Post-streptococcal uveitis is an eye inflammation that shows up after a recent streptococcal infection, most often after a sore throat, tonsillitis, or a skin infection caused by Streptococcus bacteria. “Uveitis” means the uvea is inflamed; the uvea is the middle layer of the eye that includes the iris at the front, the ciliary body in the middle, and the choroid at the back. In this condition, the infection is usually not inside the eye. Instead, your immune system reacts to the earlier strep infection and mistakenly targets parts of your eye, so the eye becomes inflamed and painful. This reaction typically begins days to a few weeks after the throat or skin illness gets better. Most people who get it are children, teens, or young adults, but adults can be affected, too. Most cases improve with standard anti-inflammatory eye drops, and vision outcomes are usually good when treated early. EyeWikiAAO Journal
Why it happens
Your immune system is trained to spot germs and protect you. After a strep infection, your immune system makes antibodies and immune cells that recognize strep proteins. Some of those strep proteins look a little like the body’s own proteins. Because of this “look-alike” problem (often called molecular mimicry), the immune system can confuse certain eye tissues for the germ and attack them by mistake. That attack leads to inflammation inside the eye, which causes pain, light sensitivity, redness, and blurred vision. Doctors group this type of problem under “post-streptococcal syndromes,” which are non-suppurative (meaning the eye is inflamed but not filled with pus from active bacteria), and they happen after the infection rather than during it. JAMA Network
Most patients report that a week or a few weeks earlier they had a sore throat, fever, or a skin infection like impetigo. Then they develop painful, red eyes with bright-light sensitivity and blurred vision. In many people the inflammation is at the front of the eye (anterior uveitis), but it can also involve the back of the eye (posterior uveitis) or the whole eye (panuveitis). Some patients have floaters if the gel in the eye (vitreous) becomes inflamed, and a few can develop inflammation of the retinal blood vessels (retinal vasculitis). Doctors confirm the uveitis at the slit lamp and look for signs of a recent strep infection with throat testing or blood tests that measure anti-streptococcal antibodies. EyeWikiPubMedPMC
Types
Below are common “types” or patterns. Think of these as simple labels doctors use to describe which parts of the eye are inflamed, how the inflammation behaves, and who tends to get it.
1) By location inside the eye
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Anterior uveitis (iritis/iridocyclitis): Inflammation mainly in the front of the eye (iris and ciliary body). This is the most common pattern in post-streptococcal cases. People feel pain, light sensitivity, and see redness around the colored part of the eye. EyeWikiAAO Journal
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Intermediate uveitis: Inflammation mainly in the middle area (the vitreous and the ciliary body region). People may notice lots of floaters and blurred vision.
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Posterior uveitis: Inflammation at the back, involving the retina or choroid. This is less common, but when present it can cause more serious vision problems like reduced central vision or blind spots. Retinal blood vessel inflammation (vasculitis) can appear in this type. PMC
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Panuveitis: Inflammation in all sections (front, middle, and back). Symptoms are a mix of the above and can be more intense.
2) By timing
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Acute: A single short-lasting episode that starts suddenly and settles with treatment.
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Recurrent: More than one episode separated by symptom-free periods. Some patients have repeat throat infections followed by repeat uveitis, which is why clinicians also pay attention to preventing new strep infections. ScienceDirect
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Chronic: Inflammation that lingers for months despite treatment. This is not common in post-streptococcal uveitis but can occur.
3) By appearance
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Nongranulomatous uveitis: The most common look in post-streptococcal cases—small, fine inflammatory deposits on the back of the cornea and brisk inflammation.
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Granulomatous uveitis: Larger “greasy” deposits and nodules; this is less typical for post-streptococcal disease but may appear in some patients.
4) By laterality (which eyes)
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Bilateral: Both eyes are inflamed, often at the same time or close together in time. This is very common in post-streptococcal uveitis.
