Kyrieleis Arteriolitis

Kyrieleis arteriolitis means there are small, bead-like white patches sitting inside the wall of the retinal arteries (the tiny blood vessels that bring blood to the retina at the back of the eye). They line up in short segments, so they look like a string of pearls or beads along the artery. Doctors also call them Kyrieleis plaques, segmental retinal arteritis/periarteritis, or nodular periarteritis. They almost always appear during a strong inflammation inside the eye (posterior uveitis) and are most often linked to infections, especially toxoplasmosis, but they can appear with a few non-infectious diseases too. On dye testing (fluorescein angiography), these plaques usually do not leak dye, which helps tell them apart from “sheathing” or frosted branch angiitis. Over time, they often fade once the eye inflammation settles, but they can persist for months in some cases. EyeWikiSpringerOpenLippincott Journals

• Retina: a thin, light-sensing layer inside the eye.

• Arteries: tubes that carry blood to the retina. Arterioles are their smaller last branches.

• Plaques: in this context, tiny white deposits that sit within the vessel wall (not floating inside the blood and not spilling outside the vessel).

• Segmental: they come in short stretches, with gaps of normal vessel in between.

• Beaded pattern: looks like little pearls dotted along the artery.

• What they mean: the eye is dealing with intense inflammation, usually from an infection near the area (such as a retino-choroiditis patch). The vessel lining (endothelium) seems to be inflamed; many studies show no dye leak and normal filling on angiography, which supports the idea of endothelitis (inflammation of the inner vessel lining) rather than a full-thickness vasculitis that leaks. EyeWiki

How doctors see them: during a dilated retinal exam, the plaques look yellow-white, glistening, and calcific-like along the arteries only (veins are typically spared). Fluorescein angiography often shows no leakage and no blockage of flow. Indocyanine green angiography and OCT (retinal scans) can show bright signals from the vessel wall, matching where the plaques sit. EyeWiki

What they are not:

• Not intraluminal emboli (cholesterol or calcium bits inside the blood column).

• Not the fluffy sheathing you see in many vasculitides.

• Not frosted branch angiitis (that condition coats both arteries and veins with thick white “frosted” sheathing and typically leaks dye). PMC

Do they harm vision by themselves? Usually no. They are more like signposts telling us there is/was strong inflammation nearby. Vision problems mostly come from the underlying disease (e.g., toxoplasma retinitis, herpetic acute retinal necrosis, or CMV retinitis), not from the plaques alone. They often disappear after the inflammation is treated, though persistence for months has been documented. Overall prognosis depends on the cause and how quickly it’s treated. EyeWikiLippincott Journals

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Types

1. By cause (most practical):

   • Infectious (the majority) versus non-infectious (autoimmune/vascular) versus drug-associated (rare). EyeWiki

2. By distribution:

   • Focal/segmental (few short bead-like stretches) versus multifocal (several segments in different places). EyeWiki

3. By timing and course:

   • Active-phase plaques (during severe inflammation) versus late-appearing or persistent plaques (becoming obvious or lingering after the retinitis calms down). EyeWikiLippincott Journals

4. By associated retina status:

   • Adjacent to active retinitis (common in toxoplasma) versus appearing while lesions resolve (reported in CMV or ARN during/after treatment). SpringerOpen

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Causes

Each item says what the cause is and why it can lead to Kyrieleis plaques (the arterial wall reacts to nearby inflammation).

