Phlyctenular Keratoconjunctivitis (PKC)

Phlyctenular keratoconjunctivitis (PKC) is an eye condition where the body’s immune system overreacts to germs or germ-related proteins and creates a small inflamed bump on the white of the eye or on the edge of the cornea. This bump is called a phlyctenule. It looks like a tiny, raised, yellow-white nodule surrounded by dilated blood vessels. It can form at the limbus (the border where the clear cornea meets the white conjunctiva) or on the conjunctiva itself. When the cornea is involved, the bump can break down on top, feel very painful, and make bright light hard to tolerate. PKC is not a direct infection of the cornea. It is an immune (delayed-type) hypersensitivity reaction to microbial antigens, most often from Staphylococcus aureus on the eyelids or from tuberculosis in areas where TB is common. Merck ManualsWebEyePubMed

PKC is an eye surface inflammation where tiny, raised, tender bumps (called phlyctenules) appear on the white part of the eye (conjunctiva) or the clear front window (cornea). These bumps are not ordinary infections. They are immune reactions—your immune system becomes over-reactive to germs (most often Staphylococcus aureus from eyelids) or, in some regions, to tuberculosis (TB) proteins. This “allergic-type” reaction (a delayed, T-cell–mediated response) inflames the surface and can cause pain, tearing, and strong light sensitivity. If the cornea is involved, it may ulcerate and scar, which can blur vision if not treated promptly. EyeWiki

In simple words, your immune system “remembers” a germ it has met before and then over-reacts on the eye’s surface when it meets that germ again. The reaction creates the little inflamed nodule. This is why treating the underlying source of antigens (often eyelid blepharitis due to staph bacteria, or TB where prevalent) is as important as calming the eye inflammation. WebEyeEyeWiki

Phlyctenules are small (often 0.5–3 mm), pinkish to yellow-white, and they frequently have a “leash of vessels” feeding them from the nearby conjunctiva. They may ulcerate on top and then heal over days to a couple of weeks. When the cornea is involved, the risk of scarring and blurred vision is higher. Vagelos College of Medicine+1Jcdr

Your eyelids and eye surface carry bacteria and other microbes. In most people, the immune system ignores them. In PKC, the immune system becomes sensitized to certain microbial proteins. Later, when the eye surface sees those proteins again, the immune system sends many defensive cells to that spot. Those cells create a nodule and sometimes a small surface ulcer. This process is called a Type IV (delayed) hypersensitivity reaction. journal.opted.org

PKC can occur at any age but is often described in children and young people. It is more likely when there is chronic eyelid margin disease (blepharitis or meibomian gland dysfunction), ocular rosacea, or when tuberculosis or other antigen sources are present in the community. It can recur if the trigger is not removed. Merck ManualsPMC

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Types of phlyctenular keratoconjunctivitis

1) By location

• Conjunctival PKC: the nodule sits on the white of the eye. It is usually less painful and often heals without scarring.

• Limbal PKC: the nodule lies at the limbus. This is very common.

• Corneal PKC: the nodule rides onto the cornea. This type causes photophobia and pain and can leave a scar.

2) By cause (trigger)

• Staphylococcal-associated PKC: linked to lash margin staph overgrowth and blepharitis.

• Tuberculin-associated PKC: linked to Mycobacterium tuberculosis exposure in endemic areas.

• Other antigen-associated PKC: rare triggers include certain bacteria, fungi, or parasites.

3) By course

• Acute, single episode: one nodule that heals and does not return.

• Recurrent PKC: repeated nodules over time, often when lid disease is uncontrolled or when the systemic source persists.

4) By severity

• Mild: small conjunctival bump, minimal symptoms.

• Moderate: limbal involvement, more redness and light sensitivity.

• Severe: corneal involvement with ulceration, scarring, or pannus (new superficial vessels), and significant light sensitivity.

(Descriptions above reflect core clinical patterns noted across standard ophthalmic sources.) WebEyeVagelos College of Medicine

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Causes

Important note: PKC is an immune reaction to antigens (proteins) from germs, most often on the lids. The items below are triggers/associations, not direct corneal infections.