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Unilateral: One eye is inflamed. This can happen but is less typical. BMJ Open
5) By age group
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Pediatric/young people: Most patients are children, teens, or young adults, because strep throat and school-based spread are common in these ages.
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Adult: Less common, but adults can develop it, especially if they have repeated strep infections or are in close contact with children who have them. AAO Journal
Causes
In post-streptococcal uveitis, the root cause is the immune reaction that follows a recent streptococcal infection. The list below breaks that single cause into common triggers and risk-shaping factors that make the immune misfire more likely.
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Recent strep throat (pharyngitis): A sore throat with fever that was caused by Streptococcus pyogenes (Group A strep) often comes 1–3 weeks before the eye inflammation. The eye problem shows up after the throat gets better. EyeWiki
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Recent tonsillitis: Inflamed tonsils due to strep can be the infection that triggers the later eye reaction. Repeated tonsillitis tends to raise the risk of repeat episodes. ScienceDirect
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Strep skin infections (impetigo): A crusty or oozing skin rash caused by strep—especially in children—can be the infection that sets off the immune reaction that later hits the eye.
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Erysipelas or cellulitis from strep: A red, hot, tender skin infection can be the trigger that the immune system “remembers,” leading to uveitis weeks later.
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Scarlet fever: A strep-related illness with fever and a sandpaper-like rash; it signals a strong strep exposure and can precede eye inflammation.
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Sinusitis caused by strep: A recent sinus infection can be the exposure that triggers the later immune-based eye problem.
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Otitis media caused by strep: Middle-ear infection from strep in children may precede the eye event.
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Perianal streptococcal dermatitis: This strep skin infection in children is another, sometimes overlooked, trigger for the post-infectious immune reaction.
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Group C or Group G streptococcal infection: Though Group A is classic, non-Group A streptococci have been linked to post-streptococcal uveitis in case reports. Taylor & Francis Online
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Incomplete or delayed antibiotic treatment: When strep infections are not treated early or completely, the immune system is stimulated longer and more strongly, which may raise the chance of a post-infectious reaction.
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Recurrent strep infections: Repeat infections stack the deck by repeatedly priming the immune system; more priming can mean higher risk later. ScienceDirect
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Close contact exposure (school or household): Living or learning in crowded spaces makes strep spread more likely, so the initial trigger is more likely.
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Tonsillar crypt colonization or carrier state: Some people carry strep in their throats without strong symptoms; this can keep the immune system simmering and occasionally triggers post-infectious problems.
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Younger age: Children and teens get strep more often, so their risk of post-streptococcal eye inflammation is higher mainly because the trigger is more common in them. AAO Journal
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A family outbreak of strep: If many people at home have strep, your chance of exposure and strong immune priming increases.
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Skin barrier problems (eczema or scratches): Broken skin lets bacteria in and raises the chance of skin strep infections that can later trigger the eye reaction.
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Constitutional “over-vigorous” immune response: Some people simply make high antibody levels to strep (very high ASO or anti-DNase B), and this strong response may spill over and affect the eye. PubMed
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Post-streptococcal reactive arthritis (PSRA): A related post-strep immune problem of joints can occur alongside uveitis in some patients, showing the whole body is reacting after the infection. PubMed
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Post-streptococcal glomerulonephritis (PSGN) in the patient’s history: This kidney reaction tells us the immune system strongly reacted to strep; some of these patients can also develop eye inflammation. Lippincott Journals
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Genetic susceptibility (general idea): While no single gene explains it, families differ in how they respond to strep. Some people may be more prone to post-infectious autoimmune-type reactions, including uveitis.
Symptoms
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Eye pain: A deep, aching pain around or inside the eye that often worsens with light or focusing.
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Redness: The white of the eye looks red, especially around the colored part of the eye (the limbus).
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Light sensitivity (photophobia): Bright light hurts, so people squint or wear sunglasses indoors.
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Blurred vision: The view is foggy or smeared, and small print is harder to read.
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Tearing: The eye waters more because of irritation and inflammation.
