Diffuse Unilateral Subacute Neuroretinitis (DUSN)

Diffuse Unilateral Subacute Neuroretinitis (DUSN) is a rare eye infection caused when a tiny worm (a nematode) gets into the layers under the retina of one eye and slowly damages the retina and optic nerve. The worm moves around beneath the retina, creating inflammation and disrupting the normal light-sensing cells. Over time, if not caught early, this leads to serious and often permanent loss of vision in the affected eye. The term “diffuse” refers to the widespread changes it causes in the retina, “unilateral” means it usually affects only one eye, “subacute” means it develops over weeks to months (not suddenly), and “neuroretinitis” reflects inflammation of both the retina and optic nerve structures. PubMed EyeWiki

Diffuse Unilateral Subacute Neuroretinitis, or DUSN, is an eye disease caused by a worm (nematode) living beneath the retina in one eye. The parasite slowly moves and releases toxins and inflammatory substances, damaging retinal cells and the optic nerve. If not caught early, this can lead to serious vision loss or blindness in that eye. It most often affects otherwise healthy children and young adults, typically in a single eye, although rare bilateral cases exist. Early signs include floating spots, mild visual decline, and subtle retinal changes; late-stage disease shows optic nerve atrophy, narrowing of retinal vessels, and diffuse degeneration of the retinal pigment epithelium. DUSN was first described in 1978 and is now known to be caused by several possible nematodes, including Baylisascaris procyonis, Ancylostoma caninum, Strongyloides, and others depending on geographic exposure. PMC EyeWiki

The worm lives in the subretinal space and sometimes intraretinally. As it moves, it physically injures tissue and releases waste products that trigger inflammation and possibly autoimmune-like damage. The outer retina usually gets localized toxic injury, while inner layers suffer more diffuse effects. Chronic inflammation and direct damage eventually cause thinning of nerve fibers, pigment changes, and optic nerve degeneration, which are often irreversible in late stages. EyeWiki

DUSN most often affects otherwise healthy children and young adults. Early recognition and treatment are critical because the damage progresses from initial inflammation to chronic degeneration like optic atrophy, which is irreversible. Dove Medical Press

---

Types / Stages

DUSN is classified mainly by stage and by the size group of the causative nematode:

1. Early stage DUSN presents when the worm is actively migrating under the retina and inflammation is still evolving. The eye may show mild to moderate vitritis (clouding in the gel), multiple small gray-white lesions in the outer retina, mild optic nerve swelling (papillitis), and subtle changes to the retinal pigment layer. Vision loss may be gradual, and sometimes the worm can be seen with careful examination. PubMedDove Medical Press

2. Late stage DUSN occurs after prolonged inflammation. The worm may no longer be visible, but permanent damage appears: optic nerve atrophy (pale, shrunken optic disc), narrowing of retinal blood vessels, widespread retinal pigment epithelium (RPE) changes, and severe loss of visual field and acuity. This stage reflects chronic scarring and neurodegeneration. PubMedDove Medical Press

3. Based on worm size, two broad groups have been described: the large nematode (typically 1,000–2,000 micrometers), often linked to raccoon roundworm (Baylisascaris procyonis), and the smaller nematodes (around 500–600 micrometers) thought to be related to dog hookworms like Ancylostoma caninum, A. ceylanicum, or A. braziliense. Molecular identification has confirmed even less common species in case reports. The worm size can influence where it is found in different regions and may slightly alter clinical suspicion, but both types produce the same damaging inflammatory process. JKMSPubMedDoctorLib

---

Causes / Risk Factors

DUSN is caused by infection with nematode larvae entering the eye, but the broader “causes” or conditions that lead to the worm getting into the subretinal space—or increase risk—include both biological agents and environmental/behavioral factors. Below are twenty such causes or risk-related contributors:

1. Baylisascaris procyonis exposure: The raccoon roundworm is a known large nematode cause; its eggs in soil can infect humans, and larvae can migrate to the eye. DoctorLib

2. Ancylostoma caninum infection: Dog hookworm species suspected in small-worm DUSN cases. JKMS

3. Ancylostoma ceylanicum: Reported in rare molecularly confirmed DUSN case; a hookworm capable of human infection. PubMed

4. Ancylostoma braziliense: Another hookworm implicated in isolated case reports of DUSN. ResearchGateAcademia

5. Unidentified small subretinal nematodes: Many DUSN cases never have the exact species identified, but similar worms are presumed to be responsible. ResearchGate

6. Living in or traveling to endemic regions: Areas with raccoons, stray dogs, poor sanitation (e.g., parts of South America, Caribbean, North America, India) raise exposure risk. CDC Travelers’ Health

