Kyrieleis vasculitis (also called Kyrieleis arteriolitis, segmental retinal arteritis, or segmental retinal periarteritis) is a rare eye finding seen on a dilated fundus exam. The doctor sees tiny, yellow-white “beads” or plaques running along a retinal artery inside the eye. These plaques sit within the artery wall (not floating inside the blood and not leaking around the vessel). They usually appear near a patch of active inflammation in the back of the eye and tell us the eye is very inflamed at that moment. Most often, this happens with infections such as ocular toxoplasmosis, but it can appear with a few other diseases too. In fluorescein angiography (a dye test), these plaques do not leak, which helps tell them apart from other kinds of vessel inflammation. EyeWikiPMC
Segmental: shows up in pieces, not the whole artery.
Retinal arteritis/arteriolitis: inflammation of a retinal artery (an “arteriole” is just a small artery).
Periarteritis: inflammation in or around the artery wall.
Plaques: small yellow-white deposits that look beaded.
Endothelium: the inner lining of blood vessels; modern imaging suggests the plaques reflect inflammation of this lining. PubMed
Kyrieleis vasculitis is a clinical sign—not a disease by itself. It means the eye’s retinal arteries show segmental, bead-like, yellow-white deposits within the vessel wall, typically beside an active focus of retinochoroiditis (inflammation of the retina and choroid). It almost always appears during severe intra-ocular inflammation, most often infectious posterior uveitis (especially toxoplasmosis), but it has also been reported with viral necrotizing retinitis (e.g., HSV/VZV), CMV retinitis, tuberculosis, syphilis, and a few non-infectious conditions. On fluorescein angiography (FA), the affected arteries fill normally and do not leak, supporting that the problem is mainly at the endothelial layer rather than a full-thickness vessel wall leak. With appropriate treatment of the underlying cause, the plaques often fade or disappear, and visual prognosis depends on the underlying disease, not the plaques themselves. EyeWikiPMCPubMed
Types
There’s no single “official” classification, so clinicians sort Kyrieleis vasculitis in ways that help with diagnosis and follow-up.
By cause
Infectious: most common (e.g., toxoplasmosis; herpes viruses like HSV/VZV in acute retinal necrosis; CMV; tuberculosis; syphilis; rickettsial infection).
Non-infectious/immune-mediated: less common (e.g., Behçet disease, Susac syndrome).
Drug-associated: rare (reported with brolucizumab-associated retinal vasculitis). EyeWikiPMC
By extent
Focal (one short segment), multifocal (several segments), or diffuse (longer stretches of artery).
By location
Posterior pole (near the optic nerve and macula) vs peripheral retina.
By timing vs. the uveitis
During active inflammation (often near the “hot” retinitis) vs during resolution (sometimes plaques become easier to see as the haze clears). EyeWiki
By host status
Immunocompetent vs immunocompromised (e.g., CMV retinitis in advanced HIV).
Causes
Remember: Kyrieleis vasculitis is a sign. You look for the underlying cause and treat that.
A. Infections (most common)
Toxoplasma gondii (ocular toxoplasmosis) – the number-one association. A parasite inflames the retina; plaques appear on nearby arteries. EyeWikiPMC
Mycobacterium tuberculosis (ocular TB) – can inflame the back of the eye and its vessels. PMC
Treponema pallidum (ocular syphilis) – the “great imitator” that can cause many uveitis patterns, including Kyrieleis-type plaques. PMC
Rickettsia conorii (Mediterranean spotted fever) – a rickettsial infection linked with retinal vasculitis and Kyrieleis plaques. PMC
Varicella-zoster virus (VZV) – causes shingles; in the eye it can trigger acute retinal necrosis (ARN) with Kyrieleis plaques. Nature
Herpes simplex virus type 1 (HSV-1) – reported with necrotizing retinitis and Kyrieleis plaques. EyeWiki
Herpes simplex virus type 2 (HSV-2) – similarly linked in ARN. EyeWiki
Cytomegalovirus (CMV) – typically in immunocompromised patients (e.g., AIDS); plaques have been described. EyeWiki
Acute retinal necrosis (ARN) syndrome – the clinical syndrome (usually HSV/VZV) that often carries the plaques as a sign. PMC
Non-specific infectious posterior uveitis – clinicians sometimes see Kyrieleis-type plaques alongside severe infectious inflammation even when the exact germ is still being confirmed. EyeWiki
