diagnostic imperative follows directly: every unexplained uveitis, retinitis, or optic neuritis warrants syphilis serology — treponemal and non-treponemal tests together — and every patient with ocular syphilis warrants HIV testing and consideration of lumbar puncture, because ocular disease implies neurosyphilis risk. Treatment is neurosyphilis-style therapy regardless of CSF results: intravenous aqueous crystalline penicillin G, 3–4 million units every four hours for 10–14 days, with desensitization where allergy precludes it; corticosteroids are adjunctive only, never a substitute. Treated early, visual recovery is often gratifying; treated late or missed, the placoid lesions resolve into permanent RPE mottling and lost vision — a reminder that this ancient disease still punishes diagnostic hesitation (CDC STI Treatment Guidelines, 2021; Mathew and Goold, 2022).
3.6 HIV: the spectrum from microangiopathy to necrotizing retinitis
The retinal manifestations of HIV span a spectrum defined by the CD4 count, and the spectrum itself has been redrawn by antiretroviral therapy. At relatively preserved immunity, the commonest finding is HIV retinopathy (microangiopathy): cotton-wool spots — often numerous and recurrent — with occasional dot-blot hemorrhages and microaneurysms, a noninfectious, usually asymptomatic marker of circulating immune complexes and early vascular damage that typically requires no ocular treatment but flags systemic immune decline. As the CD4 count falls below roughly 50 cells/μL, the door opens to opportunistic necrotizing retinopathies, and above all to cytomegalovirus retinitis, historically the commonest ocular opportunistic infection of AIDS and still its most feared. CMV retinitis presents with progressive visual field loss and floaters and displays one of the most recognizable fundi in all of medicine: a fulminant, hemorrhagic, necrotizing retinitis — confluent white necrosis advancing along vascular arcades amid hemorrhages, the celebrated "pizza-pie" or "ketchup-and-cheese" retina — or, in its indolent form, a granular peripheral retinitis with little hemorrhage; remarkably, vitritis is typically scant or absent, reflecting the very immunosuppression that permits the infection (AlZaid et al., 2026). A recent meta-analysis of 59 studies and 4,501 patients quantified modern outcomes: inflammation resolution in 90% with treatment, but retinal detachment in 11% and recurrence in 19%, with recurrence strikingly lower (10% versus 33%) in patients on effective ART — evidence that immune restoration, not antivirals alone, is the deepest therapy (Surv Ophthalmol, 2025). Treatment combines induction with intravenous ganciclovir or oral valganciclovir and intravitreal ganciclovir or foscarnet — intravitreal delivery achieving the high local levels the eye demands — followed by maintenance until immune reconstitution; ART is begun, with timing balanced against the risk of immune recovery uveitis, and vigilance for retinal detachment is lifelong, since necrotic retina tears readily. The wider HIV-associated differential completes the picture: progressive outer retinal necrosis (PORN), the fulminant VZV retinopathy of profound immunosuppression with early posterior involvement and minimal inflammation; acute retinal necrosis at higher CD4 counts; toxoplasma retinochoroiditis; ocular syphilis, often atypical and aggressive; pneumocystis choroiditis, largely historical; and the immune recovery uveitis that can paradoxically inflame a healing eye as immunity returns. The ART era has made CMV retinitis rare where treatment is available — but late presenters ensure that every ophthalmologist must still know the "pizza-pie" retina when it appears.
4. Discussion
Viewed together, these six domains teach a single grand lesson with six dialects: the retina faithfully displays the pathology of the systems that sustain it. In glaucoma it displays a neurodegeneration, in the degenerations a failure of photoreceptor and pigment epithelial maintenance, in diabetes a microangiopathy of barrier failure and ischemia, in hypertension the mechanical and sclerotic consequences of pressure, and in syphilis and HIV the retinal footprints of infection and of the immune state that governs it. For the clinician, several cross-cutting principles emerge. First, structure now precedes symptoms: OCT detects glaucomatous and diabetic change before the patient is aware, and the modern standard of care is therefore a screening standard — the fundus must be examined and imaged before it complains. Second, the fundus stratifies systemic risk: hypertensive and diabetic retinal signs predict stroke and mortality independent of office numbers, and an ophthalmoscopic finding can and should alter systemic management. Third, classification is not pedantry but prognosis and therapy — the 4-2-1 rule triggers laser or injection, Keith–Wagener grade IV triggers an emergency, and the recognition of placoid chorioretinitis triggers penicillin. Fourth, infection and immunity are inseparable: CMV retinitis is as much a disease of the missing CD4 cell as of the virus, and its definitive treatment is immune restoration. Fifth, the therapeutic arc of retina over two decades — anti-VEGF, complement inhibition, gene therapy, durable implants — shows a specialty moving from destruction (laser ablation) to modulation (cytokine blockade) to replacement (gene and cell therapy).