7. Contact with infected animals: Handling or playing with raccoons, dogs, or other animals shedding nematode eggs increases chance of accidental ingestion and aberrant larval migration. CDC Travelers’ Health

8. Soil contamination with animal feces: Eggs of nematodes survive in soil; contact with contaminated soil (especially for children playing outside) can seed infection. CDC Travelers’ Health

9. Poor hand hygiene: Not washing hands after touching soil or animals allows eggs to be ingested and eventually reach ocular tissues through abnormal migration. CDC Travelers’ Health

10. Pica or geophagia in children: Eating or mouthing dirt increases ingestion of nematode eggs. Children are a common affected group. Dove Medical Press

11. Lack of deworming in domestic animals: Dogs or pets harboring hookworms that shed eggs can seed local environments. JKMS

12. Poor sanitation systems: Uncontrolled animal waste and lack of clean environments let eggs persist and spread. CDC Travelers’ Health

13. Close proximity to wildlife reservoirs: Living near raccoon habitats or other reservoir animals increases environmental egg burden. DoctorLib

14. Young age: Children are more likely to have behaviors (playing outdoors, hand-to-mouth) that lead to infection. Dove Medical Press

15. Unwashed raw produce: Vegetables or food contaminated with soil containing nematode eggs that are not properly cleaned may be a route of accidental ingestion. (Inference based on known transmission of similar nematode infections.) CDC Travelers’ Health

16. Travel without awareness/prevention: Visiting endemic rural or wild areas without protective hygiene can expose individuals. CDC Travelers’ Health

17. Immune system variability: Although DUSN often affects healthy individuals, subtle immune differences may modulate susceptibility or severity. (Inference from the fact that DUSN can occur in healthy hosts but inflammatory response drives damage.) PubMed

18. Delayed or missed early diagnosis: Failure to recognize early inflammatory signs allows the worm to continue damaging tissue, making the condition worse and harder to treat. Dove Medical Press

19. Environmental persistence of infective eggs: Nematode eggs that survive for long periods in the environment raise cumulative exposure risk. CDC Travelers’ Health

20. Lack of awareness among clinicians: Because DUSN is rare and the worm is often not visible, it can be mistaken for other retinal diseases, delaying treatment—a systemic “cause” of progression. Cureus

---

Symptoms

Patients with DUSN usually present with a set of symptoms that begin subtly and worsen over weeks to months. The symptoms reflect both retinal inflammation and progressive nerve damage:

1. Progressive loss of vision in one eye: Vision becomes worse over time, often without pain. This is the most common presenting complaint. PubMed

2. Blind spots (scotomas): Patients notice missing areas in their sight, especially in parts of the visual field the worm has damaged. Dove Medical Press

3. Photopsia (flashes of light): The moving worm and retinal irritation cause flashes or flickers seen by the patient. ResearchGate

4. Floaters or haze: Inflammation in the vitreous (vitritis) may cause sensations of spots or cobwebs drifting in vision. PubMed

5. Photophobia (light sensitivity): Bright lights may become uncomfortable due to retinal and anterior segment inflammation. Dove Medical Press

6. Color vision changes: Colors may seem faded or altered as retinal cells and optic nerve function deteriorate. PubMed

7. Enlarged blind spot or visual field defects on testing: Patients may not always notice until formal field testing shows loss. Dove Medical Press

8. Relative afferent pupillary defect (RAPD): The damaged optic nerve conducts light signals poorly, detectable on pupillary testing. Dove Medical Press

9. Mild distortion of vision (metamorphopsia): Structural retinal changes can warp straight lines or fine detail. ResearchGate

10. Difficulty reading or focusing: Central or paracentral field loss affects near tasks. PubMed

11. Decreased night vision: Damaged retinal function impairs vision in low light. (Inference from generalized retinal injury.) PubMed

12. Optic disc swelling (early): Seen in early stages as mild swelling and sometimes blurring of the optic nerve edge. Dove Medical Press

13. Optic disc pallor or atrophy (late): As the disease progresses, the optic nerve becomes pale and shrunken, a sign of permanent damage. PubMedDove Medical Press

14. Narrowing of retinal blood vessels: Chronic inflammation causes the vessels to thin, reducing blood supply visible on exam. PubMedDove Medical Press

15. Patchy or mottled vision from RPE changes: The retinal pigment layer becomes irregular, causing shimmering or unstable vision in areas. PubMedEyeWiki

---

Diagnostic Tests

A careful combination of clinical examination, imaging, electrophysiology, and selective laboratory tests is used to make or support the diagnosis. The definitive diagnosis is often made only when the worm is seen and treated (e.g., by laser), but other tests build the case and assess damage.