1. Chronic staphylococcal blepharitis
   This is the most common association in many regions. Staph proteins on the lashes and lid margins keep the immune system “on alert” and can set off phlyctenules. Treating lid disease lowers recurrences. WebEye

2. Meibomian gland dysfunction (MGD)
   When oil glands are blocked, bacteria flourish at the lid margin. Their antigens can drive the hypersensitivity reaction that forms phlyctenules. WebEye

3. Ocular rosacea
   Rosacea often comes with blepharitis and MGD. The inflamed, bacteria-rich lid margin provides antigens that can trigger PKC. Steroid-sparing drops like cyclosporine are sometimes used when steroid tapering fails. Wiley Online LibraryPMC

4. Mycobacterium tuberculosis (TB)
   In TB-endemic areas, sensitization to TB proteins is a classic trigger. In such settings, TB screening is important. IJDVLPMC

5. Chlamydia trachomatis
   This organism can rarely be linked to phlyctenules through antigen exposure and hypersensitivity. Merck Manuals

6. Herpes simplex virus (antigen exposure)
   Some reports list herpes simplex antigen exposure as a possible but uncommon trigger. This is not the same as active herpetic keratitis. EyeWiki

7. Streptococcus viridans (rare)
   Uncommon bacterial associations are documented, including S. viridans, via antigen exposure. EyeWiki

8. Dolosigranulum pigrum (rare case reports)
   This unusual bacterium has been reported in association with bilateral PKC in a child. Taylor & Francis Online

9. Intestinal parasite—Hymenolepis nana
   Studies from some regions show frequent H. nana infections in children with phlyctenular eye disease, suggesting parasite antigens can trigger PKC. PubMedjesp.journals.ekb.eg

10. Intestinal parasite—Ascaris lumbricoides
    Helminth antigens can sensitize the immune system and have been linked to phlyctenular disease in observational studies. PubMedResearchGate

11. Intestinal parasite—Ancylostoma duodenale
    Hookworm has been mentioned as a possible trigger in secondary sources. Local epidemiology matters. Medical News Today

12. Candida species (rare)
    Fungal antigens such as Candida have been cited rarely as triggers for a similar hypersensitivity response. PMC

13. Coccidioides (rare)
    Coccidioidomycosis has been listed among rare infectious associations in case-based literature. PMC

14. Demodex infestation of lashes
    Mites increase lid inflammation and bacterial load; managing Demodex can reduce antigen exposure. (Considered an indirect trigger through blepharitis.)

15. Chronic poor lid hygiene
    Inadequate cleansing allows bacterial overgrowth and biofilm, increasing antigen exposure at the lid margin.

16. Chronic conjunctivitis from other bacteria
    Any long-standing lid or conjunctival colonization can prime the immune system and promote phlyctenules.

17. Dacryocystitis (chronic tear sac infection)
    A chronically infected lacrimal sac can shed bacteria onto the ocular surface, adding antigen load.

18. Atopic tendency (general allergic background)
    People with strong atopic backgrounds can be more reactive to environmental and microbial antigens, making PKC more likely to flare.

19. Malnutrition/Vitamin A deficiency (indirect risk)
    A poor ocular surface and reduced immunity can make lid disease stubborn and antigen exposure persistent, enabling PKC recurrences.

20. Recent exposure to TB household contact (contextual trigger)
    In TB-endemic settings, household exposure increases the chance of tuberculin sensitization, which can manifest as PKC. IJDVL

(Items 14–19 reflect common clinical contributors that raise antigen exposure or immune reactivity on the lids and conjunctiva; the core, well-documented triggers remain staph blepharitis and TB.)