Infectious (most common):

1. Toxoplasma gondii retinochoroiditis — the classic association; a hot retinal infection beside an artery can inflame the artery wall, making segmental plaques. EyeWiki

2. Cytomegalovirus (CMV) retinitis — in immunosuppressed eyes, CMV can cause retinal necrosis; plaques may increase early in treatment then fade over months. SpringerOpen

3. Varicella-zoster virus (VZV) acute retinal necrosis (ARN) — aggressive herpetic infection with arterial involvement; plaques reported in VZV-ARN. PMC

4. Herpes simplex virus type 1 (HSV-1) ARN — similar mechanism; cases show plaques with HSV-1 ARN. PMC

5. Herpes simplex virus type 2 (HSV-2) ARN — same family, same pattern; reported with Kyrieleis plaques. PMC

6. Mycobacterium tuberculosis (ocular TB) — posterior uveitis from TB can inflame arteries and produce plaques, including TB-related serpiginous-like disease. revistas.rcaap.pt

7. Syphilis (Treponema pallidum) uveitis — spirochetal infection can mimic many eye diseases and has been linked to plaques. EyeWiki

8. Rickettsia conorii (Mediterranean spotted fever) — rickettsial posterior uveitis may involve arteries segmentally. EyeWiki

9. CMV retinitis in advanced HIV/AIDS — profound immune suppression (very low CD4) predisposes to CMV retinitis, in which plaques can appear. PMC+1

10. Post-herpetic encephalitis with subsequent ARN — HSV-1 encephalitis can be followed by herpetic ARN and plaques. PMC

Non-infectious autoimmune/vasculitic:

1. Behçet disease uveitis — a systemic vasculitis; rare reports show bilateral Kyrieleis plaques. Frontiers
2. Susac syndrome — a micro-arteriolopathy of brain, retina, and inner ear; plaques have been described in this setting. PMC
3. Serpiginous choroiditis — a chronic inflammatory choroidopathy; plaques have been imaged in some cases. UCR Library Search
4. Tubercular serpiginous-like choroiditis (TB-SLC) — a TB-related serpiginous pattern; arterial wall involvement may present as plaques. revistas.rcaap.pt
5. Idiopathic posterior uveitis — sometimes no cause is found; plaques still signal intense intraocular inflammation. EyeWiki

Drug-associated / iatrogenic (very rare):

1. Brolucizumab-associated retinal vasculitis/inflammation — a recognized complication of this anti-VEGF drug; Kyrieleis-like periarterial plaques have been described among its features. EyeWikiAAO Journal
   17) Rifabutin-associated uveitis with segmental retinal arteritis — reported as segmental arteritis (the Kyrieleis pattern) in an immunocompromised patient. ScienceDirect

Contextual infectious variants (overlap with above but useful in practice):

1. VZV progressive outer retinal necrosis (PORN) in HIV — a severe herpetic variant with marked arterial involvement; plaques can be a clue. casereports.bmj.com
   19) CMV retinitis in transplant or steroid-treated patients — iatrogenic immunosuppression (not only HIV) can lead to CMV retinitis and plaques. PMC
   20) Atypical toxoplasmosis presentations — multifocal segmental arteritis and even optic-nerve-head plaques have been reported. PMCNature

Note: The list above focuses on documented associations. Reports exist across both infectious and autoimmune spectra. Your local prevalence (TB, toxoplasma, herpetic disease, HIV/CMV) often shapes what’s most likely. EyeWiki

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Symptoms

1. Blurred vision — the most common complaint when the retina is inflamed.

2. Floaters — dark specks or cobwebs from inflammatory cells in the vitreous gel.

3. Photopsia — brief flashes of light from irritated retina.

4. Scotoma — a “missing spot” in the field of vision when the inflamed area affects photoreceptors.

5. Metamorphopsia — lines look wavy if central retina is disturbed.

6. Color desaturation — colors look dull or “washed out.”

7. Reduced contrast sensitivity — everything looks foggier than usual.

8. Light sensitivity (photophobia) — inflamed eye is uncomfortable in bright light.

9. Mild eye ache or fullness — less common than in front-of-the-eye uveitis, but possible.

10. Glare/halos — scattered light from media haze (vitritis).

11. Poor night vision — if the outer retina is affected.

12. Peripheral vision loss — if necrosis or inflammation is away from the center.

13. Sudden vision drop — if the macula or optic nerve becomes involved.

14. Red eye — often subtle with posterior disease.

15. Systemic symptoms (from the cause) — fever, headache, skin rash, oral/genital ulcers (Behçet), or neurologic/hearing issues (Susac). (These help point to the cause rather than to the plaques themselves.) PMC