Physical and Clinical Examination

1. Visual acuity measurement: Standard charts (e.g., Snellen or logMAR) quantify how much central vision is lost. This is the first basic test. Dove Medical Press

2. Pupillary reflex testing (to detect RAPD): Using swinging flashlight test reveals asymmetric optic nerve function due to DUSN damage. Dove Medical Press

3. Visual field testing (perimetry): Formal testing shows scotomas, enlarged blind spot, and peripheral field loss; essential to map functional impact. Dove Medical Press

4. Color vision testing: Tools like Ishihara plates detect subtle color deficits from optic/retinal injury. Academia

5. Contrast sensitivity testing: Reduced ability to see low-contrast objects reflects early retinal dysfunction. (Inference from retinal involvement.) PubMed

Manual / Ophthalmic Clinical Techniques

6. Indirect ophthalmoscopy with scleral depression: A thorough retinal exam to try to locate the moving worm and see multiple gray-white retinal lesions. This is the core clinical inspection. Dove Medical Press

7. Slit-lamp biomicroscopy with fundus lenses: Allows closer view of vitreous inflammation, optic disc changes, and retinal lesions. Cureus

8. Fundus photography (color): Documentation of lesions, vessel narrowing, optic disc appearance, and any visible worm for comparison over time. ResearchGate

9. Wide-field or ultra-widefield imaging: Captures the full extent of peripheral retinal changes that might be missed in standard views. Cureus

10. Infrared/confocal scanning laser ophthalmoscopy: Helps in locating the worm, sometimes by showing subtle motion or contrast. Cureus

Laboratory / Pathological

11. Serologic testing for nematode antibodies: Blood tests for antibodies against parasites like Baylisascaris or related species can support systemic exposure, though they are not always definitive for ocular involvement. DoctorLib

12. Complete blood count with differential (including eosinophils): May be done to screen for systemic parasitic infection; eosinophilia is not always present in isolated ocular disease but can provide context. CDC Travelers’ Health

13. PCR analysis of intraocular fluid: If available, aqueous or vitreous samples can be tested for nematode DNA to try to identify causative species—used in difficult or atypical cases. PubMed

14. Cytology of ocular fluid: Microscopic examination of fluid obtained during diagnostic tap may identify inflammatory cell patterns or, very rarely, larvae fragments. (Inference based on general ophthalmic infectious workup.) Dove Medical Press

Electrodiagnostic Tests

15. Full-field electroretinography (ERG): Measures overall retinal electrical responses; reduced signals indicate diffuse retinal dysfunction from the inflammatory damage. athenaeum.uiw.edu

16. Multifocal ERG: Gives localized functional mapping of the retina to see which retinal areas have decreased function, helpful when the worm is near critical areas like the macula. Academia

17. Visual evoked potentials (VEP): Tests the signal transmission from the retina through the optic nerve to the brain; delays or reduced amplitude reflect optic nerve compromise. athenaeum.uiw.edu

Imaging

18. Optical coherence tomography (OCT): High-resolution cross-sectional imaging shows structural retinal damage, edema, thinning, and, in some cases, the worm if it lies in the macular region. It also visualizes early outer retina changes and later atrophy. ResearchGate

19. Fluorescein angiography: Dye test showing leakage, window defects from RPE damage, and vascular narrowing; helps distinguish active inflammation from chronic scars. Dove Medical Press

20. Fundus autofluorescence: Highlights retinal pigment epithelium dysfunction; areas of abnormal autofluorescence correlate with RPE stress or loss, helping gauge disease extent even when the worm is not seen. EyeWiki.

Non-Pharmacological Treatments

1. Prompt Diagnosis with Regular Eye Exams: Early identification through dilated fundus exam, OCT, fluorescein angiography, and visual field testing allows earlier intervention before irreversible damage. Monitoring stabilizes disease and guides treatment. EyeWiki

2. Laser Light Direction to Mobilize Worm: Using a focused bright slit-lamp beam can sometimes coax a motile worm to migrate from critical areas (like the macula) toward safer peripheral zones before killing it. This manipulation reduces collateral damage. ophed.com

3. Visual Rehabilitation (Low Vision Therapy): After some vision loss, patients benefit from trained use of magnifiers, contrast-enhancing devices, large-print materials, and occupational therapy to maximize remaining vision and adapt daily tasks. This does not reverse damage but improves function.