B. Non-infectious/immune
Behçet disease – a systemic inflammatory disease that can inflame retinal vessels and rarely show Kyrieleis plaques. EyeWiki
Susac syndrome – an autoimmune endotheliopathy (brain–retina–ear) where retinal arterial wall plaques can appear with branch retinal artery occlusions; these can resemble Kyrieleis-type changes. PubMed
Sarcoidosis – granulomatous inflammation can involve retinal vessels; Kyrieleis-type plaques have been reported in association. PMC
Idiopathic retinal vasculitis – rarely, no clear cause is found; the pattern still signals active intra-ocular inflammation. EyeWiki
C. Drug-associated
Brolucizumab-associated retinal vasculitis – a rare immune-mediated vasculitis after this anti-VEGF injection has been linked with Kyrieleis-like plaques. EyeWiki
D. Additional, less common infectious contexts reported in the literature
Ocular tuberculosis presenting as uveitis (distinct from item 2 when the uveitis is the main presentation). EyeWiki
Syphilitic retinitis (distinct clinical phenotype within syphilis). Nature
CMV retinitis in advanced HIV (explicitly in the immunocompromised setting). EyeWiki
Rickettsial vasculitis beyond the classic MSF presentation (broader rickettsioses spectrum noted in reviews). Longdom
Herpetic encephalitis with secondary ocular ARN (a clinical pathway reported in case literature). PMC
Symptoms
Symptoms come from both the inflamed retina and any nearby macular or optic-nerve involvement. Many cases are painless; some are not.
Blurred vision—the most common complaint.
New floaters—tiny moving specks or cobwebs from vitreous inflammation.
A patch of missing vision (scotoma)—a “hole” or shadow in part of the view.
Distorted lines (metamorphopsia)—straight lines look wavy.
Light sensitivity (photophobia)—bright light feels uncomfortable.
Reduced contrast—“faded” or washed-out look to scenes.
Trouble with night vision—harder to see in dim light.
Glare—oncoming headlights or sunlight scatter more.
Color desaturation—colors look dull.
Peripheral field loss—edges of vision feel “cut off.”
Transient flashing lights (photopsias)—from retinal irritation.
Eye redness—especially if there’s anterior uveitis too.
Mild ache or eye discomfort—not universal.
Headache—non-specific, sometimes from eye strain.
Symptoms of the underlying disease—e.g., fever or rash (in infections) or mouth/genital ulcers (in Behçet), hearing changes (in Susac).
(Symptoms are variable; the plaques themselves aren’t what you “feel”—they’re what the doctor sees. What matters clinically is finding and treating the cause.)
Diagnostic tests
Kyrieleis vs. frosted branch angiitis: Kyrieleis plaques are shiny, beaded, intramural deposits that affect arteries only and don’t leak on FA. Frosted branch angiitis causes fluffy, white sheathing of arteries and veins, with dye leakage. PMC
Kyrieleis vs. emboli/atheroma: Emboli usually sit at bifurcations and may cause filling defects; Kyrieleis plaques show normal arterial filling without blockage or non-perfusion on FA. EyeWiki
Total = 20 tests. Each test’s value is explained in plain English.
A) Physical examination
Vital signs and general exam
Fever, rash, weight loss, or other systemic clues can point toward infection or systemic inflammation (e.g., TB, syphilis, rickettsial illness, Behçet, sarcoid).Skin and mucosal exam
Rashes (rickettsial), mouth/genital ulcers (Behçet), or nodules (sarcoid) can steer the work-up toward a cause.Respiratory exam
Cough, lymph-node enlargement, or chest findings can hint at TB or sarcoidosis.Neurologic and ear exam
Headache, confusion, or hearing changes can raise suspicion for Susac syndrome (brain–retina–ear triad). PubMed
B) Manual/bedside eye tests
Best-corrected visual acuity
Baseline and follow-up measure of how well you see, which tracks disease activity.Amsler grid
A simple square grid to detect distortion or missing spots from macular or nearby retinal inflammation.Confrontation visual fields
Quick bedside check for field defects from retinal lesions.Ishihara color plates
Screens color vision changes that sometimes accompany macular/optic involvement.Swinging-flashlight (pupillary) test
Looks for a relative afferent pupillary defect (RAPD) if there’s significant unilateral retinal or optic-nerve dysfunction.