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Diagnostic tests

A) Physical exam

1. Visual acuity — reading charts to measure how sharp the vision is; sets a baseline and tracks response.

2. Dilated fundus exam — eye drops enlarge the pupil so the doctor can directly see the retina and spot the beaded white plaques along arteries only. This is the key clinical sign. EyeWiki

3. Intraocular pressure (IOP) & pupil reflexes — checks for pressure spikes and relative afferent pupillary defect if the nerve/retina are severely affected.

B) Manual/bedside functional tests

4. Amsler grid — a small checkerboard held at reading distance; wavy lines or missing squares suggest macular involvement.

5. Confrontation visual fields — quick bedside mapping of blind spots or side-vision loss.

6. Color vision (Ishihara plates) — detects color drop-out from macular/nerve dysfunction.

7. Photostress recovery — shining light then timing recovery of reading ability; delayed recovery suggests macular dysfunction.

C) Laboratory & pathological tests

8. Toxoplasma serology (IgG/IgM) — supports or argues against toxoplasmosis.

9. Syphilis tests — a screen (RPR/VDRL) plus a confirmatory treponemal test (FTA-ABS/TPPA).

10. Tuberculosis testing — IGRA (Quantiferon-TB Gold) or PPD skin test; sometimes chest imaging if TB is suspected.

11. Rickettsial serology — when travel/exposure suggests Mediterranean spotted fever.

12. HIV test and immune profile (CD4 count) — because CMV retinitis and severe herpetic disease are far more likely in advanced immunosuppression. PMC

13. Aqueous or vitreous PCR & Goldmann–Witmer coefficient — molecular tests on a tiny fluid sample from the eye to detect pathogen DNA (HSV-1/2, VZV, CMV, Toxoplasma) or local antibody production. These tests can pin down the cause when the exam alone is not enough. MDPI

D) Electrodiagnostic tests

14. Full-field ERG (electroretinogram) — measures the electrical responses of the retina; helps gauge retinal damage beyond what we see.

15. VEP (visual evoked potential) — measures the brain’s response to visual signals; helpful if the optic nerve or pathways might be affected (e.g., in Susac or widespread disease).

E) Imaging tests

16. Color fundus photography — documents the appearance and location of plaques and tracks change over time.

17. Fluorescein angiography (FA) — an IV dye test; Kyrieleis plaques classically show no leakage, and arterial filling remains normal. This helps separate plaques from “sheathing” or frosted branch angiitis, which do leak. EyeWikiSpringerOpen

18. Indocyanine green angiography (ICG) — a different dye that binds proteins; can highlight plaques clearly and supports endothelial involvement. EyeWiki

19. Optical coherence tomography (OCT) — non-contact scan; shows bright (hyper-reflective) vessel walls exactly where plaques sit, and checks the retina for edema or damage. MDPI

20. Fundus autofluorescence (FAF) or OCT-A — FAF may show bright signal over plaques; OCT-angiography can show narrowed flow signal

Non-pharmacological treatments

These measures support healing and safety. They do not replace antimicrobial/antiviral therapy when an infection is present.