4. Protective Eyewear and Light Management: Limiting unnecessary bright light exposure and using sunglasses with UV protection helps reduce secondary phototoxic stress on already inflamed and vulnerable retinal tissue. UV and blue-light filtering may reduce oxidative strain. MDPI

5. Anti-inflammatory Lifestyle (Diet and Behavior): Eating a diet rich in anti-inflammatory foods (leafy greens, omega-3s, berries) and avoiding smoking helps blunt chronic low-grade inflammation that could worsen retinal injury. Lifestyle factors also support general ocular health. MDPIVerywell Health

6. Smoking Cessation: Smoking increases oxidative stress and impairs microcirculation in the eye; quitting supports the microenvironment for damaged retinal tissue and reduces risk of progression of secondary degenerations. MDPI

7. Stress and Mental Health Support: Sudden vision loss is emotionally difficult. Counseling or support groups help patients cope, maintain compliance with treatment, and reduce psychosomatic worsening of perceived vision.

8. Close Follow-up Imaging: Serial OCT and visual field testing allow tracking of structural changes; early detection of worsening can trigger timely additional interventions. EyeWiki

9. Use of Magnification/Contrast Aids in Daily Life: Helps with reading and navigation when central or peripheral vision is compromised—training combined with devices supports independence.

10. Patient Education on Exposure Risks: Teaching about the sources of infection (e.g., contact with raccoon/dog feces, undercooked fish) helps patients and caregivers reduce reinfection or exposure for family members. EyeWiki

11. Eye Movement and Field Awareness Training: Occupational therapists can train patients to scan more effectively, compensating for field defects from retinal damage.

12. Controlled Light Stimulation to Localize Worm Before Treatment: Strategic light exposure can help localize a moving worm prior to laser, improving targeting and minimizing collateral burns. ophed.com

13. Avoidance of Eye Trauma or Strain: Reducing activities that could exacerbate intraocular inflammation (e.g., heavy straining) during active disease may help the eye stabilize.

14. Optimization of Systemic Health: Controlling comorbid conditions (e.g., diabetes, hypertension) that impair microvascular health helps support retinal recovery and prevents compounding injury.

15. Hydration and Ocular Surface Care: Maintaining lubrication and avoiding dry-eye–related reflex irritation prevents additional ocular surface stress, which can cloud assessment and comfort.

16. Use of Tinted/Filtered Displays for Screen Use: Reducing glare and blue light when using computers reduces strain for compromised vision.

17. Community and Public Health Awareness in Endemic Areas: Informing communities about DUSN’s existence, risk exposures, and early symptoms increases early presentation and decreases disease burden. EyeWiki

18. Adaptive Environmental Modifications: Improving lighting, high-contrast markings, and safe navigation at home/work to compensate for vision deficits and lower accident risk.

19. Support for Care Coordination: Ensuring coordination among retina specialists, low-vision therapists, and primary care fosters holistic care, early detection of complications, and adherence.

20. Avoidance of Known Carriers: Behavior modification such as not handling raccoon or stray animal feces directly, using gloves for gardening, and supervising children in potentially contaminated sandboxes reduces exposure risk. EyeWiki

---

Drug Treatments

Note: DUSN has only a few well-established medical drugs. Some “treatments” are supportive or investigational. Here, each is explained with class, typical use, purpose/mechanism, dosing (where established), timing, and side effects.

1. Albendazole

   • Class: Anti-helminthic (benzimidazole)

   • Purpose: Treat presumed DUSN when worm is not visible or as adjunct when visualization fails to kill all organisms.

   • Mechanism: Inhibits parasite microtubule formation and impairs glucose uptake, leading to worm death.

   • Dosage/Time: Common regimen in reported series is 400 mg orally once or twice daily for 30 days; sometimes high-dose protocols are used based on clinician judgment. EyeWikiPMC

   • Side Effects: Gastrointestinal upset, dizziness, rash, transient liver enzyme elevation, alopecia; contraindicated in pregnancy due to teratogenic risk. EyeWiki

2. Thiabendazole

   • Class: Anti-helminthic

   • Purpose: Historical use in DUSN, though limited effectiveness in confirmed cases.

   • Mechanism: Disrupts parasite energy metabolism.

   • Dosage/Time: Previously used orally; exact regimen varied, but in practice has fallen out of favor for DUSN because the worm often remains mobile after treatment. PubMed

   • Side Effects: Nausea, dizziness, liver enzyme elevation, central nervous system symptoms at high doses.

3. Prednisone (Systemic Corticosteroid)

   • Class: Anti-inflammatory / immunosuppressant

   • Purpose: Control secondary inflammation after killing the worm or when inflammation threatens further retinal damage.

   • Mechanism: Broad suppression of inflammatory cytokines and immune cell activation.