C) Lab and pathological tests
Toxoplasma serology (IgG/IgM)
Positive IgG supports prior exposure; with the classic clinical picture, it helps confirm ocular toxoplasmosis, the leading association. PMCSyphilis testing
Non-treponemal (RPR/VDRL) plus treponemal (FTA-ABS/TPPA) to identify ocular syphilis. (Syphilis is a major cause of posterior uveitis.) NCBITuberculosis testing
IGRA blood test or tuberculin skin test, plus chest imaging if needed, to detect ocular TB. EyeWikiViral testing (HSV-1/2, VZV, CMV)
Aqueous or vitreous PCR (when available) can detect viral DNA in necrotizing retinitis or CMV retinitis. EyeWikiAutoimmune markers
Depending on the story: HLA-B51 (Behçet context), ANA/ANCA (vasculitis screen), and ACE/lysozyme (sarcoid). These do not diagnose Kyrieleis, but they support a systemic cause. EyeWikiHIV test (with consent)
Important when CMV retinitis or unusual infections are suspected; guides both diagnosis and safety. (CMV plaques have been reported.) EyeWiki
D) Electrodiagnostic
Full-field electroretinogram (ERG)
Measures retina’s electrical function; not specific for Kyrieleis, but helps document how much the retina is affected in widespread disease.Visual evoked potential (VEP)
Checks the optic pathway from eye to brain; useful if vision is poor and the exam is hazy, to separate retinal from optic-nerve issues.
E) Imaging tests
Fundus photography (color and widefield)
Records the appearance and distribution of plaques and the nearby retinitis for comparison over time.Fluorescein angiography (FA)
The key test: arteries with Kyrieleis plaques fill normally and show no leakage. This finding separates Kyrieleis from “sheathing” vasculitis and emboli. EyeWikiPMCAdvanced multimodal imaging (FAF, ICG, OCT, OCT-A)
FAF: plaques often show hyper-autofluorescence.
ICG: can highlight plaques clearly, sometimes better than FA.
SD-OCT: shows hyper-reflective artery wall where plaques sit.
OCT-A: may show narrowing of flow signal over plaques.
These support the idea that the endothelium (inner lining) is the main site of inflammation. PubMed
Non-pharmacological (non-drug) treatments
These options do not cure an infection, but they protect vision, reduce strain, and support recovery while the underlying cause is treated (usually with medicines). Each item includes what it is, purpose, and simple mechanism.
Observation with tight follow-up (selected cases).
Purpose: If a lesion is small and far from the macula/optic nerve, a specialist may watch closely.
Mechanism: Some plaques fade as inflammation resolves; careful monitoring avoids overtreatment and catches worsening early. EyeWikiProtective light management (sunglasses/hat).
Purpose: Reduce photophobia and glare while the eye is inflamed.
Mechanism: Lowers retinal light stress and patient discomfort during healing.Activity pacing and eye-strain breaks.
Purpose: Cut down on near-work strain during acute episodes.
Mechanism: Less accommodative effort and fewer inflammatory flares from fatigue.Optimize systemic health (blood sugar, blood pressure, lipids).
Purpose: Better vascular health supports retinal recovery.
Mechanism: Stable microcirculation and less endothelial stress.Smoking cessation.
Purpose: Improve ocular perfusion and healing.
Mechanism: Reduces vasoconstriction/oxidative stress harmful to retinal vessels.Infection-source control and hygiene (food, cats, soil).
Purpose: Lessen Toxoplasma exposure (undercooked meat, unwashed produce, cat litter), and reduce re-exposure risk.
Mechanism: Cuts parasitic load and prevents new infections. (General toxoplasma prevention.)Vaccination where appropriate (e.g., shingles vaccine).
Purpose: Reduce VZV reactivation risk that can cause acute retinal necrosis.
Mechanism: Recombinant zoster vaccine (RZV) boosts VZV-specific immunity in eligible adults. CDCManage immunosuppression thoughtfully.
Purpose: In transplant/HIV or autoimmune patients, balance needed immunosuppression with infection risk.
Mechanism: ID/uveitis teams tailor antirejection/biologic dosing and may use CMV prophylaxis if indicated. PMCAdherence coaching and written action plans.
Purpose: Complex regimens are hard; simple schedules reduce missed doses.