1. Close observation after infection control – plaques often fade gradually; watching avoids overtreatment. PubMed

2. Light management (sunglasses, hats) – reduces photophobia and improves comfort.

3. Home vision checks (Amsler grid, one eye at a time) – catches new central distortion early.

4. Symptom diary (floaters, flashes, “curtain”) – helps detect retinal detachment promptly.

5. Activity pacing (rest during flares) – lowers visual strain while the macula is irritable.

6. Strict treatment adherence – finishing the full antimicrobial course prevents relapse or resistance. NCBI

7. Do not start steroids alone for suspected infection – steroids without antimicrobial cover can worsen infectious uveitis. PMC

8. Follow the “24–48-hour rule” – add systemic steroids after antimicrobial therapy has begun (when infection is being treated). NCBI

9. Blood sugar control (if diabetic) – high glucose fuels inflammation and infection risk.

10. Blood pressure control – stabilizes fragile retinal circulation during healing.

11. Smoking cessation – reduces oxidative stress that harms retinal vessels.

12. Sleep optimization – supports immune function and tissue repair.

13. Stress reduction (breathing, mindfulness) – high stress raises systemic inflammatory signals.

14. Eye protection (avoid eye trauma, careful with contact lenses during active inflammation).

15. Hydration – supports overall perfusion and comfort.

16. Low-vision aids (magnifiers, better lighting) – pragmatic help while the retina recovers.

17. Regular follow-ups (keep appointments for exam/FA/OCT) – lets the team adjust therapy quickly.

18. Primary-care coordination – review vaccinations (e.g., shingles vaccine in eligible adults) to reduce future viral risks.

19. Nutrition pattern (Mediterranean-style) – anti-inflammatory dietary base (details below).

20. Safe-driving advice – avoid driving until vision is stable and safe.

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Drug treatments

Doses below are typical adult starting points. Final choices depend on your doctor’s assessment, kidney/liver function, pregnancy status, and local guidelines.

1. Pyrimethamine + sulfadiazine + folinic acid (Class: antiparasitic + sulfonamide + leucovorin rescue)
   Dose: pyrimethamine loading 50–100 mg day 1, then 25–50 mg daily; sulfadiazine 1–1.5 g every 6 h; folinic acid 5–25 mg with each pyrimethamine dose for marrow protection; duration usually 4–8 weeks.
   Purpose: first-line for ocular toxoplasmosis.
   Mechanism: blocks folate metabolism in T. gondii; sulfonamide blocks folate synthesis; folinic acid protects host bone marrow.
   Common side effects: nausea, rash; serious: bone-marrow suppression (hence folinic acid), sulfa allergy. CDCNCBI

2. Trimethoprim–sulfamethoxazole (TMP-SMX, “Bactrim DS”) (Class: folate antagonists)
   Dose: 160/800 mg twice daily, often 4–6 weeks; sometimes used for maintenance.
   Purpose: alternative for toxoplasmosis (effective, widely used).
   Mechanism: dual folate blockade in the parasite.
   Side effects: rash, hyperkalemia, marrow suppression (rare). AAO Journal

3. Clindamycin (Class: lincosamide antibiotic)
   Dose: 300 mg four times daily, often added to pyrimethamine regimens.
   Purpose: adjunct for toxoplasma retinitis.
   Mechanism: inhibits parasite protein synthesis.
   Side effects: diarrhea, C. difficile risk. AAO Journal

4. Azithromycin (Class: macrolide)
   Dose: 500 mg daily (regimens vary) as an alternative in toxoplasmosis (especially if sulfa allergy).
   Purpose: alternative anti-toxoplasma option.
   Mechanism: protein synthesis inhibition in T. gondii.
   Side effects: GI upset, QT prolongation (rare). AAO Journal

5. Prednisone (systemic corticosteroid)
   Dose: 0.5–1 mg/kg/day, then taper. Start only after antimicrobials have begun for infectious uveitis (often 24–48 h later).
   Purpose: reduces retinal inflammation, edema, and pain.
   Mechanism: broad anti-inflammatory gene regulation.
   Side effects: glucose elevation, mood changes, infection risk, cataract, glaucoma. PMC