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A feeling of grit or irritation: It can feel like sand in the eye because the front of the eye is inflamed.
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Headache or brow ache: The nerves around the eye carry the pain upward into the forehead or temples.
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Floaters: Small spots or threads drifting across the vision, especially if the middle gel of the eye (vitreous) is inflamed.
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Decreased contrast or color dullness: Colors can look less bright when the back of the eye is involved.
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Glare and halos: Lights can seem to glare or show halos, especially at night.
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Mild discharge: A small amount of watery or mucus discharge can occur because the eye surface is irritated.
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Eyelid swelling: The lids can look puffy because of nearby inflammation.
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Reduced sharpness (acuity): Vision chart scores can drop during flares and usually improve with treatment.
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Systemic clue: recent sore throat or skin infection: People often remember a throat illness, fever, or a skin rash a week or a few weeks earlier. EyeWiki
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Joint aches or malaise: Some feel achy or tired, reflecting the body-wide immune reaction that can accompany the eye problem. PubMed
Diagnostic tests
Doctors use eye-exam tools to confirm uveitis and lab tests to prove the recent strep exposure or to rule out other causes. Below are 20 tests grouped by type. You will not need all of them. Your eye doctor chooses based on your history and what they see in your eyes.
A) Physical exam tests (done right in the clinic without complex machines)
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Visual acuity test: Reading the eye chart tells how much the inflammation is affecting sharpness. A drop in letters supports that the eye is irritated or the view is hazy.
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External eye inspection: The doctor looks at lid swelling, the pattern of redness, and any light sensitivity when shining a light; the ring of redness around the cornea suggests front-of-eye inflammation.
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Pupil and swinging-flashlight test: Checking how the pupils react to light can uncover a relative afferent pupillary defect if the back of the eye is affected.
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Confrontation visual fields: Simple finger-counting tests check for any missing areas in the side vision that could hint at inflammation near the retina or optic nerve.
B) Manual / bedside ophthalmic tests (hands-on instruments at the slit lamp)
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Slit-lamp biomicroscopy: A bright microscope examines the front of the eye for cells and flare in the anterior chamber, tiny deposits on the cornea, and inflammation at the iris. This is how anterior uveitis is confirmed. EyeWiki
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Intraocular pressure (tonometry): Eye pressure can go up (from steroid response or blocked drainage) or down (from inflamed ciliary body). Measuring pressure guides safe treatment.
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Dilated fundus examination (indirect ophthalmoscopy): Drops widen the pupil so the doctor can look at the vitreous, retina, optic nerve, and blood vessels. This can show vitritis (inflammatory cells in the gel), retinal vasculitis, or macular edema in posterior disease. PMC
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Phenylephrine blanching test (for differential): If the eye is very red and sore, a drop of phenylephrine can help tell episcleritis (blanches) from scleritis (does not blanch). This is useful because these conditions can mimic uveitis-related redness.
C) Laboratory and pathological tests (to prove recent strep and rule out mimics)
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Throat culture or rapid strep test: If you still have a sore throat, these tests can show an active Group A strep infection. A positive result supports a link to the eye inflammation. EyeWiki
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Antistreptolysin-O (ASO) titer: A blood test that rises after strep infections; a high or rising level over time supports recent exposure even if the throat is now normal. PubMed
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Anti-DNase B titer: Another anti-strep antibody that tends to rise after skin infections or throat infections; together with ASO it strengthens the case that a strep infection happened recently. American Academy of Ophthalmology
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C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR): General inflammation blood tests; they often rise during immune-system flares and help track severity.
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Complete blood count (CBC) with differential: Looks for white-cell changes or anemia; helps exclude other infections or inflammatory diseases that can also cause uveitis.
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Urinalysis: Checks for blood or protein in the urine that might point to post-streptococcal kidney involvement (PSGN), which sometimes accompanies the immune reaction.
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Complement C3 level: C3 can drop in post-streptococcal kidney disease; when low, it supports a recent systemic immune response to strep.