Mechanism: Improves time-on-therapy and outcomes.Home symptom diary (floaters, blur, new dark curtain).
Purpose: Catch recurrence/retinal detachment early.
Mechanism: Patients report changes promptly for urgent care.Nutritional support (adequate protein, micronutrients).
Purpose: Healing needs building blocks.
Mechanism: Supports immune and tissue repair (see diet section).Sleep optimization and stress reduction.
Purpose: Aid immune regulation.
Mechanism: Better cytokine balance and resilience.Eye protection after injections/procedures.
Purpose: Lower infection risk.
Mechanism: Hygiene and shields reduce inoculation or rubbing.Treat dry eye if present (lubricants, lid hygiene).
Purpose: Comfort and visual stability during recovery.
Mechanism: Smooths tear film to reduce fluctuating vision.Glucose control in diabetes.
Purpose: Improve retinal microvascular stability.
Mechanism: Less endothelial dysfunction and edema.Blood pressure control.
Purpose: Protect fragile retinal vessels.
Mechanism: Reduces stress on inflamed arteries.Educate on “no steroid alone” for infections.
Purpose: Avoid worsening infection.
Mechanism: Steroids must be paired with the correct antimicrobial when infection is suspected (important in ocular toxoplasmosis/ARN). Hopkins GuidesHousehold/partner screening when indicated (e.g., syphilis).
Purpose: Prevent reinfection and catch silent disease.
Mechanism: Public health/partner treatment. CDCFall-risk/low-vision aids during flares.
Purpose: Safety when acuity is temporarily reduced.
Mechanism: Lighting, contrast tools, and magnifiers.Prophylaxis in select cases (toxoplasmosis recurrence).
Purpose: Prevent future flares that can create new plaques.
Mechanism: Intermittent TMP-SMX reduces recurrent ocular toxoplasmosis. PubMed+1
Drug treatments
Important: The right drug depends on the cause. Doctors treat the uveitis driving the plaques; the plaques themselves fade as inflammation resolves.
Pyrimethamine + sulfadiazine + leucovorin (classic “triple therapy” for ocular toxoplasmosis).
Class: Antifolate + sulfonamide + folinic acid rescue.
Dose/time: Common adult approach: pyrimethamine oral loading then ~25–50 mg/day, sulfadiazine 1–1.5 g every 6 h, leucovorin 10–25 mg several times weekly; steroid added 24–48 h after antiparasitic start; 4–6 weeks typical. (Exact regimen individualized.)
Purpose: Clear Toxoplasma tachyzoites and protect bone marrow.
Mechanism: Dual blockade of folate pathway in the parasite; leucovorin protects human marrow.
Key AEs: Cytopenias, rash, GI upset; sulfa allergy; monitor CBC. ASM JournalsHopkins GuidesAAO JournalTrimethoprim–sulfamethoxazole (TMP-SMX) for ocular toxoplasmosis (treatment and recurrence prevention).
Class: Antifolate combo.
Dose/time: Frequently 160/800 mg (DS) twice daily ~45 days for active disease; intermittent dosing used for recurrence prophylaxis.
Purpose: Alternative to classic triple therapy; cost-effective and accessible.
Mechanism: Folate pathway inhibition in parasite.
Key AEs: Rash, cytopenias, hyperkalemia; avoid in severe sulfa allergy. PubMedPMCIntravitreal clindamycin + dexamethasone (IVCD) for toxoplasmosis.
Class: Local antibiotic + steroid.
Dose/time: Given as periodic intravitreal injections; often 1–4 injections over several weeks.
Purpose: Comparable efficacy to systemic therapy in trials; useful when systemic therapy is risky or not tolerated.
Mechanism: High intraocular clindamycin concentration against T. gondii; steroid to calm inflammation.
Key AEs: Procedure risks (endophthalmitis, pressure spikes). PubMedAAO JournalValganciclovir for CMV retinitis.
Class: Antiviral (guanosine analog, oral prodrug of ganciclovir).
Dose/time: 900 mg orally twice daily for 21 days (induction), then 900 mg once daily (maintenance); adjust for kidneys.
Purpose: Treat CMV driving retinitis/plaque associations.
Mechanism: Inhibits viral DNA polymerase.
Key AEs: Neutropenia, anemia, renal toxicity, GI upset. FDA Access DataIntravitreal ganciclovir (adjunct for CMV).