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Common symptoms

1. Red eye
   The eye looks red because surface blood vessels are inflamed around the nodule.

2. Foreign-body sensation
   It feels like grit or sand is in the eye because the surface is uneven and irritated. Vagelos College of Medicine

3. Tearing (watering)
   Reflex tears increase to “wash out” the irritation.

4. Photophobia (light sensitivity)
   Light hurts, especially when the cornea is involved, because corneal nerves are exposed and inflamed. Vagelos College of Medicine

5. Burning or stinging
   Inflamed surface nerves send pain signals.

6. Soreness or pain
   Pain becomes worse when a corneal ulcer forms on top of the nodule.

7. Mucous discharge
   Thick strings of mucus may appear due to surface inflammation.

8. Blurry vision
   Vision blurs when the cornea is irregular, when tears are unstable, or when a scar forms.

9. Eyelid crusting
   Crusts on the lashes in the morning suggest blepharitis, a common driver of antigen exposure.

10. Itching
    Itching is usually mild compared with classic allergic conjunctivitis but can be present.

11. Lid swelling
    The lids can puff up from local inflammation.

12. Eye fatigue
    People blink more and squint because the eye is uncomfortable.

13. Stringy feeling when moving the eye
    The inflamed area rubs under the lid with each blink.

14. Sensitivity to wind or smoke
    Any drying or irritant exposure can worsen symptoms.

15. Headache around the eye
    Strain and inflammation can produce a dull ache around the affected eye.

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Diagnostic tests

Below are the usual ways clinicians confirm PKC and look for the cause. Many cases are diagnosed at the slit lamp by an eye specialist. Only a subset of the tests below are needed for each person. I list 20 for completeness and group them as requested.

A) Physical exam

1) External eye and eyelid inspection
The doctor looks at the lashes and lids for crusting, redness, and blocked oil glands. This helps uncover blepharitis or rosacea, which commonly drive PKC. WebEye

2) Visual acuity testing (letters chart)
This checks how clearly you see. It is important because corneal involvement can blur vision.

3) Pupillary and light reflex exam
This rules out deeper eye problems and checks how the eye reacts to light.

4) Conjunctival and limbal inspection with a bright light
The clinician notes a small, raised, pink-white nodule with a surrounding leash of vessels, often near the limbus. Jcdr

5) General health review
A brief systemic screen looks for TB risk (contact, cough, weight loss, night sweats) or skin signs of rosacea that might explain the trigger. IJDVL

B) Manual office tests

6) Slit-lamp biomicroscopy
This is the key exam. The microscope shows the phlyctenule, any surface ulcer, and surrounding inflammation. It confirms whether the cornea is involved. Vagelos College of Medicine

7) Fluorescein staining of the cornea
A safe orange dye highlights surface breaks and shows if the top of the nodule has ulcerated. The dye glows under blue light.

8) Lissamine green or rose bengal staining
These dyes map damaged or unprotected surface cells, which helps judge irritation around the lesion.

9) Lid eversion and meibomian gland expression
Flipping the lid shows the tarsal surface for bumps or inflammation. Gentle pressure checks if the oil glands are blocked. This pinpoints MGD, a frequent driver. WebEye

10) Tear film break-up time (TBUT) and Schirmer test
These quick tests check tear quality and quantity. Tear instability can worsen surface irritation and symptoms.

C) Lab and pathological tests

11) Eyelid margin swab for bacterial culture
This looks for staphylococcal overgrowth or other bacteria at the lid margin so the doctor can target treatment. WebEye

12) Lash sampling for Demodex (microscopy)
Lashes are gently removed and examined to detect mites that worsen blepharitis.

13) Tuberculosis skin test (Mantoux) or IGRA blood test
If TB is possible, these tests check for tuberculin sensitization, which is a classic PKC trigger in endemic regions. IJDVL

14) Chest imaging and TB microbiology (guided by risk)
If TB tests are positive or suspicion is high, doctors may order sputum studies and chest imaging to look for active disease. (Imaging specifics appear under the “Imaging” section.)