6. Valacyclovir / Acyclovir (Class: anti-herpes antivirals)
   Dose: Acyclovir 10 mg/kg IV q8h initially for acute retinal necrosis (ARN), then valacyclovir 1 g three times daily orally; duration varies with response.
   Purpose: treats HSV/VZV-driven ARN.
   Mechanism: inhibits viral DNA polymerase after phosphorylation in infected cells.
   Side effects: kidney injury (hydrate), nausea; neurotoxicity (rare). AAO Journal

7. Intravitreal antivirals (ganciclovir 2 mg/0.1 mL or foscarnet 2.4 mg/0.1 mL)
   Timing: given in addition to systemic therapy during induction; often 1–2×/week until regression.
   Purpose: immediate, high antiviral levels inside the eye for ARN.
   Mechanism: direct viral DNA polymerase inhibition in the vitreous/retina.
   Side effects: procedure-related (infection risk, retinal tear/detachment—rare). PMC

8. Valganciclovir (Class: anti-CMV antiviral)
   Dose: 900 mg twice daily for 14–21 days (induction), then 900 mg daily (maintenance) for CMV retinitis (adjust for renal function).
   Purpose: treats CMV retinitis associated with Kyrieleis plaques.
   Mechanism: inhibits CMV DNA polymerase.
   Side effects: bone-marrow suppression, GI upset. PMC

9. Penicillin G (IV) for ocular syphilis
   Dose: 18–24 million units/day IV for 10–14 days (standard neurosyphilis regimen also treats ocular syphilis).
   Purpose: eradicates Treponema pallidum.
   Mechanism: β-lactam cell-wall inhibition.
   Side effects: allergic reactions, Jarisch–Herxheimer reaction (transient fever/worsening). PMC

10. Anti-TB therapy (RIPE: isoniazid, rifampin, pyrazinamide, ethambutol) when ocular TB is suspected/confirmed
    Dose: per national TB guidelines and weight.
    Purpose: treats TB-associated uveitis contributing to Kyrieleis plaques.
    Mechanism: multi-drug kill of Mycobacterium tuberculosis.
    Side effects: liver toxicity (monitor), optic neuritis (ethambutol). PMC

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Advanced/immune” medicines

There are no approved stem-cell or regenerative drugs for Kyrieleis arteriolitis. In severe non-infectious uveitis, specialists sometimes use advanced immune-modulating therapies to control inflammation and protect vision:

1. Adalimumab (anti-TNF-α)
   Dose: 80 mg loading, then 40 mg every 2 weeks subcutaneously (adult NIU label).
   Function/mechanism: blocks TNF-α to dampen retinal inflammation.
   Notes: FDA-approved for non-infectious intermediate/posterior/panuveitis; watch for infection risk. FDA Access DataRetina Today

2. Infliximab (anti-TNF-α, IV)
   Dose: 5–10 mg/kg at weeks 0, 2, 6, then q4–8 weeks.
   Function: TNF-α blockade for refractory uveitis.
   Notes: infusion reactions, infection risk; used off-label in NIU. PMCAAO Journal

3. Tocilizumab (anti-IL-6)
   Dose: IV 4–8 mg/kg monthly or SC weekly/biweekly (specialist-guided).
   Function: blocks IL-6 signaling; helpful in macular edema from NIU.
   Notes: monitor lipids, liver enzymes, infection risk. AAOPMC

4. Interferon-α2a
   Dose: regimens vary (e.g., 3–6 million IU SC several times/week, tapered).
   Function: immunomodulatory; classic option in Behçet uveitis.
   Notes: flu-like symptoms, mood changes; specialist care required. PMCJAMA Network

5. Mycophenolate mofetil (MMF)
   Dose: 1–1.5 g twice daily in NIU as a steroid-sparing agent.
   Function: inhibits lymphocyte proliferation.
   Notes: GI upset, leukopenia; lab monitoring needed. EyeWikiPubMed

6. Methotrexate
   Dose: 15–25 mg once weekly (with folic acid).
   Function: antimetabolite; long-used steroid-sparing therapy in NIU.
   Notes: liver, marrow monitoring; avoid in pregnancy. (Head-to-head data with MMF exist in NIU.) JAMA Network

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Surgeries/procedures

These are not for the plaques themselves; they are for complications of the underlying disease—especially acute retinal necrosis (ARN).