Class: Antiviral, local injection.
Dose/time: Induction ~2 mg twice weekly ×3 weeks, then weekly maintenance (protocols vary).
Purpose: Rapid local viral suppression, especially for sight-threatening lesions.
Mechanism: High intraocular concentrations block CMV replication.
Key AEs: Injection risks; retinal tears rare. AAOValacyclovir (for HSV/VZV acute retinal necrosis).
Class: Antiviral (prodrug of acyclovir).
Dose/time: Often 1–2 g orally three times daily after/with IV acyclovir; duration weeks, tailored; intravitreal foscarnet/ganciclovir may be added.
Purpose: Halt necrosis, protect the fellow eye.
Mechanism: Inhibits viral DNA polymerase in HSV/VZV.
Key AEs: GI upset, kidney issues (acyclovir IV), neurotoxicity if renal failure. PMCsurveyophthalmol.comAqueous crystalline penicillin G (for ocular syphilis).
Class: Beta-lactam antibiotic.
Dose/time: 3–4 million units IV every 4 hours (or continuous infusion 18–24 MU/day) for 10–14 days.
Purpose: Eradicate Treponema pallidum in ocular/neuro syphilis.
Mechanism: Cell-wall inhibition.
Key AEs: Jarisch–Herxheimer reaction, allergy. (Ceftriaxone is an alternative when appropriate.) AAOCDCDoxycycline (for rickettsial causes).
Class: Tetracycline antibiotic.
Dose/time: 100 mg orally twice daily, typically 7–14 days (tailor to disease).
Purpose: Treat rickettsial retinal vasculitis associations.
Mechanism: Inhibits bacterial protein synthesis.
Key AEs: Photosensitivity, esophagitis; avoid in pregnancy/young children.Anti-TB regimen (for ocular TB).
Class: Multi-drug (e.g., isoniazid, rifampin, pyrazinamide, ethambutol) per national guidelines.
Dose/time: Standard RIPE phases, directed by infectious disease/ophthalmology.
Purpose: Eradicate M. tuberculosis driving posterior uveitis/vasculitis.
Mechanism: Multiple targets in mycobacterial metabolism.
Key AEs: Hepatotoxicity, optic neuropathy (ethambutol—monitor color vision).Albendazole (for ocular toxocariasis—selected cases).
Class: Anti-helminthic.
Dose/time: Often 400 mg twice daily for 1–2 weeks (regimens vary) plus oral steroids to control inflammation.
Purpose: Kill Toxocara larvae in ocular involvement.
Mechanism: Inhibits parasite microtubules.
Key AEs: GI upset, liver enzyme elevation (monitor). CDCPMC
Important steroid note: In infectious uveitis, steroids are adjuncts only—they are added after appropriate antimicrobial coverage has started. Using steroids alone can worsen infection. Hopkins Guides
Dietary molecular & supportive supplements
These do not treat infection, but they can support overall ocular/immune health while you’re on the correct medicines. Always clear supplements with your clinician to avoid interactions (e.g., with methotrexate, cyclosporine, warfarin).
Omega-3 (EPA/DHA) 1–2 g/day.
Function: Anti-inflammatory milieu.
Mechanism: Competes with arachidonic acid; pro-resolving mediators.Lutein + zeaxanthin (10–20 mg/2–4 mg daily).
Function: Macular pigment support.
Mechanism: Antioxidants in photoreceptors.Vitamin C (500–1000 mg/day).
Function: Antioxidant/cofactor for collagen repair.
Mechanism: Free-radical scavenging in inflamed tissues.Vitamin E (≤400 IU/day).
Function: Lipid antioxidant.
Mechanism: Protects cell membranes.Zinc (10–25 mg elemental/day) with copper (1–2 mg/day).
Function: Enzyme and immune support.
Mechanism: Cofactor in immune/retinal enzymes.Vitamin D (target serum 25-OH-D ~30–50 ng/mL; dose per labs).
Function: Immune modulation.
Mechanism: T-cell regulation.B-complex with folate (dietary).
Function: Marrow support during long courses; note leucovorin is the medical “rescue” if on pyrimethamine.
Mechanism: DNA synthesis support (do not replace prescribed leucovorin).Protein 1.0–1.2 g/kg/day (food first).
Function: Tissue repair.