15) Stool exam for ova and parasites (selected settings)
Where parasitic infections are common, stool testing can detect Hymenolepis nana, Ascaris, or others that may supply antigens linked to PKC in observational studies. PubMed

16) Conjunctival swab NAAT (e.g., for Chlamydia trachomatis)
This is done when symptoms and context suggest chlamydial exposure. It supports finding a treatable trigger. Merck Manuals

D) Electrodiagnostic tests  rarely needed

17) Corneal esthesiometry (electronic/gas esthesiometer)
This measures corneal nerve sensitivity. It is not routine for PKC but can help when pain seems out of proportion or when nerve issues are suspected.

18) Blink reflex testing (trigeminal electrophysiology)
This is very rarely used and mainly for unusual cases with suspected nerve problems. It is not part of standard PKC work-ups.
(These two tests are listed for completeness because you asked for an electrodiagnostic category; in typical PKC, they are unnecessary.)

E) Imaging tests

19) Anterior segment OCT / in-vivo confocal microscopy (specialty use)
These imaging tools can document corneal thickness, surface changes, inflammatory cells, and early scarring after severe or recurrent PKC. They help track healing in difficult cases.

20) Chest X-ray (when TB is suspected)
If TB screening is positive or there are risk factors, a chest X-ray supports evaluation for active tuberculosis, which changes the overall treatment plan. IJDVL

Non-pharmacological treatments (therapies & daily practices)

These steps lower the antigen load (especially Staph) and calm surface inflammation. They’re safe to start early and continue long-term.

1. Warm compresses (5–10 minutes, 1–2×/day).
   Purpose: melts thick eyelid oils and loosens crusts.
   Mechanism: gentle heat softens meibum so it can flow, reducing stagnation and bacterial overgrowth. NCBItfosdewsreport.org

2. Lid massage after warmth.
   Purpose: expresses thickened oil from meibomian glands.
   Mechanism: mechanical pressure along the lid margin clears blockages. esht.nhs.uk

3. Lid scrubs/cleansers (commercial foams/wipes).
   Purpose: remove debris and lower bacterial load.
   Mechanism: surfactants lift crusts and biofilm from lashes/lid edges. Evidence supports symptom relief in blepharitis. CochraneCollege Optometrists

4. Demodex hygiene (if present).
   Purpose: reduce mite burden that worsens lid inflammation.
   Mechanism: tea-tree–based wipes/solutions disturb mites; improves lid margin. (Supportive evidence in blepharitis literature.)

5. Blink training and screen breaks.
   Purpose: improve tear spread and reduce evaporative stress.
   Mechanism: frequent full blinks refresh the lipid layer; the “20-20-20 rule” helps.

6. Humidify your air, avoid drafts/smoke.
   Purpose: reduce tear evaporation and surface irritation.
   Mechanism: higher humidity preserves tear film; avoiding smoke removes irritants. PubMed

7. Sunglasses outdoors.
   Purpose: reduce wind/UV triggers and photophobia.
   Mechanism: physical barrier decreases environmental irritation and light-induced discomfort.

8. Warm-heat masks or FDA-cleared warming devices (at home).
   Purpose: more consistent, therapeutic heat than a washcloth.
   Mechanism: controlled heat improves meibum quality and symptoms. PMCScienceDirect

9. Professional eyelid exfoliation (in-office when needed).
   Purpose: deeply removes biofilm/collarettes.
   Mechanism: micro-exfoliation decreases bacterial load and inflammation. ScienceDirect

10. Thermal pulsation (e.g., LipiFlow®) or meibomian probing (clinic procedures).
    Purpose: open blocked glands and restore flow.
    Mechanism: heat + pressure/pulsation liquefies meibum; probing mechanically opens ducts. AAO

11. Intense pulsed light (IPL) for rosacea-MGD (select patients).
    Purpose: tamp down lid-margin vascular inflammation.
    Mechanism: IPL targets telangiectatic vessels and inflammatory mediators. AAO

12. Hand hygiene and no eye-rubbing.
    Purpose: prevent re-seeding bacteria to lids/eyes.
    Mechanism: lowers antigen exposure that drives flares.

