Kyrieleis plaques are tiny, bright, yellow-white “beads” that sit in the wall of the retinal arteries (the small blood vessels that bring blood to the light-sensing layer at the back of the eye). They show up in short, segmental stretches—so the artery looks dotted or beaded rather than uniformly coated. These plaques are inside the vessel wall (not loose clots inside the blood stream and not fuzzy sheathing outside the vessel). They usually appear during or after strong inflammation in the back of the eye (posterior uveitis/retinitis). They were first described in 1933 in a patient with presumed ocular tuberculosis, and modern imaging confirms they’re closely linked to severe intra-ocular inflammation rather than true emboli. EyeWiki

Common alternative names you may see in papers and reports: Kyrieleis arteriolitis, Kyrieleis vasculitis, nodular periarteritis, segmental retinal periarteritis/arteritis—all describing the same beaded arterial wall deposits. EyeWiki

Kyrieleis plaques are tiny, yellow-white, bead-like deposits that line segments of the retinal arteries (the small blood vessels that carry blood into the back of the eye). They show up during severe inflammation in the eye, most often when an infection or, less commonly, an autoimmune disease inflames the retina. Doctors also call them Kyrieleis arteriolitis, segmental retinal periarteritis/arteritis, or nodular periarteritis. They were first described in 1933, and we still don’t have tissue proof of their exact makeup, but modern imaging suggests they are inflammatory material (immune cells and debris) in or stuck to the artery wall. Importantly, they affect arteries (not veins), do not behave like cholesterol emboli, and on fluorescein angiography typically do not block flow or leak dye, which helps doctors tell them apart from other look-alikes. EyeWikiPubMedPMC+1

---

How do they differ from other white vessel changes?

• Not emboli (e.g., Hollenhorst plaques): emboli sit inside the blood column and can block flow; Kyrieleis plaques live within the wall and do not cause arterial filling defects on dye tests. EyeWiki

• Not “frosted branch angiitis” or general perivascular sheathing: those conditions usually involve veins as well as arteries and leak dye on fluorescein angiography (FA); Kyrieleis plaques are arterial-only and do not leak. SpringerOpenNatureEyeWiki

---

Types

There’s no official universal classification, but this simple framework helps when you’re reading charts or seeing patients:

1. Infectious-associated Kyrieleis plaques
   Most commonly linked to ocular toxoplasmosis; also seen with herpes-family retinal infections (acute retinal necrosis from VZV/HSV, CMV retinitis), tuberculosis, syphilis, and rickettsial infections. EyeWikiPMCNatureSpringerOpen

2. Non-infectious/immune-mediated plaques
   Uncommonly reported in Behçet disease and drug-associated retinal vasculitis (e.g., after brolucizumab). EyeWikiPMC

3. By timing

   • Active-phase: appear near or during active retinitis/uveitis.

   • Resolving-phase: sometimes become more obvious as the “storm” calms and the view clears; they may persist for months and then fade. PMCSpringerOpen

4. By extent

   • Focal: short artery segments near a single lesion.

   • Multifocal: several arteries or longer stretches involved, sometimes in atypical toxoplasmosis or ARN. PMC

---

Causes and associations

Think of Kyrieleis plaques as fingerprints left on the artery wall by a strong inflammatory trigger—usually an infection in or near the retina.

Most-supported infectious causes

1. Ocular toxoplasmosis (Toxoplasma gondii). The most frequently reported cause; plaques often appear near the retino-choroiditis focus. EyeWikiPMC

2. Varicella-zoster virus (VZV) – Acute retinal necrosis. Severe viral retinitis that can produce arterial plaques without FA leakage. Nature

3. Herpes simplex virus-1 (HSV-1) – ARN. Similar mechanism to VZV; plaque pattern along arteries. ScienceDirect

4. Herpes simplex virus-2 (HSV-2) – ARN. Another herpes ARN variant reported with plaques. EyeWiki

5. Cytomegalovirus (CMV) retinitis. Especially in immunocompromised hosts; plaques may increase transiently as retinitis improves; no leakage on FA. SpringerOpen