Mechanism: Provides amino acids for healing.Carotenoids (beta-carotene from foods).
Function: Retinal support.
Mechanism: Antioxidant vitamin A precursor (avoid high-dose pills in smokers).Selenium (55–100 mcg/day).
Function: Antioxidant enzymes (GPx).
Mechanism: Redox balance.CoQ10 (100–200 mg/day).
Function: Mitochondrial support.
Mechanism: Electron transport cofactor.Curcumin (meriva/BCM-95 forms, ~500–1000 mg/day).
Function: Adjunct anti-inflammatory.
Mechanism: NF-κB modulation (watch anticoagulants).Probiotics (per label, multi-strain).
Function: Gut-immune axis.
Mechanism: Barrier and cytokine tuning.Magnesium (200–400 mg/day).
Function: Vascular tone, sleep.
Mechanism: Cofactor in >300 enzymes.Hydration target (urine pale straw).
Function: Kidney safety on antivirals/antibiotics; comfort.
Mechanism: Maintains renal perfusion (important with acyclovir/valacyclovir).
Regenerative” medicines
These are for non-infectious uveitis or after infection is excluded. Use under uveitis specialist care.
Adalimumab (anti-TNF-α).
Use: Steroid-sparing in non-infectious intermediate/posterior/panuveitis; FDA-approved.
Dose: 80 mg loading, then 40 mg every 2 weeks.
Mechanism: Blocks TNF-α inflammatory signaling.
Key risks: Serious infections, TB reactivation; lab and TB screening required. New England Journal of MedicineFDA Access DataInfliximab (anti-TNF-α, IV).
Use: Behçet-type severe uveitis unresponsive to others.
Dose: Weight-based IV infusions (e.g., 3–5 mg/kg at weeks 0, 2, 6, then q6–8 w).
Mechanism: TNF-α blockade.
Risks: Infusion reactions, infections. PMCMethotrexate (antimetabolite).
Use: Steroid-sparing in non-infectious uveitis.
Dose: Weekly oral/subcutaneous (e.g., 7.5–25 mg/week) + folic acid.
Mechanism: Dampens lymphocyte proliferation.
Risks: Hepatotoxicity, cytopenias (labs required).Mycophenolate mofetil.
Use: Common steroid-sparing alternative.
Dose: Typically 1–1.5 g twice daily.
Mechanism: Inhibits lymphocyte purine synthesis.
Risks: GI upset, leukopenia, teratogenic.Azathioprine.
Use: Another antimetabolite option.
Dose: ~1–2 mg/kg/day.
Mechanism: Purine analog → fewer active lymphocytes.
Risks: Cytopenias, hepatotoxicity; TPMT status matters.Cyclosporine (calcineurin inhibitor).
Use: T-cell-targeted steroid-sparing.
Dose: 2–5 mg/kg/day in divided doses.
Mechanism: Blocks IL-2 signaling.
Risks: Kidney toxicity, hypertension.
About “stem-cell drugs”: There are no approved intravitreal stem-cell treatments for Kyrieleis plaques or uveitis, and unapproved injections have blinded patients. If you see clinics offering this, be extremely cautious. AAOPew Charitable Trusts
Surgeries/procedures
Prophylactic laser barricade (selected ARN cases).
Why: Create a “wall” to reduce retinal detachment risk around necrotic zones (evidence mixed; discussed with patient).
Procedure: Argon laser rows encircling lesions. PubMedNaturePars plana vitrectomy (PPV) for retinal detachment from ARN or non-clearing vitreous).
Why: Reattach retina, clear vitreous, deliver antivirals.
Procedure: Remove vitreous, repair breaks, often silicone oil tamponade. Ophthalmology RetinaBioMed CentralIntravitreal antiviral/antibiotic injections (office procedure).
Why: Rapid, high local drug levels for CMV/ARN or toxoplasmosis (clindamycin).
Procedure: Small-needle injection under aseptic technique. PMCAAO JournalCataract surgery (after quiet eye).
Why: Steroid-related or inflammation-related cataract preventing vision.
Procedure: Phacoemulsification with careful peri-op inflammation control.Glaucoma surgery (trabeculectomy/valve) if steroid-induced or inflammatory glaucoma persists.
Why: Protect optic nerve when drops fail.
Procedure: Create new outflow pathway; close follow-up needed.