13. Separate face towels and makeup hygiene.
    Purpose: reduce cross-contamination.
    Mechanism: limits shared bacteria/allergens.

14. Treat scalp dandruff/seborrhea.
    Purpose: improve anterior blepharitis.
    Mechanism: anti-seborrheic care reduces flaking into lashes.

15. Manage skin rosacea.
    Purpose: decrease ocular rosacea flares.
    Mechanism: systemic/derm care reduces lid margin inflammation.

16. Balanced diet with vitamin A–rich foods and adequate protein.
    Purpose: support a resilient ocular surface.
    Mechanism: vitamin A maintains mucous membranes; protein supports healing. (Vitamin A deficiency damages cornea; nutrition matters.) World Health Organization

17. Hydration (regular water intake).
    Purpose: supports tear volume.
    Mechanism: good hydration helps aqueous tear production.

18. Cold compress for pain/photophobia during flares.
    Purpose: short-term comfort.
    Mechanism: vasoconstriction reduces surface hyperemia and pain signaling.

19. Non-preserved lubricating drops/gel.
    Purpose: dilute inflammatory mediators; cushion epithelium.
    Mechanism: isotonic polymers stabilize the tear film (adjunct to the steps above). PubMed

20. Address household TB risk when relevant.
    Purpose: remove the antigen source.
    Mechanism: screening/treatment of latent/active TB in patients/contacts lowers re-exposure risk. CDC

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Drug treatments

Doses below are typical adult starting patterns used clinically; exact regimens must be individualized by an eye-care professional, especially in children, pregnancy, glaucoma, or TB risk.

1. Prednisolone acetate 1% (topical corticosteroid).
   Dose: 1 drop 4×/day for 1–2 weeks, then slow taper based on response.
   Purpose: quickly calm inflammation and stop the “march” of corneal phlyctenules.
   Mechanism: blocks multiple inflammatory pathways.
   Side effects: ↑eye pressure, cataract risk, infection masking—must be supervised. EyeWiki

2. Fluorometholone 0.1% (soft steroid).
   Dose: 1 drop 3–4×/day, taper.
   Purpose: similar to prednisolone but with typically lower IOP risk.
   Mechanism: corticosteroid anti-inflammatory.
   Side effects: still can raise IOP; watch carefully. (General steroid references apply.)

3. Loteprednol etabonate 0.5% (ester steroid).
   Dose: 1 drop 3–4×/day, taper.
   Purpose/mechanism: steroid with lower average IOP impact; good for recurrent cases.
   Side effects: burning, rare IOP rise; still requires monitoring.

4. Topical azithromycin 1–1.5%.
   Dose (common): 1 drop BID for 2 days, then QD up to several weeks (local product instructions vary).
   Purpose: treat lid-margin Staph load and ocular rosacea-MGD component.
   Mechanism: macrolide antibiotic plus anti-inflammatory effects on meibomian glands.
   Side effects: transient blur/stinging. Evidence supports benefit in PKC with ocular rosacea. EyeWikiOphthalmology TimesSciELO

5. Erythromycin 0.5% ophthalmic ointment (topical).
   Dose: small ribbon to lid margins/inside lower lid at bedtime (or 1–3×/day) for weeks.
   Purpose: lowers Staph bioburden; helpful for children.
   Mechanism: macrolide antibiotic; also lubricates overnight.
   Side effects: blur after application, mild irritation. WebEye

6. Oral doxycycline (systemic tetracycline; adults only).
   Dose (MGD): 50–100 mg once daily (or 50 mg twice daily) for several weeks, then taper per clinician.
   Purpose: reduces meibomian inflammation and alters meibum composition; steroid-sparing.
   Mechanism: anti-inflammatory MMP inhibition in addition to antibacterial action.
   Side effects: photosensitivity, GI upset; avoid in pregnancy and in children <8 y. AAOScienceDirect