6. Mycobacterium tuberculosis (ocular TB). Described in the earliest reports; modern cases include “Kyrieleis(-like)” plaques during ocular TB uveitis. EyeWikiPMC

7. Syphilis (Treponema pallidum) – posterior uveitis. Reported with periarterial plaque formation. EyeWiki

8. Rickettsia conorii. Mediterranean spotted fever organism; retinal involvement can include these plaques. EyeWiki

Less-common non-infectious/other settings

9. Behçet disease uveitis. Rare but documented association; plaques behave similarly (arterial, non-leaking). PMC

10. Brolucizumab-associated retinal vasculitis. Drug-triggered intraocular inflammation can show a Kyrieleis-like arterial plaque pattern. EyeWiki

Broader/related infectious contexts where “Kyrieleis-like” periarterial plaques may be described

(Terminology varies across reports; the look can mimic classic Kyrieleis plaques.)

11. Varicella-zoster uveitis (without full ARN). Severe VZV uveitis has shown plaques on adaptive optics imaging. MDPI

12. Remote-site vasculitis in toxoplasmosis under treatment. Plaques may appear at a distance as the main lesion settles. PMC

13. Post-rickettsial retinitis spectrum. Authors describe Kyrieleis plaques in some rickettsial retinitis cases. PMC

14. Broader “infectious retinal vasculitis” category. Reviews of retinal vasculitis note Kyrieleis arteriolitis as a characteristic periarterial plaque pattern in inflammatory arterial disease. Karger

---

Common symptoms

The plaques themselves are silent. Symptoms usually come from the underlying retinitis/uveitis that triggered them.

1. Blurry vision—from retinal swelling or nearby inflammation.

2. Floaters—from cells/debris in the vitreous gel.

3. A small dark spot (scotoma)—if inflammation is near the macula.

4. Distorted lines (metamorphopsia).

5. Light sensitivity (photophobia).

6. Eye redness—if there’s anterior uveitis as well.

7. Mild eye ache or soreness.

8. Reduced contrast or color “washed-out” feeling—in inflamed maculae.

9. Worse vision in dim light—if wide retinal areas are affected.

10. Peripheral shadow or curtain—rare, but suggests a related complication like retinal detachment in severe necrotizing retinitis. Lippincott Journals

11. Headache—nonspecific, sometimes from eye strain.

12. Glare/halos—if inflammation spreads to the front of the eye.

13. Intermittent improvement/worsening—as inflammation waxes and wanes.

14. No symptoms at all—plaques are sometimes noticed only on exam after the main inflammation settles. EyeWiki

15. Systemic clues—fever, rash, oral/genital ulcers, cough, weight loss, or neurologic symptoms can point toward the trigger (infection or autoimmune disease).

---

Diagnostic tests

Doctors do two things at once: (1) look carefully at the retina and (2) hunt for the cause. The tests below are the common building blocks.

A) Physical exam in the clinic

1. Best-corrected visual acuity. Checks how much sight is affected and tracks recovery during treatment.

2. Pupil exam (swinging flashlight test). Looks for a relative afferent pupillary defect (RAPD), which suggests significant retinal/nerve impact.

3. Intraocular pressure (IOP). Some uveitis types (especially herpetic) raise IOP; tracking it guides therapy.

4. Slit-lamp evaluation of the front of the eye and vitreous. Finds inflammatory cells/flare in the anterior chamber and vitritis in the gel—both support active uveitis.