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Autoimmune screen (e.g., ANA) and targeted infectious tests (e.g., syphilis serology, TB screening) when needed: These do not diagnose PSU directly, but they rule out other causes of uveitis so the doctor can be more confident about the post-streptococcal diagnosis.
D) Electrodiagnostic tests (used in selected cases with back-of-eye involvement)
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Electroretinography (ERG): Measures how the retina’s light-sensing cells are working; it is rarely needed but can show dysfunction if posterior inflammation has been severe.
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Visual evoked potentials (VEP): Measures the brain’s electrical response to visual signals; used when optic nerve involvement is suspected.
E) Imaging tests (to map inflammation and fluid)
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Optical coherence tomography (OCT): A painless scan that shows cross-section pictures of the retina and macula; it can reveal macular edema or subtle structural changes that explain blurred vision.
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Fluorescein angiography (FA): A dye test with photos that shows retinal blood vessels leaking or inflamed; very helpful for retinal vasculitis or macular edema in posterior disease. B-scan ultrasound may be added if the view is cloudy to check for retinal detachment or dense vitritis. PMC
Non-pharmacological treatments (therapies & “other” supports)
Each item explains what it is, why it helps, and how it works in simple terms.
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Clear diagnosis and education
Understanding PSU reduces worry and improves adherence. Your doctor confirms the link to a recent strep infection, rules out other causes, and explains warning signs. Education improves medication use and early reporting of flares, which lowers complication risk. -
Strict follow-up schedule
Regular eye checks (often weekly at first) allow timely steroid tapering and pressure checks. This prevents steroid-related pressure spikes and cataract progression because dosing is adjusted to the smallest effective amount. -
Sunglasses and indoor light control
Dark, wrap-around sunglasses and dimmer screens reduce photophobia (light pain). Less light reduces stimulation of the irritated iris and ciliary muscle, which lowers pain and spasm. -
Cold compresses (short sessions)
Cool packs for 5–10 minutes, 2–3 times daily, can ease surface discomfort. Cooling narrows surface blood vessels and calms nerve endings, which reduces soreness (note: this does not treat the internal inflammation itself). -
Preservative-free lubricating drops
Artificial tears (no redness removers) soothe surface dryness from frequent medicine use and light avoidance. Lubrication dilutes inflammatory debris on the surface and improves comfort, helping you tolerate necessary steroid drops. -
Cycloplegia adherence aids (timers/reminders)
Cycloplegic drops prevent the iris from sticking to the lens. Phone reminders and written schedules reduce missed doses, limiting pain and posterior synechiae (sticky adhesions). -
Avoid contact lenses during active inflammation
Contacts can trap inflammatory proteins and reduce oxygen to the cornea. Stopping lenses reduces irritation and infection risk, and it improves drop penetration. -
Healthy sleep routine
7–9 hours of regular sleep supports immune balance and healing. Good sleep down-regulates stress hormones that can fuel inflammation. -
Hydration
Proper fluid intake maintains tear production and overall health. Good hydration optimizes ocular surface and supports metabolism during steroid and NSAID use. -
Anti-inflammatory eating pattern
Meals rich in vegetables, fruits, whole grains, legumes, nuts, fish help calm body-wide inflammation. Omega-3 fats (from fish/flax) shift immune signaling toward a less inflammatory profile. -
Smoking cessation
Smoke irritates eyes and raises systemic inflammation. Quitting improves ocular blood flow and reduces flare risk over time. -
Alcohol moderation
Alcohol can worsen sleep and interact with medicines (e.g., methotrexate). Limiting alcohol reduces drug side-effect risks and supports liver health. -
Manage systemic conditions (BP, diabetes)
Good control lowers the chance of treatment complications (e.g., steroid-related glucose spikes). Stable health improves eye healing capacity. -
Gentle aerobic activity
Walking or light cycling improves mood and circulation without eye strain. Better circulation supports tissue recovery; avoiding high-impact activities reduces jarring eye pain. -
Stress-reduction skills (breathing, mindfulness)
Short daily practices lower stress hormones (like cortisol surges) that can worsen immune dysregulation, helping symptoms feel more manageable. -
Work/school accommodations
Temporary screen breaks, larger fonts, and flexible deadlines reduce visual strain, allowing treatment to work without constant irritation. -
Home lighting and screen adjustments
Warm light, screen filters, and lower brightness reduce glare and pain from photophobia. -
Eye protection
Safety glasses during dusty or windy activities limit mechanical irritation and reduce surface inflammation. -
Infection-control hygiene
Good handwashing, replacing toothbrushes after strep, and avoiding shared utensils lower strep exposure and reduce the chance of recurrent immune triggers. -
Low-vision supports (if needed during flares)
Magnifiers, audio books, and high-contrast settings bridge temporary vision dips, maintaining independence and safety while inflammation settles.