7. Oral azithromycin (alternative to doxycycline in some cases).
   Dose: regimens vary (e.g., pulse dosing); used when doxycycline isn’t suitable.
   Purpose/mechanism: macrolide anti-inflammatory effect on MGD and lids.
   Side effects: GI upset, QT risk in predisposed patients; clinician-directed. AAO

8. Topical cyclosporine A 0.05% (steroid-sparing immunomodulator).
   Dose: 1 drop BID long term in recurrent/steroid-dependent PKC.
   Purpose: reduce flares and minimize chronic steroid exposure.
   Mechanism: calcineurin inhibitor that quiets T-cell–driven surface inflammation.
   Side effects: burning on instillation; slow onset (weeks). EyeWiki

9. Cycloplegic drops (e.g., cyclopentolate 1% or homatropine 2–5%).
   Dose: typically BID–TID during painful corneal flares (short course).
   Purpose: relax the ciliary muscle to reduce pain and photophobia.
   Mechanism: anticholinergic mydriasis/cycloplegia.
   Side effects: light sensitivity, blurred near vision; use under guidance. ScienceDirect

10. Treat the infectious trigger when present (systemic therapy).
    Examples: standard TB regimens for active TB (per national/CDC guidelines); azithromycin or doxycycline for confirmed chlamydial infection; weight-based oral erythromycin in young children when tetracyclines are contraindicated—these are prescribed and monitored by your physician. The eye quiets better once the trigger is treated. CDC

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Dietary molecular supplements

Supplements may help the eyelid/tear film environment but do not replace medical therapy for PKC. Evidence is stronger for some (omega-3) and weaker/mixed for others. Always discuss with your clinician.

1. Omega-3 fatty acids (EPA/DHA) — 1000–2000 mg/day total EPA+DHA.
   Function: may improve meibum quality and tear stability in some MGD patients.
   Mechanism: anti-inflammatory lipid mediators.
   Evidence note: mixed; some RCTs show limited benefit overall, others show improvement in MGD subsets. New England Journal of MedicinePMCMDPI

2. Vitamin A (dietary intake; supplement only if deficient).
   Function: maintains healthy conjunctiva/cornea.
   Mechanism: supports mucin-secreting epithelium and immunity.
   Safety: high-dose supplements can be toxic—test and supervise; deficiency is sight-threatening. World Health Organization

3. Vitamin D (e.g., 1000–2000 IU/day unless advised otherwise).
   Function: immune modulation; may aid dry eye in deficient individuals.
   Mechanism: vitamin-D–receptor pathways reduce inflammatory signaling.
   Evidence: meta-analyses suggest benefit in deficiency; results vary—check levels first. PMCScienceDirect

4. Zinc (up to diet-recommended doses).
   Function: supports innate/adaptive immunity and healing.
   Mechanism: cofactor for immune enzymes.
   Safety: excess can upset copper balance; stay at RDA unless directed.

5. Curcumin (turmeric extract 500–1000 mg/day).
   Function: general anti-inflammatory adjunct.
   Mechanism: NF-κB pathway dampening; limited ocular-specific data.

6. Probiotics (standard daily CFU per product).
   Function: may balance microbial communities; ocular evidence limited.
   Mechanism: gut-immune interactions; consider only as supportive.

7. N-acetylcysteine (NAC 600 mg/day).
   Function: mucolytic/antioxidant; sometimes used for filamentary keratitis; adjunct only.

8. Evening primrose oil (GLA 240–320 mg/day).
   Function: potential anti-inflammatory lipid modulation for dry eye; data mixed.

9. Lutein/zeaxanthin (dietary focus).
   Function: ocular surface antioxidant support (stronger data in retina; optional here).

10. Collagen peptides (food-grade, optional).
    Function: general wound-healing support; no PKC-specific evidence.

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Regenerative” options

There are no approved “stem-cell drugs” for PKC. The helpful tools here are steroid-sparing immunomodulators and biologic surface therapies used off-label for severe, recurrent disease or surface damage—always under specialist care.