B) “Manual” bedside tests

5. Amsler grid. Quick macular function check for distortions or missing areas.

6. Pinhole test. Distinguishes refractive blur from retinal disease.

7. Color vision (Ishihara or red desaturation). Macular/optic changes dull color perception.

8. Photostress recovery. Prolonged recovery hints at macular dysfunction from the retinal lesion.

C) Laboratory & pathological tests

9. Toxoplasma serology (IgG/IgM) ± intraocular antibody ratio (Goldmann–Witmer) or PCR on aqueous/vitreous. Confirms or supports ocular toxoplasmosis—the most common setting for Kyrieleis plaques. EyeWiki

10. Syphilis testing (non-treponemal + treponemal, e.g., RPR/VDRL and TPPA/FTA-ABS). Catches a treatable systemic cause of posterior uveitis with plaques. EyeWiki

11. Tuberculosis testing (IGRA or TST) with TB assessment. TB can drive posterior uveitis and Kyrieleis(-like) plaques. EyeWiki

12. Herpes-family viral PCR (HSV-1/2, VZV, CMV) from aqueous/vitreous. Very helpful in acute retinal necrosis or CMV retinitis. NatureSpringerOpen

13. Rickettsial serology (immunofluorescence). Consider in the right geography/exposure. EyeWiki

14. HIV test and basic bloods (CBC, ESR/CRP). HIV status guides CMV risk; ESR/CRP support an inflammatory process.

D) Electrodiagnostic tests

15. Full-field ERG (electroretinogram). If disease is widespread or chronic, ERG quantifies global retinal function.

16. VEP (visual evoked potential). Used when optic-nerve involvement is suspected or visual loss is out of proportion.

E) Imaging tests

17. Dilated fundus photography. Baseline and follow-up pictures document plaque segments and retinitis borders.

18. Fluorescein angiography (FA). In Kyrieleis plaques the arteries fill, and the plaques do not leak, helping separate them from frosted branch angiitis or emboli. SpringerOpenNature

19. Indocyanine green angiography (ICGA). Often shows plaques more clearly and can outline them throughout the study. EyeWiki

20. Optical coherence tomography (OCT) ± OCT-angiography. Shows a brightened artery wall where plaques sit, and OCT-A can show narrowed flow signal along the affected segment. EyeWiki

Non-pharmacological treatments

Important: Kyrieleis plaques are a sign. Non-drug steps support eye health and safety, but the cause (infection/autoimmunity) still needs proper medicines.

1. Urgent ophthalmology care and close follow-up — fast diagnosis and frequent checks limit complications.
   Purpose/Mechanism: Early recognition of infectious vs non-infectious disease guides safe therapy (e.g., antibiotics before steroids in toxoplasmosis). WebEye

2. Observation only (selected cases) — tiny, peripheral, non-threatening lesions may be watched while inflammation settles.
   Mechanism: Avoids overtreatment when risk to vision is low.

3. Activity modification — rest the eyes during acute inflammation (limit strenuous near work, bright screens).
   Mechanism: Reduces symptom triggers like glare/strain.

4. Photoprotection — sunglasses/filters.
   Mechanism: Decreases photophobia and light-induced discomfort.

5. Avoid contact lenses during active uveitis.
   Mechanism: Lowers irritation/infection risk.

6. Hygiene education for toxoplasma — wash hands, clean cutting boards, avoid cross-contamination.
   Mechanism: Reduces re-exposure to T. gondii oocysts in food prep. CDC

7. Food safety — thoroughly cook meat; wash fruits/veggies; avoid unpasteurized milk.
   Mechanism: Cuts parasitic and bacterial exposure (toxoplasma, others). CDC

8. Cat-litter precautions (if pregnant/immunocompromised) — gloves; change daily; someone else does it if possible.
   Mechanism: Avoids toxoplasma oocysts. CDC

9. Smoking cessation.
   Mechanism: Smoking worsens vascular and inflammatory eye disease risk.

10. Optimize systemic health — diabetes, hypertension, lipids.
    Mechanism: Healthier vessels, fewer complications.

11. HIV testing and antiretroviral adherence when appropriate.
    Mechanism: Restores immunity and lowers CMV retinitis risk. EyeWiki

12. Safe-sex practices and partner testing (syphilis prevention).
    Mechanism: Lowers ocular syphilis risk. CDC

13. TB control — screening/treatment in high-risk settings.
    Mechanism: Prevents ocular TB vasculitis. Karger

14. Shingles (VZV) vaccination where indicated.
    Mechanism: Reduces VZV reactivation and risk of ARN. (Discuss with physician.) EyeWiki