Drug treatments
Always follow your ophthalmologist’s plan. Doses below are typical ranges, individualized to you. Never start/stop without medical advice.
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Topical corticosteroid (Prednisolone acetate 1%)
Class: Ophthalmic glucocorticoid.
Dose/Timing: 1 drop every 1–2 hours while awake for severe flares, then taper slowly over weeks as directed.
Purpose: First-line to quiet intraocular inflammation.
Mechanism: Blocks inflammatory genes and cytokines via glucocorticoid receptors.
Side effects: Raised eye pressure (glaucoma risk), cataract over time, delayed healing, infection masking—requires regular pressure checks. -
Cycloplegic/mydriatic (Homatropine 5% or Cyclopentolate 1%)
Class: Antimuscarinic.
Dose/Timing: 1 drop 2–3×/day.
Purpose: Pain relief and prevention of iris-lens adhesions (posterior synechiae).
Mechanism: Temporarily relaxes the ciliary muscle and dilates the pupil, stopping spasm.
Side effects: Blurred near vision, light sensitivity, dry mouth; rare angle-closure in predisposed eyes. -
Oral NSAID (e.g., Ibuprofen or Naproxen)
Class: Nonsteroidal anti-inflammatory.
Dose/Timing: Ibuprofen 400–600 mg every 6–8 h with food; or Naproxen 250–500 mg twice daily.
Purpose: Pain control and systemic anti-inflammatory support.
Mechanism: COX inhibition lowers prostaglandins.
Side effects: Stomach upset/bleeding risk, kidney strain, fluid retention; avoid with certain heart/kidney issues. -
Topical NSAID (e.g., Bromfenac 0.09%)
Class: Ophthalmic NSAID.
Dose/Timing: Typically 1 drop once daily as adjunct.
Purpose: Additional pain/photophobia relief; not a substitute for steroids.
Mechanism: Local COX-2 inhibition.
Side effects: Surface irritation; rarely corneal problems if overused—use only if prescribed. -
Oral corticosteroid (Prednisone)
Class: Systemic glucocorticoid.
Dose/Timing: ~0.5–1 mg/kg/day, then slow taper under supervision.
Purpose: For moderate to severe or back-of-the-eye inflammation.
Mechanism: Strong systemic immunosuppression.
Side effects: Insomnia, mood change, high blood sugar, blood pressure rise, infection risk, bone loss with long use—do not stop abruptly. -
Periocular steroid injection (Triamcinolone acetonide 40 mg)
Class: Long-acting corticosteroid injection (sub-Tenon’s).
Dose/Timing: One injection; effect weeks–months.
Purpose: Targets inflammation when drops aren’t enough.
Mechanism: Depot steroid near the inflamed tissues.
Side effects: Eye pressure rise, cataract acceleration, rare infection—needs close follow-up. -
Intravitreal dexamethasone implant (0.7 mg)
Class: Intraocular corticosteroid implant.
Dose/Timing: Single in-office procedure; may repeat if indicated.
Purpose: Back-of-the-eye inflammation and macular edema.