1. Topical cyclosporine A 0.05% (Rx; immunomodulator).
   Dose: 1 drop BID long term.
   Function: reduces T-cell–driven inflammation and relapses; steroid-sparing. EyeWiki

2. Topical tacrolimus 0.03% ointment to lid margins or compounded eye drops (off-label).
   Dose: often QHS–BID to lids; drops if prescribed.
   Function: calcineurin inhibitor similar to cyclosporine; used in stubborn allergic/rosacea-type disease.
   Evidence: steroid-sparing in allergic surface disease; used by cornea specialists when needed. AMBOSS

3. Lifitegrast 5% (off-label in PKC).
   Dose: 1 drop BID.
   Function: blocks LFA-1/ICAM-1 interaction to reduce T-cell activation; mainly a dry-eye drug; sometimes tried in chronic inflammatory lid/ocular surface states.

4. Autologous serum tears (AST) 20–50% (compounded).
   Dose: typically QID (varies by center).
   Function: provides growth factors and vitamins similar to natural tears; promotes epithelial healing after severe surface damage. PMC+1

5. Platelet-rich plasma (PRP) eye drops (compounded).
   Dose: often QID; protocols vary.
   Function: rich in growth factors; may aid healing and symptoms in severe ocular surface disease. PMCNature

6. Amniotic membrane (biologic graft or extract; see surgeries below).
   Function: anti-inflammatory, anti-scarring substrate that accelerates corneal epithelial healing in persistent defects/ulcers. Not a drug, but a regenerative tissue therapy. Nature

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Procedures/surgeries

1. Amniotic membrane transplantation (AMT)—in office (self-retaining ring) or in OR.
   Why: speeds healing of persistent epithelial defects or ulcers, reduces pain and scarring risk when PKC ulcers are severe or non-healing. Nature

2. Cyanoacrylate corneal gluing (with/without bandage contact lens).
   Why: emergency seal for small corneal perforations or impending perforation from an ulcer—buys time for healing or later graft if needed. Lippincott Journals

3. Corneal patch graft or lamellar/penetrating keratoplasty (rare).
   Why: restores corneal integrity and clarity if perforation or dense scar affects vision despite other care. EyeWiki

4. Thermal pulsation / meibomian probing (in-office procedures).
   Why: reopen blocked meibomian glands to reduce blepharitis-MGD that fuels PKC relapses. AAO

5. Targeted anti-VEGF for aggressive corneal neovascularization (specialist use).
   Why: in selected, vision-threatening cases with active new corneal vessels, subconjunctival or topical anti-VEGF may be considered to quiet vessels and protect the visual axis. (Off-label; careful monitoring required.) PMCOphthalmology Science

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Prevention habits

1. Daily lid hygiene (warmth → massage → scrub). EyeWiki

2. Treat dandruff/rosacea to calm lid margins.

3. No eye-rubbing; wash hands often.

4. Replace eye makeup regularly; don’t share it.

5. Sunglasses outdoors to cut wind/UV triggers.

6. Humidify air; avoid smoke/dust. PubMed

7. Balanced diet with vitamin A and adequate protein. World Health Organization

8. Address TB risk (test and treat per public-health guidance where relevant). CDC

9. Keep contact lenses clean; consider glasses during flares.

10. Follow-up visits as advised to catch early recurrence before scarring.

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When to see a doctor

• Severe light sensitivity, pain, or blurred vision—especially if it worsens over hours/days.

• A visible white/yellow bump on the eye or a painful corneal ulcer appearance.

• Recurrent flares despite good lid care.

• You live in or traveled to an area with TB or have TB symptoms/contacts.