   • Dosage/Time: Typical described dose is 40–60 mg/day orally with gradual taper over 2–4 weeks depending on response. EyeWiki

   • Side Effects: Elevated blood sugar, mood changes, weight gain, increased infection risk, hypertension, osteoporosis with long-term use.

4. Topical Corticosteroids (e.g., Prednisolone Eye Drops)

   • Class: Anti-inflammatory

   • Purpose: Manage anterior segment inflammation if present (e.g., mild anterior uveitis accompanying DUSN).

   • Mechanism: Local reduction of inflammatory mediators.

   • Dosage: Eye drop frequency adjusted by inflammation severity (e.g., 4–6 times daily with taper).

   • Side Effects: Increased intraocular pressure, cataract formation with prolonged use.

5. Intravitreal Corticosteroid (e.g., Triamcinolone acetonide injection)

   • Class: Local anti-inflammatory

   • Purpose: Severe intraocular inflammation not controlled with systemic or topical therapy; used cautiously.

   • Mechanism: Direct suppression of ocular inflammation by sustained local steroid.

   • Side Effects: Elevated intraocular pressure, cataract progression, risk of infection.

6. Anti-VEGF Agents (e.g., Bevacizumab) – for Complications

   • Class: Vascular endothelial growth factor inhibitor

   • Purpose: Treat secondary neovascular complications if they arise (rare in DUSN but possible from chronic ischemic stimulus or inflammatory sequelae).

   • Mechanism: Blocks VEGF to prevent abnormal blood vessel growth and leakage.

   • Dosage: Intravitreal injection per standard retinal protocols (often monthly initially).

   • Side Effects: Rare endophthalmitis, transient increase in intraocular pressure.

7. Neuroprotective Agents under Investigation (e.g., Brimonidine)

   • Class: Alpha-2 agonist (used for glaucoma) with some neuroprotective interest

   • Purpose: Experimental adjunct to protect retinal ganglion cells from degeneration.

   • Mechanism: May increase neurotrophic support and reduce apoptotic signaling.

   • Evidence: Limited; used in other optic neuropathies, not standard for DUSN.

   • Side Effects: Eye redness, dry mouth, fatigue.

8. Citicoline (CDP-Choline)

   • Class: Neuroprotective / nootropic compound

   • Purpose: Support optic nerve health after injury (used in optic neuropathies), as adjunct in chronic retinal damage.

   • Mechanism: Enhances phospholipid synthesis, mitochondrial function, and neuronal membrane repair.

   • Dosage: Oral formulations vary (e.g., 500–1000 mg/day in divided doses).

   • Evidence: Preliminary; not a primary treatment for DUSN but sometimes used for residual optic nerve compromise.

9. Systemic Nonsteroidal Anti-inflammatory Drugs (NSAIDs)

   • Class: Anti-inflammatory

   • Purpose: Mild control of inflammation when corticosteroids are contraindicated or as adjunct.

   • Mechanism: COX inhibition reducing prostaglandin-mediated inflammation.

   • Caution: Limited benefit compared to steroids; not first-line for posterior segment inflammation. Side effects include gastrointestinal irritation and renal stress.

10. Off-label Immunomodulators (e.g., in refractory inflammatory response)

• Class: Various (methotrexate, mycophenolate)

• Purpose: Rarely considered in severe, persistent immune-mediated retinal inflammation after the worm is eliminated; only under specialist guidance.

• Mechanism: Suppresses aberrant immune activity.

• Evidence: Very limited in DUSN context; used cautiously due to systemic immunosuppression risks.

Note: Ivermectin was studied and found ineffective in confirmed DUSN cases, so it is not a recommended therapy for killing the worm in this condition. PubMed

---

Dietary Molecular Supplements

These supplements support retinal health, reduce oxidative stress, and may help the injured eye tolerate damage better. None replace primary therapy, but they are commonly used in general retinal neuroprotection strategies.

1. Lutein

   • Dosage: Typical supplemental doses 10–20 mg/day.

   • Function: Antioxidant concentrated in the macula, filters blue light, supports retinal cell integrity.

   • Mechanism: Scavenges free radicals, modulates inflammation, and improves photoreceptor survival. PMCPMC

2. Zeaxanthin

   • Dosage: 2–10 mg/day as part of combined macular formulas.

   • Function: Works with lutein to maintain macular pigment and protect against light-induced damage.

   • Mechanism: Antioxidant and photoprotective carotenoid. MDPI

3. Omega-3 Fatty Acids (DHA/EPA)

   • Dosage: 500–1000 mg EPA/DHA combined per day (often from fish oil).