Mechanism: Sustained steroid delivery inside the eye.
Side effects: Pressure spikes, cataract progression, rare endophthalmitis. -
Methotrexate
Class: Antimetabolite immunomodulator (steroid-sparing).
Dose/Timing: 10–25 mg once weekly + folic acid.
Purpose: For recurrent or steroid-dependent uveitis.
Mechanism: Dampens rapidly dividing immune cells and cytokines.
Side effects: Nausea, mouth sores, liver enzyme elevation, low blood counts; avoid pregnancy; needs regular blood tests. -
Mycophenolate mofetil
Class: Antimetabolite immunomodulator.
Dose/Timing: 1–1.5 g twice daily.
Purpose: Steroid-sparing control of chronic/recurrent disease.
Mechanism: Inhibits lymphocyte nucleotide synthesis.
Side effects: GI upset, infection risk, low blood counts; avoid pregnancy; routine labs needed. -
Adalimumab
Class: Anti-TNF-α biologic (subcutaneous).
Dose/Timing: 80 mg loading, then 40 mg every other week (some need weekly).
Purpose: For moderate–severe noninfectious uveitis not controlled by conventional therapy.
Mechanism: Neutralizes TNF-α, a key inflammatory signal.
Side effects: Infection risk, injection-site reactions; screen for TB and hepatitis B beforehand.
Special note on antibiotics: Because PSU is post-infectious, antibiotics do not treat the eye inflammation, but your clinician may prescribe penicillin or amoxicillin to eradicate residual strep carriage (for example: Penicillin V 250–500 mg twice daily for 10 days, or one dose of benzathine penicillin G 1.2 million units IM in adults) when indicated by throat culture or public-health reasons. Report allergies.
Dietary molecular supplements
These do not replace medical treatment. Discuss with your clinician—supplements can interact with medicines.
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Omega-3 fatty acids (EPA/DHA)
Dose: 1–2 g/day combined EPA+DHA.
Function/Mechanism: Produces pro-resolving mediators that help turn off inflammation and support retinal health. -
Vitamin D3
Dose: 1000–2000 IU/day (or per blood level guidance).
Function/Mechanism: Immune modulation; low vitamin D is linked with higher inflammatory activity in many conditions. -
Curcumin (with piperine)
Dose: 500–1000 mg curcumin/day of a bioavailable form.
Function/Mechanism: NF-κB pathway calming; may ease inflammatory signaling. -
Quercetin
Dose: ~500 mg/day.
Function/Mechanism: Antioxidant and mast-cell stabilizing effects that may reduce ocular surface irritation. -
Lutein + Zeaxanthin
Dose: Lutein 10 mg + Zeaxanthin 2 mg/day.
Function/Mechanism: Concentrate in the macula; antioxidant shield for retinal cells. -
N-Acetylcysteine (NAC)
Dose: 600–1200 mg/day.
Function/Mechanism: Replenishes glutathione, a major antioxidant; may reduce oxidative stress in inflamed tissues. -
Probiotics (Lactobacillus/Bifidobacterium blends)
Dose: ≥10^9 CFU/day as labeled.
Function/Mechanism: Gut–immune axis modulation; a healthier microbiome can steady immune responses. -
Zinc (elemental)
Dose: 10–25 mg/day with food.
Function/Mechanism: Supports innate and adaptive immunity and ocular surface repair; avoid long-term high doses. -
Vitamin C
Dose: 500–1000 mg/day.
Function/Mechanism: Water-soluble free-radical scavenger aiding tissue recovery. -
Resveratrol
Dose: 100–250 mg/day.
Function/Mechanism: Sirtuin activation and antioxidant effects that may dampen excessive inflammation.
Regenerative approaches
There are no approved stem-cell or “immunity-booster” drugs for PSU. The options below are specialist-only and, in many places, clinical-trial-restricted. They are listed for awareness, not as recommendations.