15. Imaging-guided monitoring — serial photos/FA/OCT to ensure no ischemia or macular edema.
    Mechanism: Early detection of complications. EyeWiki

16. Protective eyewear if work/hobby risks eye trauma.
    Mechanism: Avoids secondary inflammation/infection.

17. Stress and sleep optimization.
    Mechanism: Supports immune balance and recovery.

18. Nutritional support (balanced diet; see “What to eat”).
    Mechanism: General ocular and immune support.

19. Avoid starting steroids on your own.
    Mechanism: Steroids without antimicrobial cover can worsen infectious retinitis such as toxoplasmosis. PMChopkinsguides.com

20. Medication safety review (if on intravitreal brolucizumab, report new floaters/pain immediately).
    Mechanism: Early catch of drug-associated retinal vasculitis. AAO

---

Drug treatments

Strong caution: Doses below are typical references. Individual care varies. Never start/stop these on your own. Infectious causes must be covered before any steroid.

1. Trimethoprim-sulfamethoxazole (TMP-SMX) — antiparasitic alternative for ocular toxoplasmosis.
   Dose/Time: Commonly 160/800 mg twice daily for ~45 days; used in trials and cohorts with good healing; also used long-term (e.g., every other day) to prevent recurrences.
   Purpose/Mechanism: Blocks folate pathway in T. gondii.
   Key side effects: Rash, cytopenias, kidney effects; check interactions. PubMed+1

2. Pyrimethamine + sulfadiazine + leucovorin (folinic acid) — classic toxoplasmosis regimen.
   Dose: Pyrimethamine 25–50 mg/day (often after a loading dose) + sulfadiazine 2–4 g/day divided + leucovorin 10–25 mg/day to protect bone marrow; typically 4–6 weeks.
   Purpose/Mechanism: Dual folate-pathway block vs T. gondii; leucovorin prevents toxicity.
   Side effects: Bone-marrow suppression (monitor CBC), rash, GI upset. hopkinsguides.com

3. Clindamycin (systemic) — alternative/add-on for toxoplasmosis.
   Dose: Commonly 300 mg orally every 6 hours with other agents for 4–6 weeks.
   Purpose: Inhibits protein synthesis in T. gondii.
   Side effects: GI upset, C. difficile risk. EyeWiki

4. Azithromycin — alternative in selected toxoplasmosis cases.
   Dose: Often 500 mg/day with pyrimethamine or alone in some reports.
   Side effects: GI upset, QT prolongation. EyeWiki

5. Oral prednisone (systemic steroid) — only after antimicrobial cover if significant inflammation threatens vision.
   Dose: Common starting ~0.5–1 mg/kg/day, then taper; start 24–72 hours after anti-infective therapy begins; stop before antimicrobials end.
   Purpose/Mechanism: Dampens damaging inflammation; preserves macula/nerve.
   Side effects: Hyperglycemia, hypertension, infection risk; avoid as monotherapy in infection. PMCWebEye

6. Intravitreal clindamycin (± dexamethasone) — local therapy for toxoplasmosis when systemic therapy is risky or not tolerated.
   Dose: Clindamycin 1 mg + dexamethasone 400 μg, 1–3 injections as needed, shown non-inferior to classic systemic therapy in trials.
   Side effects: Procedure risks (infection, pressure spikes); needs specialist. PubMedAAO Journal

7. Acyclovir/valacyclovir — antivirals for ARN (HSV/VZV).
   Dose: Common protocols include IV acyclovir 10 mg/kg every 8 hours for 7–10 days, followed by high-dose oral valacyclovir; practice varies and may include intravitreal antivirals.
   Purpose: Stops viral DNA replication.
   Side effects: Kidney effects (hydrate, adjust dose). PMCEyeWiki

8. Valganciclovir — first-line oral therapy for CMV retinitis.
   Dose: 900 mg twice daily for 21 days (induction), then 900 mg once daily (maintenance).
   Side effects: Neutropenia, anemia; pregnancy precautions. EyeWikiDrugs.com