   • Function: Anti-inflammatory support for retinal tissues and maintenance of photoreceptor cell membranes.

   • Mechanism: Modulates inflammatory eicosanoids, supports retinal cell membrane fluidity. MDPI

4. Vitamin C (Ascorbic Acid)

   • Dosage: 500–1000 mg/day, adjusted to tolerance.

   • Function: Potent antioxidant that helps recycle other antioxidants and protect ocular tissues.

   • Mechanism: Neutralizes reactive oxygen species in retinal microenvironment. EyeWiki

5. Vitamin E

   • Dosage: 100–400 IU/day (usually mixed tocopherols).

   • Function: Lipid-soluble antioxidant protecting photoreceptor membranes from peroxidation.

   • Mechanism: Interrupts lipid free radical chain reactions. EyeWiki

6. Zinc

   • Dosage: 25–80 mg/day (often with copper to prevent deficiency).

   • Function: Cofactor in many enzymes critical for retinal metabolism and antioxidant defense.

   • Mechanism: Stabilizes cell membranes, supports antioxidant enzymes like superoxide dismutase. EyeWiki

7. Selenium

   • Dosage: 50–200 mcg/day.

   • Function: Component of glutathione peroxidase; supports the body’s antioxidant system.

   • Mechanism: Helps detoxify peroxides that can damage retinal cells. EyeWiki

8. Alpha-Lipoic Acid (ALA)

   • Dosage: 300–600 mg/day.

   • Function: Regenerates other antioxidants and combats oxidative stress in neural tissue.

   • Mechanism: Acts both in lipid and aqueous compartments to neutralize free radicals and regenerate glutathione. EyeWiki

9. N-Acetyl Cysteine (NAC)

   • Dosage: 600–1200 mg/day.

   • Function: Precursor to glutathione; supports endogenous antioxidant capacity.

   • Mechanism: Boosts intracellular glutathione to mitigate oxidative damage. EyeWiki

10. Astaxanthin

    • Dosage: 4–12 mg/day.

    • Function: Very potent antioxidant with neuroprotective properties in retinal cells.

    • Mechanism: Crosses blood-retinal barrier, reduces inflammation, and prevents photoreceptor apoptosis; used adjunctively in many eye health regimens. (Supported by general antioxidant literature and emerging eye health supplements consensus). MDPI

---

Experimental / Regenerative / “Hard Immunity” / Stem Cell–Related Approaches

These are not proven standard treatments for DUSN but are being explored in retinal degeneration or neuroprotection contexts; their applicability to DUSN is theoretical or investigational.

1. Human Embryonic Stem Cell–Derived Retinal Pigment Epithelium (hESC-RPE) Transplant

   • Purpose: Replace damaged retinal pigment epithelial cells to support photoreceptor survival.

   • Mechanism: Transplanted RPE cells integrate and perform phagocytosis, nutrient transport, and growth factor support.

   • Status: Clinical trials in geographic atrophy/AMD; no established protocol for DUSN but conceptually targeted at repairing outer retinal damage. PMCHerald Open Access

2. Induced Pluripotent Stem Cell (iPSC)–Derived Retinal Progenitor Cells

   • Purpose: Provide precursor cells that can differentiate into retinal neurons or supportive cells.

   • Mechanism: iPSCs from patient or donor are guided to retinal lineage, then injected/subretinally placed to replace lost/degenerating cells.

   • Evidence: Early-phase trials in degenerative retinal disease; application to inflammatory injury like DUSN remains experimental. PMCHerald Open Access

3. Mesenchymal Stem Cell (MSC) Intravitreal Injection

   • Purpose: Neuroprotection and immune modulation after retinal injury.

   • Mechanism: MSCs secrete trophic factors, anti-inflammatory cytokines, and may modulate microglial activation, supporting retinal cell survival.

   • Delivery: Intravitreal injection in investigational protocols; dosing varies by trial.

   • Note: Not targeted at the worm but for residual neurodegeneration. Herald Open Access

4. Ciliary Neurotrophic Factor (CNTF) via Encapsulated Cell Implant (NT-501)

   • Purpose: Provide sustained delivery of neurotrophic support to retinal neurons.

   • Mechanism: Encapsulated cells release CNTF locally, which supports photoreceptor and retinal ganglion cell survival.

   • Status: Investigated in retinitis pigmentosa and geographic atrophy; could hypothetically help in chronic neural loss after DUSN. PMC

5. Autologous Bone Marrow–Derived Mononuclear/Stem Cells

   • Purpose: Systemic or local delivery aiming at immune modulation and paracrine support for ischemic/inflammatory retinal injury.

   • Mechanism: Release growth factors, anti-inflammatory mediators, and may promote microenvironment stabilization.