Prevention tips
Cook meat well; wash fruits/veggies; handle cat litter with gloves (toxoplasma).
Shingles (RZV) vaccination if eligible to cut VZV risk. CDC
Condom use/partner testing (syphilis). CDC
CMV prevention/prophylaxis when immunosuppressed per ID guidance. PMC
Control diabetes and blood pressure.
Don’t stop/adjust immunosuppressants on your own.
Avoid steroid eye drops without a diagnosis (can worsen infections). Hopkins Guides
Report new floaters, flashes, or a dark curtain immediately (possible detachment).
Follow prophylaxis plans (e.g., intermittent TMP-SMX to prevent toxoplasma recurrences when prescribed). PubMed
Keep vaccination and screening up to date (TB, syphilis, HIV when indicated).
When to see a doctor
Urgent (same day): sudden blur, new floaters, flashes, a gray/black curtain, eye pain, or rapid drop in vision—especially if you’re known or suspected to have ARN or CMV.
Soon (days): persistent light sensitivity, mild blur, eye redness, or if you see new “string-of-pearls” vessels on photos from a previous visit.
Always: if you’re on pyrimethamine, valganciclovir, or other marrow-suppressing drugs and develop fever, mouth sores, unusual bruising—you need blood tests.
What to eat and what to avoid
What to eat:
Protein-rich foods (fish, eggs, legumes, lean meats) to help tissues repair.
Colorful produce (leafy greens for lutein/zeaxanthin; berries/citrus for vitamin C).
Healthy fats (olive oil, nuts, seeds; fatty fish for omega-3s).
Whole grains for steady glucose (retinal microvasculature likes stability).
Plenty of water—especially if on antivirals (helps kidneys).
What to avoid (or limit):
Undercooked meat, unwashed produce, unpasteurized dairy (toxoplasma risk).
Alcohol when on methotrexate/azathioprine (liver risk) or metronidazole (disulfiram-like reactions).
Grapefruit if you take cyclosporine (raises drug levels).
Mega-dose vitamin A supplements (smokers at higher risk; food sources are fine).
Random supplements without checking interactions.
Frequently asked questions
Are Kyrieleis plaques dangerous by themselves?
Usually no—they’re a sign of nearby severe inflammation; vision risk comes from the underlying disease (e.g., toxoplasmosis, ARN). Plaques often fade with treatment. EyeWikiDo they block blood flow or cause a stroke in the eye?
Typically no—dye tests show normal flow without leakage, suggesting limited endothelial involvement. EyeWikiWhat’s the most common cause?
Ocular toxoplasmosis. EyeWikiCan viruses cause them?
Yes—CMV and HSV/VZV (acute retinal necrosis) may be associated. NatureHow are they different from “frosted branch” angiitis?
Kyrieleis plaques don’t leak dye and stay within arteries; frosted branch leaks and often involves veins and surrounding tissue. PMCWill I need injections in my eye?
Sometimes—intravitreal clindamycin (toxoplasma) or intravitreal antivirals (ARN/CMV) can save sight quickly. AAO JournalPMCDo steroids help?
As adjuncts (after antimicrobials start), they lower damaging inflammation. Never use steroid alone in infectious uveitis. Hopkins GuidesCan they come back?
Yes, if the underlying disease recurs (e.g., recurrent toxoplasmosis). TMP-SMX prophylaxis can reduce recurrences in selected patients. PubMedWhat if tests are all negative?
Doctors may treat empirically based on the retinal pattern and response, and evaluate for non-infectious uveitis causes.Is surgery ever needed?
Not for plaques themselves—but retinal detachment from ARN may need vitrectomy/laser. Ophthalmology RetinaDo these plaques mean permanent damage?
Not necessarily; many resolve without a trace once inflammation is controlled. EyeWikiCan both eyes be involved?
Yes, depending on the cause (e.g., ARN can spread to the fellow eye). PMCHow long does treatment last?
Varies—weeks for toxoplasma; weeks to months for viral retinitis; 10–14 days IV penicillin for ocular syphilis; months for TB. AAOFDA Access DataAre stem-cell injections an option?
No—unapproved stem-cell eye injections have blinded patients. Avoid them outside regulated trials. AAOWhat specialists should I see?
A retina/uveitis specialist and, depending on cause, infectious disease and rheumatology.
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.