9. Aqueous crystalline penicillin G (IV) — ocular syphilis.
   Dose: 18–24 million units/day IV (3–4 million q4h or continuous) for 10–14 days; may add benzathine penicillin afterward depending on stage.
   Side effects: Allergy, electrolyte shifts; Jarisch–Herxheimer reaction. CDC

10. Standard anti-TB regimen (RIPE) — for ocular TB.
    Dose: Isoniazid + rifampin + pyrazinamide + ethambutol per TB guidelines, under specialist care.
    Purpose: Eradicate TB; reduce ocular vasculitis.
    Side effects: Drug-specific (liver, optic nerve, etc.); close monitoring required. Karger

---

Regenerative” medicines

These are immune-modulating agents used when the cause is autoimmune (e.g., Behçet) or when inflammation persists after infections are excluded/treated. They are not used to treat the plaques directly.

1. Adalimumab (anti-TNF-α)
   Dose: 80 mg loading, then 40 mg every 2 weeks (some go weekly if needed).
   Function/Mechanism: Blocks TNF-α to calm uveitis/vasculitis.
   Notes: FDA-approved for non-infectious posterior uveitis; screen for TB/HBV. New England Journal of Medicinehumira.com

2. Infliximab (anti-TNF-α, IV)
   Dose: ~5 mg/kg at weeks 0, 2, 6, then every 8 weeks.
   Mechanism: TNF-α neutralization; rapid control in Behçet flares.
   Notes: Infusion reactions; infection screening needed. PMC

3. Rituximab (anti-CD20)
   Dose: 1 g IV, two doses 2 weeks apart (uveitis protocols vary).
   Mechanism: Depletes B cells driving inflammation.
   Notes: Monitor for infusion reactions/infections. PMC

4. Tocilizumab (anti-IL-6 receptor)
   Dose: 162 mg SC weekly or 8 mg/kg IV monthly.
   Mechanism: Blocks IL-6–mediated inflammation; helpful in refractory uveitis or macular edema. PMC

5. Methotrexate (antimetabolite)
   Dose: 7.5–25 mg once weekly with folic acid.
   Mechanism: Broad immunomodulation to reduce relapse.
   Notes: Lab monitoring (CBC/LFTs); avoid in pregnancy. PMC

6. Cyclophosphamide (alkylator) — reserved for severe vasculitis (e.g., Behçet with vascular complications).
   Dose: Pulsed IV regimens individualized.
   Mechanism: Potent immunosuppression when vision is at high risk.
   Notes: Fertility, marrow, bladder toxicity risks; specialist only. PMC

(There are no approved “stem cell drugs” for Kyrieleis plaques or retinal vasculitis; stem-cell approaches remain experimental.)

---

Procedures/surgeries

1. Intravitreal antiviral or antibiotic injections (e.g., foscarnet for ARN; ganciclovir for CMV; clindamycin for toxoplasma).
   Why: Delivers high local drug levels when the macula is threatened. EyeWikiPubMed

2. Pars plana vitrectomy.
   Why: Clears dense vitreous opacity or hemorrhage, treats traction, and allows endolaser or drug delivery when needed.

3. Laser photocoagulation to ischemic retina (selected vasculitis).
   Why: Reduces risk of neovascularization/bleeding when blood flow is severely reduced. EyeWiki

4. Retinal detachment repair (scleral buckle or vitrectomy with tamponade).
   Why: In ARN or severe retinitis, retinal breaks/detachments can occur; urgent repair saves vision.