   • Evidence: Used in broader vision loss trials (e.g., SCOTS for optic nerve/retinal conditions), but DUSN-specific data are lacking. ClinicalTrials.gov

6. Retinal Progenitor Cell Implantation (from fetal or derived sources)

   • Purpose: Replace degenerating retinal neurons directly.

   • Mechanism: Introduced cells attempt to integrate into retinal layers and restore function.

   • Evidence: Very early stage; theoretical benefit for late-stage damage after DUSN. PMCHerald Open Access

Important: All regenerative/stem cell strategies carry uncertainties, are mostly in clinical trial phases, and should only be pursued under specialized centers with ethical oversight. PMCHerald Open Access

Surgeries / Procedural Interventions (What They Are and Why Done)

1. Laser Photocoagulation of the Worm

   • Procedure: Focused laser burns are applied directly to the visible worm (or bounding it) to kill it. Parameters often include 200 µm spots at around 200 mW with brief durations, sometimes enclosing the worm then applying confluent burns.

   • Why Done: Direct destruction of the causative nematode stops further migration and toxin release, halting progression of vision loss. Early application can yield visual improvement. EyeWikiophed.com

2. Pars Plana Vitrectomy with Direct Worm Extraction

   • Procedure: Surgical entry into the vitreous cavity, followed by aspiration or removal of the worm when located in difficult-to-treat areas (e.g., macula) or when laser is unsuitable.

   • Why Done: Physical removal prevents continued retinal damage in cases where the worm is mobile and in critical visual zones. PMCEyeWiki

3. Epiretinal Membrane Peeling

   • Procedure: If chronic inflammation leads to scar tissue over the macula (epiretinal membrane), a surgeon removes this membrane microsurgically to relieve traction.

   • Why Done: Improve distortion and some visual acuity loss due to secondary traction from membrane formation after DUSN-related damage.

4. Vitrectomy for Persistent Vitreous Opacities or Traction

   • Procedure: Removal of vitreous gel in cases of long-standing inflammation or vitreoretinal traction causing further visual distortion.

   • Why Done: Clear media and relieve mechanical stress that may contribute to vision impairment, improving visualization for ongoing management.

5. Interventional Treatment of Secondary Complications (e.g., Intravitreal Injections for Neovascularization)

   • Procedure: Injection of anti-VEGF agents or steroids directly into the eye if new abnormal vessels or inflammation threaten vision.

   • Why Done: Manage late complications that could compound vision loss after the primary insult from DUSN. EyeWiki

---

Preventions (How to Reduce Risk of DUSN)

1. Avoid Contact with Raccoon Feces and Their Habitats: Baylisascaris procyonis is carried by raccoons; avoid handling or exposure to their droppings. EyeWiki

2. Regular Deworming of Pet Dogs and Control of Stray Dogs: Prevent spread of nematodes like Ancylostoma caninum that can contribute to ocular larva migrans-type infections. EyeWiki

3. Cook Fish and Meat Thoroughly: Gnathostoma and other parasites can enter humans through raw or undercooked seafood; proper cooking kills larvae. EyeWiki

4. Good Hand Hygiene After Soil or Animal Contact: Washing hands reduces inadvertent ingestion of eggs or larvae from contaminated surfaces. EyeWiki

5. Cover Sandboxes and Play Areas: Prevent contamination from animals shedding infective eggs where children play. EyeWiki

6. Use Gloves When Gardening or Handling Soil: Some nematodes can penetrate skin; protective gloves add a barrier. EyeWiki

7. Public Education in Endemic Regions: Inform communities about risk behaviors and early symptoms so people seek care quickly. EyeWiki

8. Avoid Drinking Untreated Water in High-risk Areas: Though retinal nematodes usually require intermediary hosts, general hygiene reduces opportunistic exposures.

9. Prompt Evaluation After Exposure or Early Visual Symptoms: Early ophthalmologic assessment at first sign of visual change increases chances of saving vision. EyeWiki

10. Pet and Wildlife Control to Limit Carrier Contact: Manage and limit access to potential wild carrier animals near living spaces. EyeWiki

---

When to See a Doctor (Red Flags)

• Sudden or progressive vision loss in one eye. EyeWiki

• New floaters or dark spots that were not present previously. EyeWiki

• Visual field deficits (missing areas in side or central vision). EyeWiki

• Appearance of gray-white or yellow-white outer retinal lesions. EyeWiki

• Any unexplained change in color perception or contrast.