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Intravenous immunoglobulin (IVIG)
Dose: Common autoimmune protocols use 2 g/kg total over 2–5 days (hospital setting).
Function/Mechanism: Provides pooled antibodies that neutralize auto-antibodies and rebalance immune signaling.
Use case: Extremely refractory, systemic, or multi-system post-infectious immune reactions under subspecialist care.
Risks: Headache, clots, kidney strain; costly. -
Tocilizumab (anti-IL-6 biologic)
Dose: SC 162 mg every 1–2 weeks, or IV per protocol; off-label for some uveitis cases.
Function/Mechanism: Blocks IL-6, a strong inflammation driver.
Use case: Refractory uveitis with macular edema not responding to anti-TNF or antimetabolites.
Risks: Infection risk; lab monitoring required. -
Rituximab (anti-CD20)
Dose: Various IV regimens (e.g., 1000 mg day 1 and 15) off-label.
Function/Mechanism: Depletes B-cells that can present auto-antigens and make auto-antibodies.
Use case: Select, severe autoimmune uveitis phenotypes.
Risks: Infusion reactions, infection risk; specialist oversight. -
Hematopoietic stem-cell transplantation (HSCT)
Dose: No standard dose; done only in trials/tertiary centers.
Function/Mechanism: Resets the immune system with high-dose chemo, then reinfusion of stem cells.
Use case: Exceptionally rare for uveitis; only for catastrophic, systemic autoimmune disease.
Risks: Serious; not routine for PSU. -
Mesenchymal stem-cell (MSC) therapy
Dose: Experimental only (IV or targeted delivery in trials).
Function/Mechanism: MSCs release anti-inflammatory and trophic factors that may modulate immunity.
Use case: Research settings; not standard for PSU.
Risks: Unknown long-term safety; avoid outside trials. -
Autologous platelet-derived products (e.g., PRP)
Dose: Protocols vary; largely used for ocular surface, not intraocular uveitis.
Function/Mechanism: Growth factors that support surface healing.
Use case: Rare adjunct for surface discomfort; does not treat intraocular inflammation.
Risks: Procedure-related irritation; limited applicability to PSU.
Surgeries
Surgery is only considered after inflammation is quiet for several months or for urgent complications.
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Cataract surgery (phacoemulsification with IOL)
Why done: Treats uveitic or steroid-related cataract causing vision loss.
Procedure: Ultrasound breaks and removes the cloudy lens; a clear artificial lens is implanted. Pre-/post-op steroids keep inflammation quiet. -
Glaucoma surgery (trabeculectomy or drainage implant)
Why done: For uncontrolled eye pressure (uveitic glaucoma) despite maximal medical therapy.
Procedure: Creates a new drainage path to lower pressure and protect the optic nerve. -
Pars plana vitrectomy (PPV)
Why done: Dense vitreous opacities, persistent floaters, traction, or diagnostic sampling.
Procedure: Removes the gel inside the eye to clear the visual axis and allow better treatment of the retina. -
Synechiolysis and pupilloplasty
Why done: To break iris-lens adhesions and re-shape the pupil if it is stuck and visually disabling.
Procedure: Mechanical separation during surgery, often combined with cataract surgery. -
Retinal membrane peel / macular surgery
Why done: To remove epiretinal membranes or treat complications affecting central vision.
Procedure: Micro-instruments delicately peel scar tissue to restore macular contour.
Practical prevention tips
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Treat strep throat early as guided by a clinician.
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Complete any antibiotic course fully when prescribed.
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Good hygiene: handwashing, no sharing utensils during respiratory illnesses.
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Replace toothbrushes after confirmed strep infection.
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Keep vaccinations current (e.g., flu), which lowers secondary infections that complicate care.
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Avoid smoking and secondhand smoke to reduce baseline inflammation.
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Protect eyes from UV and irritants with sunglasses and safety glasses.
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Maintain healthy weight, blood pressure, and glucose, which makes steroid courses safer.
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Follow your taper plan precisely to reduce rebound flares.