5. Intravitreal corticosteroid implant (e.g., dexamethasone) for non-infectious macular edema.
   Why: Controls inflammation-related edema once infection is excluded. PMC

---

Prevention tips

1. Cook meat well; wash produce (toxoplasma). CDC

2. Handle cat litter safely (or avoid it if pregnant/immunocompromised). CDC

3. Practice safer sex; test/treat partners (syphilis). CDC

4. HIV testing and ART adherence to prevent CMV retinitis. EyeWiki

5. Vaccinate for shingles when eligible (discuss with your clinician). EyeWiki

6. Screen for TB and treat latent infection if indicated. Karger

7. Don’t self-start steroids for red, painful eyes. See an eye doctor first. PMC

8. Control diabetes, blood pressure, and lipids to protect retinal vessels.

9. Quit smoking.

10. Seek care early for new floaters, flashes, or a dark curtain in vision.

---

When to see a doctor (and how fast)

• Same day / urgent: Sudden vision drop, new flashes/floaters, a dark curtain, severe pain, or if you’re immunocompromised (HIV, chemotherapy, transplant) and develop any new eye symptoms. This could be ARN or CMV retinitis, which need immediate antivirals. EyeWiki+1

• Prompt appointment (within days): Blurry vision, persistent redness, or photophobia without severe pain.

• If pregnant and exposed to undercooked meat/unclean litter plus visual symptoms — seek care promptly (toxoplasma risk). PMC

---

What to eat — and what to avoid

Helpful (for general eye/immune health; these don’t treat infections):

• Leafy greens & colored veggies (spinach, kale, peppers): lutein/zeaxanthin for retinal support.

• Fish rich in omega-3s (2–3 times/week) or as advised by your clinician.

• Lean proteins, whole grains, legumes, and adequate hydration to support healing.

• Vitamin-D–containing foods (or per clinician-guided supplementation if deficient).

Avoid/limit:

• Undercooked meat and unpasteurized milk/cheese (toxoplasma risk). CDC

• Excess alcohol, high-sugar ultra-processed foods, and smoking, all of which hinder recovery and vascular health.

---

 FAQs

1) Are Kyrieleis plaques dangerous by themselves?
Usually no. They’re a marker of inflammation. The danger comes from the underlying disease (like toxoplasma or ARN), which needs proper treatment. EyeWiki

2) How do doctors tell Kyrieleis plaques from cholesterol emboli?
Plaques line segments of arteries and don’t block flow or leak on FA, unlike emboli that cause blockages and ischemia. SpringerOpen

3) Can they occur without infection?
Yes, rarely in autoimmune uveitis (e.g., Behçet). PMC

4) Do they affect veins?
No — arteries only, which helps in diagnosis. EyeWiki

5) Will they go away?
Often fade over weeks to months after inflammation is controlled, though some can linger. EyeWiki

6) What imaging is most helpful?
FA (shows normal arterial filling, no leakage) and OCT (bright vessel wall). OCT-A can show reduced flow at plaques. PMCEyeWiki

7) Is steroid eye-drop use safe?
Only under an ophthalmologist’s guidance. In infectious retinitis, steroids without antimicrobials can worsen disease. PMC

8) What’s first-line treatment for ocular toxoplasmosis?
Many clinicians use TMP-SMX or pyrimethamine+sulfadiazine+leucovorin; approach varies, and steroids are added later if needed. PubMedhopkinsguides.com

9) How is CMV retinitis treated?
Valganciclovir (900 mg twice daily for 21 days, then 900 mg daily) or IV ganciclovir, with HIV care optimized. EyeWiki

10) How is ocular syphilis treated?
IV penicillin G 18–24 million units/day for 10–14 days. CDC

11) Are biologics like adalimumab used?
Yes, for non-infectious uveitis/retinal vasculitis, under specialist care. New England Journal of Medicine

12) Can anti-VEGF shots cause similar vasculitis?
Brolucizumab has been linked with retinal vasculitis; report any sudden symptoms after injections. AAO

13) Do Kyrieleis plaques always mean bad prognosis?
Not by themselves; they track with inflammation and often don’t worsen vision once the cause is treated. EyeWiki

14) Can they appear as the eye gets better?
Yes — they may become more visible as haze clears or even appear during recovery. PMC

15) What’s the fastest way to protect vision if I have these plaques?
See a uveitis/retina specialist quickly, follow the plan for the underlying cause, and keep close follow-up. 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 10, 2025.

PDF Document For This Disease Conditions References