1. Barrier laser photocoagulation around necrotic retina
   Why: may lower the risk of retinal detachment (RD) by “welding” the retina to underlying tissue at the edge of necrosis. PubMedOphthalmology Advisor

2. Pars plana vitrectomy (PPV) for RD or dense vitreous debris
   Why: reattaches the retina, removes traction/infectious debris; silicone oil or gas may be used. Outcomes vary; RD from ARN often has guarded visual prognosis. PMCScienceDirect

3. Scleral buckle (sometimes with PPV) for rhegmatogenous RD
   Why: supports the retinal wall externally to help seal breaks related to necrosis. Lippincott Journals

4. Diagnostic vitreous tap/biopsy (PCR)
   Why: obtains intraocular fluid to identify the pathogen when the diagnosis is uncertain—guides precise therapy. Nature

5. Cataract or glaucoma surgery (if needed later)
   Why: long-term steroids/inflammation can cause cataract or high eye pressure; surgery treats these complications to improve/maintain vision.

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Dietary & supportive supplements

No supplement treats Kyrieleis plaques directly. Some have evidence for general retinal or immune support—mostly from AMD or uveitis research. Always discuss with your clinician.

1. AREDS2 antioxidant mix (Vitamin C 500 mg, Vitamin E 400 IU, Zinc 80 mg [or 25 mg formulations], Copper 2 mg, Lutein 10 mg, Zeaxanthin 2 mg) – slows AMD progression; neutral safety profile when beta-carotene is replaced by lutein/zeaxanthin. National Eye InstituteNational Institutes of Health (NIH)JAMA Network

2. Lutein + Zeaxanthin (as above) – carotenoids concentrated in the macula; antioxidant/blue-light filtering. JAMA Network

3. Zinc (with copper) – part of AREDS2; supports retinal enzymes; avoid high-dose without guidance. National Eye Institute

4. Omega-3 (EPA/DHA ~1 g/day) – mixed ocular evidence; general anti-inflammatory effects; not proven to help AMD progression in AREDS2. PentaVision

5. Vitamin D (800–2000 IU/day) – broad immune effects; recent large meta-analyses show little or no prevention of respiratory infections in the general population; still useful to correct deficiency. The LancetThe Washington Post

6. N-acetylcysteine (NAC 600 mg 1–2×/day) – antioxidant/glutathione precursor; promising retinal cell protection signals in lab and early clinical work. PMCScienceDirect

7. Curcumin (e.g., 500 mg 1–2×/day with piperine or enhanced formulations) – anti-inflammatory; small uveitis studies and reviews suggest benefit, but bioavailability is a challenge. PubMedFrontiers