• History of exposure to potential nematode sources (raccoons, raw fish, dogs) with visual complaints. EyeWiki

• Persistent eye inflammation (vitritis) not resolving with standard care. EyeWiki

• New onset of afferent pupillary defect (suggesting optic nerve involvement). EyeWiki

• Worsening vision after presumed treatment (suggests complication or incomplete worm elimination).

• Any sign of optic nerve swelling or atrophy observed by a clinician. EyeWiki

---

What to Eat and What to Avoid

What to Eat (Supports Retinal Health)

1. Leafy Green Vegetables (Spinach, Kale): High in lutein and zeaxanthin, help protect the macula. Verywell Health

2. Fatty Fish (Salmon, Tuna): Rich in omega-3 fatty acids (DHA/EPA) for anti-inflammatory support. MDPI

3. Colorful Fruits (Berries, Citrus): Provide vitamin C and antioxidants to fight oxidative stress. Verywell Health

4. Nuts and Seeds: Sources of vitamin E and zinc precursors which help maintain retinal cell membrane health. Verywell Health

5. Eggs: Contain lutein/zeaxanthin in a bioavailable form and support macular pigment. Prevention

What to Avoid

1. Excessive Sugar and Refined Carbs: Promote inflammation and oxidative stress which can worsen retinal injury. MDPI

2. Trans Fats / Highly Processed Foods: Linked to systemic inflammation; avoiding them supports ocular microcirculation. MDPI

3. Smoking / Tobacco Products: Increases risk of further retinal degeneration; cessation is critical. MDPI

4. Excessive Alcohol: Can dehydrate and impair nutrient absorption needed for retinal repair.

5. Over-supplementation of Fat-Soluble Vitamins (e.g., Vitamin A in excess): High doses without supervision may have toxicity; balance is safer.

---

Frequently Asked Questions (FAQs)

1. What causes DUSN?
   DUSN is caused by a living nematode (worm) beneath the retina. Species vary by region and include Baylisascaris procyonis, Ancylostoma caninum, and others. EyeWiki

2. Can DUSN affect both eyes?
   It is usually unilateral (one eye), but rare bilateral cases have been reported. EyeWiki

3. How is DUSN diagnosed?
   Diagnosis is clinical, based on retinal findings, symptoms, and imaging. Direct visualization of the worm confirms it but only occurs in ~25–40% of cases. EyeWiki

4. What happens if the worm is seen?
   Immediate laser photocoagulation to kill the worm is preferred and can halt progression. EyeWikiophed.com

5. What if the worm cannot be seen?
   Doctors may start anti-helminthic treatment (e.g., albendazole) and control inflammation with corticosteroids based on clinical suspicion. EyeWikiPMC

6. Is vision fully recoverable?
   Early treated cases can stabilize or improve somewhat; late-stage damage (optic atrophy, widespread degeneration) is often irreversible. EyeWiki

7. Are anti-parasitic pills enough?
   Albendazole can help when worm isn’t seen, but killing a visible worm directly with laser gives the best chance to stop damage. Some traditional drugs like thiabendazole and ivermectin have shown limited or no effectiveness alone. PubMedPMC

8. Do I need surgery?
   Surgery (laser or vitrectomy) is needed if the worm is visible or if complications arise that threaten vision. EyeWiki

9. Can diet help?
   Yes. Eating foods rich in antioxidants (like lutein, zeaxanthin, vitamins C/E), omega-3s, and zinc supports retinal resilience and reduces inflammation. MDPIEyeWiki

10. Should I take supplements?
    Supplements such as lutein, zeaxanthin, omega-3s, and zinc may be beneficial as adjuncts for retinal health; they do not replace primary anti-worm and anti-inflammatory treatments. EyeWiki

11. Is DUSN contagious?
    No. You cannot catch it from someone else directly. Infection comes from environmental exposure to nematode eggs or larvae via animal carriers. EyeWiki

12. Can stem cell therapy cure DUSN damage?
    Not currently. Stem cell approaches are experimental and aimed at degenerative retinal diseases; their use in DUSN-related damage is theoretical and under investigation. PMCHerald Open Access

13. What are common side effects of treatment?
    Anti-parasitic drugs can cause stomach upset and dizziness; corticosteroids have systemic effects like elevated sugar; laser can cause localized retinal injury if misapplied. EyeWiki

14. How often should I follow up?
    Frequent early follow-up with retinal imaging (OCT, visual fields) is important to assess treatment response, then periodically to monitor for late complications. EyeWiki

15. Can the worm come back after treatment?
    Reinfection is possible if new exposures occur, but the same worm, once destroyed, does not “regrow.” Prevention of re-exposure is key. EyeWiki

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 02, 2025.

PDF Document For This Disease Conditions References