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Attend all follow-ups, even if you feel fine—silent pressure rises can harm vision.
When to see a doctor—urgent vs. routine
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Seek urgent eye care now if you develop sudden vision loss, severe eye pain, halos around lights, intense redness, nausea with headache, new large floaters, or flashes of light. These can signal high eye pressure, severe inflammation, or retinal problems.
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Book prompt follow-up if light sensitivity, mild pain, or blur returns while tapering drops.
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For routine care, keep every scheduled visit for pressure checks and medication adjustments—this prevents permanent damage.
What to eat and what to avoid
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Eat: fatty fish (salmon/sardines) 2–3×/week for omega-3s that help resolve inflammation.
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Eat: colorful vegetables and fruits daily (spinach, kale, peppers, berries) for antioxidants that protect the retina.
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Eat: nuts, seeds, olive oil, and legumes for healthy fats and fiber that support an even immune tone.
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Eat: whole grains instead of refined carbs to steady blood sugar, especially if on steroids.
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Eat: fermented foods (yogurt, kefir, kimchi) to support the gut–immune axis.
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Avoid or limit: excess salt, which worsens fluid retention during steroid therapy.
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Avoid: high-sugar drinks and sweets that spike inflammation and blood sugar.
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Avoid: excess alcohol, which interferes with sleep and some medicines (e.g., methotrexate).
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Avoid: smoked/charred foods that add oxidative stress.
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Discuss before using: grapefruit products if you take certain oral medicines that are CYP-interacting (your pharmacist can check).
Frequently asked questions
1) Is PSU an infection inside my eye?
No. PSU is an immune reaction that happens after a strep infection. There are no living bacteria inside the eye in typical PSU.
2) Can PSU make me blind?
Permanent vision loss is uncommon with early treatment and close follow-up. Risk rises if inflammation is untreated, recurrent, or if pressure stays high.
3) Do I need antibiotics for my eyes?
Antibiotics do not treat the inflammation. Your doctor may use antibiotics to clear throat carriage if tests suggest it, but eye treatment relies on anti-inflammatory medicines.
4) How long does recovery take?
Many improve within days to weeks, but full control and safe steroid taper can take several weeks. Timelines vary by severity and location in the eye.
5) Why are steroid drops tapered slowly?
A slow taper prevents rebound inflammation. The immune system needs time to settle so the eye does not “flare back up.”
6) Will I need long-term medicines?
Some people have a single episode. Others have recurrent flares and may need a steroid-sparing medicine (like methotrexate or mycophenolate) to prevent frequent relapses.
7) Are biologic injections safe?
Biologics like adalimumab can help difficult cases. They suppress specific immune signals and require infection screening and periodic labs to stay safe.
8) Can I wear contact lenses?
Avoid them during active inflammation. Once the eye is quiet and comfortable, ask your doctor when you can safely resume.
9) Is PSU the same as PANDAS or rheumatic fever?
They are all post-streptococcal immune conditions, but they affect different organs. PSU mainly affects the eye.
10) Do blue-light filters help?
They do not treat inflammation, but many people find less glare and strain, which improves comfort during recovery.
11) Can I drive?
Only if vision and light sensitivity are safe for you and your doctor agrees. Driving with poor contrast or severe glare is unsafe.
12) What about pregnancy or breastfeeding?
Several medicines used for uveitis are not safe in pregnancy (e.g., methotrexate, mycophenolate). Discuss family planning with your ophthalmologist and obstetrician.
13) Will I definitely get PSU again if I catch strep?
Not necessarily. Many never recur. Early strep treatment and good hygiene may reduce risk. Keep an eye care plan ready.
14) Are supplements required?
No. Supplements are optional adjuncts. Focus first on prescribed medicines, diet quality, sleep, and follow-up.
15) What warning signs mean “go in now”?
Rapid vision drop, severe pain, halos, nausea/vomiting, new large floaters, or flashes—seek urgent eye care.
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 22, 2025.