8. Vitamin A (as diet, not high-dose pills) – essential for photoreceptors; avoid excess supplements (toxicity).

9. Vitamin C (already in AREDS2) – antioxidant support. National Eye Institute

10. Vitamin E (already in AREDS2) – antioxidant; avoid very high doses without supervision. National Eye Institute

11. Copper (2 mg with high-dose zinc) – prevents copper-deficiency anemia when taking zinc. National Eye Institute

12. Selenium (55–100 mcg/day) – antioxidant enzymes (GPx); keep within safe limits.

13. Coenzyme Q10 (100–200 mg/day) – mitochondrial support; human ocular data limited.

14. Probiotics – gut-immune modulation is being explored; evidence in ocular inflammation is early.

15. Resveratrol/Bilberry – antioxidant polyphenols; evidence for uveitis/retina remains preliminary.

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Prevention tips

1. Food safety for toxoplasma: cook meat well; wash fruits/vegetables; avoid unpasteurized milk.

2. Cat-litter hygiene: avoid handling if pregnant/immunosuppressed; wear gloves; wash hands.

3. Shingles (VZV) vaccination if eligible (prevents reactivation that can lead to ARN).

4. Safe sex & STI screening: reduces syphilis risk.

5. TB control: screen/treat latent TB in high-risk settings.

6. Tick bite prevention when traveling to rickettsial-endemic areas.

7. HIV prevention & treatment: PrEP where appropriate; if HIV-positive, stay on ART to protect immune function.

8. Avoid unsupervised steroid bursts for red, painful eyes—get examined first to rule out infection.

9. Control diabetes and blood pressure: reduces vascular stress.

10. Don’t smoke: lowers oxidative injury to retinal vessels.

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When to see a doctor (red flags)

• Sudden blur, new floaters, flashes, or a shadow/curtain in your vision (possible retinal detachment—urgent).

• Rapidly worsening vision or severe light sensitivity.

• Eye symptoms with fever or new rash, especially if you have HIV, are on immunosuppressants, or recently had shingles.

• Pregnancy with suspected toxoplasma exposure (special management).

• Any new eye symptom if you have known uveitis or are starting/stopping steroids or biologics.

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What to eat & what to avoid

Eat more of:

• A Mediterranean-style pattern: leafy greens (spinach, kale), orange/yellow veggies, citrus/berries, legumes, whole grains, nuts, seeds, fish (salmon, sardines) 1–2×/week, olive oil as main fat.

• Hydrating fluids (water, infused water, unsweetened tea).

• Protein from fish, eggs, legumes, poultry for healing.

Limit/avoid:

• Undercooked meats; unwashed produce; unpasteurized dairy (toxoplasma risk).

• Excess alcohol (inflammation, drug interactions).

• High-sugar ultra-processed foods (pro-inflammatory).

• Smoking/vaping (vessel and retina harm).

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FAQs

1) Are Kyrieleis plaques dangerous?
By themselves, no—they are a sign of inflammation/infection in the retina. The underlying disease (e.g., toxoplasma or ARN) is what can threaten vision. EyeWiki

2) Do the plaques block blood flow?
Typically no. FA usually shows normal arterial filling without blockage. EyeWiki

3) Are they cholesterol clots?
No. They are inflammatory wall deposits, not cholesterol emboli (Hollenhorst). NCBI

4) Will they go away?
Often yes—they can fade over months as inflammation resolves. PubMed

5) Can they move?
No. They are in the vessel wall, not free-floating. EyeWiki

6) What causes them most often?
Ocular toxoplasmosis is the most reported association; viruses that cause acute retinal necrosis are also common. EyeWikiNature

7) How are they diagnosed?
By dilated exam and imaging (FA/OCT). PCR of eye fluid may identify the exact germ when needed. Nature

8) Are steroids helpful?
Yes, as add-on after starting the correct antimicrobial; never use steroids alone for suspected infection. PMC

9) Do I need surgery?
Not for the plaques. Surgery is for complications like retinal detachment in ARN. PMC

10) How long will treatment take?
Antimicrobial/antiviral courses often run weeks, with follow-up imaging to confirm healing. (Exact length varies by cause.) NCBIAAO Journal

11) Can supplements cure this?
No. Supplements may support general retinal health, but they do not treat Kyrieleis plaques. Use only as advised. National Eye Institute

12) Could this come back?
Yes, if the underlying infection or uveitis recurs. Maintenance therapy is sometimes used in high-risk cases. AAO Journal

13) Is it contagious?
The sign isn’t; some causes (e.g., syphilis, VZV) are infectious—your doctor will guide precautions. PMC

14) What about both eyes?
Usually one eye; both eyes can be affected in some infections (e.g., ARN). PubMed

15) What’s the outlook?
If caught early and treated, prognosis is generally good for the plaques; outcome depends on the disease behind them. PMC

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 10, 2025.

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