This review has limitations. It is a narrative synthesis, not a systematic review, and each domain could support an article of its own; the fast-moving fields of anti-VEGF durability, geographic atrophy therapeutics, and retinal gene therapy may outdate specifics; and imaging criteria evolve with each device generation. The student is urged to pair this survey with the primary guidelines cited.
5. Conclusion
The fundus is medicine's most honest window. Through it, glaucoma writes its slow arithmetic of dying ganglion cells, macular degeneration its accumulating debris, diabetes its leaking and ischemic microvasculature, hypertension its silvered and nicking arterioles, syphilis its placoid masquerade, and HIV its spectrum from innocent cotton-wool spots to necrotizing catastrophe. To learn these patterns is to acquire not merely ophthalmic knowledge but a general medical instrument, one that detects disease before symptoms, stratifies systemic risk, and occasionally saves both sight and life at a single glance. The ophthalmoscope — now joined by OCT and artificial intelligence — remains what it has always been: a small instrument that opens onto a very large field.
References
Vilares-Morgado R, et al. Age-related changes in optical coherence tomography glaucoma-related parameters: a systematic review. Surv Ophthalmol. 2025;70(5) (S0039-6257(25)00104-3).
Weinreb RN, Aung T, Medeiros FA. The pathophysiology and treatment of glaucoma: a review. JAMA. 2014;311(18):1901–1911.
Jonas JB, Aung T, Bourne RR, et al. Glaucoma. Lancet. 2017;390(10108):2183–2193.
Bahr TA, Bakri SJ. Update on the management of diabetic retinopathy: anti-VEGF agents for the prevention of complications and progression of nonproliferative and proliferative retinopathy. Life (Basel). 2023;13(5):1098.
American Academy of Ophthalmology. Diabetic Retinopathy Preferred Practice Pattern, 2024.
Gross JG, Glassman AR, Jampol LM, et al. Panretinal photocoagulation vs intravitreous ranibizumab for proliferative diabetic retinopathy: a randomized clinical trial (DRCR Protocol S). JAMA. 2015;314(20):2137–2146; and 5-year outcomes, JAMA Ophthalmol. 2019.
Early Treatment Diabetic Retinopathy Study Research Group. Photocoagulation for diabetic macular edema: ETDRS Report No. 1. Arch Ophthalmol. 1985;103(12):1796–1806.
Maturi RK, et al. Effect of intravitreous anti-VEGF vs sham treatment for prevention of vision-threatening complications of diabetic retinopathy: the PANORAMA randomized clinical trial. JAMA Ophthalmol. 2021;139(7):701–712.
The Diabetic Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications. N Engl J Med. 1993;329:977–986; and UK Prospective Diabetes Study (UKPDS) Group, BMJ 1998;317:703–713.
Wong TY, Mitchell P. Hypertensive retinopathy. N Engl J Med. 2004;351(22):2310–2317.
Keith NM, Wagener HP, Barker NW. Some different types of essential hypertension: their course and prognosis. Am J Med Sci. 1939;197:332–343.
Mitchell P, Liew G, Gopinath B, Wong TY. Age-related macular degeneration. Lancet. 2018;392(10153):1147–1159.
Age-Related Eye Disease Study 2 (AREDS2) Research Group. Lutein + zeaxanthin and omega-3 fatty acids for age-related macular degeneration. JAMA. 2013;309(19):2005–2015.
Heier JS, Lad EM, Holz FG, et al. Pegcetacoplan for the treatment of geographic atrophy secondary to age-related macular degeneration (OAKS and DERBY). Lancet. 2023;402(10411):1434–1448.
Verbakel SK, van Huet RAC, Boon CJF, et al. Non-syndromic retinitis pigmentosa. Prog Retin Eye Res. 2018;66:157–186.
Russell S, Bennett J, Wellman JA, et al. Efficacy and safety of voretigene neparvovec in patients with RPE65-mediated inherited retinal dystrophy. Lancet. 2017;390(10097):849–860.
Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021 (ocular syphilis and neurosyphilis recommendations). MMWR Recomm Rep. 2021;70(RR-4):1–187.
Mathew RGT, Goold P. Ocular syphilis: epidemiology, clinical features and management. Eye (Lond) / clinical reviews. 2022.
AlZaid A, et al. CMV retinitis: the diagnostic challenges and long-term outcomes — the experience of a tertiary eye center. Int J Retina Vitreous. 2026;12:00572-3.
Antiviral therapy for cytomegalovirus retinitis: a systematic review and meta-analysis of 59 studies. Surv Ophthalmol. 2025;70(3) (S0039-6257(24)00141-3).