• Children with red, very light-sensitive eyes—they need prompt pediatric eye evaluation. (Early care prevents scars.) EyeWiki

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What to eat  & what to avoid

Eat more of:

1. Vitamin-A–rich foods (leafy greens, carrots, sweet potatoes, eggs, liver in moderation).

2. Omega-3-rich fish (salmon, sardines) 2–3×/week.

3. Protein (fish, lean meats, legumes) for healing.

4. Colorful vegetables & fruits (antioxidants).

5. Fermented foods (yogurt, kefir) if tolerated—microbiome support.

6. Nuts/seeds (walnuts, flax, chia).

7. Plenty of water throughout the day.

8. Whole grains for steady energy.

9. Spices like turmeric in meals (curcumin).

10. Vitamin-D sources (oily fish, fortified foods) and safe sunlight per local guidance.

Prefer to limit/avoid:

1. Smoking and secondhand smoke (surface irritant).

2. Very dry, windy, dusty environments (or protect with eyewear/humidification).

3. Rubbing eyes (spreads antigens and irritates).

4. Old/contaminated eye makeup; share none.

5. High-sugar ultra-processed foods (pro-inflammatory pattern).

6. Excess trans fats (may worsen inflammatory milieu).

7. Allergen triggers known to you (dust mites, pet dander) around bedding.

8. Over-the-counter drops with benzalkonium chloride used too often—prefer preservative-free lubricants in frequent use.

9. Unverified “immune booster” products—many claims, little evidence.

10. Contact lenses during active flares (switch to glasses until quiet).

If your doctor suspects TB exposure, they may order PPD or IGRA tests and a chest X-ray. If TB infection is confirmed, systemic TB treatment following national/CDC/ATS/IDSA guidance is crucial. Treating the trigger dramatically reduces recurrences of PKC. (Eye drops alone are not enough if TB is present.) CDC

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Frequently asked questions

1) Is PKC contagious?
No. The reaction is your immune system’s response. But the triggers (like eyelid Staph or TB) can be infectious—so hygiene and appropriate medical treatment matter. EyeWiki

2) Do I always need steroid drops?
Steroids are often the fastest way to stop the painful flare and protect the cornea, then they’re tapered. In frequent relapses, doctors add steroid-sparing immunomodulators (like cyclosporine) and step up lid care. EyeWiki

3) Will it come back?
It can. Good lid hygiene and treating the underlying trigger (blepharitis, rosacea, TB/chlamydia when present) reduce recurrences. EyeWiki

4) Can it make me blind?
Vision loss is uncommon with proper care, but corneal scarring can reduce vision if flares are severe or untreated. Seek prompt care for corneal symptoms. EyeWiki

5) Are antibiotics always needed?
Topical antibiotics are used when ulcers/erosions are present or to treat lid bacteria. Oral antibiotics (like doxycycline) help MGD/rosacea lids, not the phlyctenule itself. EyeWiki

6) What about omega-3 fish oil?
Some people with MGD feel better on omega-3s; research is mixed. It’s reasonable to try with your doctor’s advice, especially if your diet lacks oily fish. New England Journal of MedicinePMC

7) Can children take doxycycline?
No—avoid tetracyclines under 8 years (tooth discoloration). Pediatricians often use erythromycin instead when an oral antibiotic is needed. EyeWiki

8) Are “stem-cell drops” a thing for PKC?
No approved stem-cell drugs for PKC. Autologous serum/PRP and amniotic membrane are biologic/regenerative options for severe surface damage under specialist care. PMCNature

9) Why do bright lights hurt so much?
Corneal nerve endings are exposed/irritated by inflammation or tiny ulcers—cycloplegic drops and anti-inflammatory therapy ease this. ScienceDirect

10) How long until it gets better?
With the right regimen, symptoms often improve within days; corneal healing and vessel regression take weeks. Tapers and maintenance lid care prevent relapse. EyeWiki

11) Can I use contact lenses during a flare?
Best to pause until the surface heals; lenses can worsen irritation and increase infection risk.

12) Do artificial tears help?
Yes—non-preserved tears/gel dilute inflammatory mediators and cushion the surface; they’re supportive, not curative. PubMed

13) Do I need TB tests even if I feel fine?
If you live in or have traveled to TB-endemic areas or have TB contacts, yes—testing guides treatment that reduces PKC relapses. EyeWiki

14) Can IPL/thermal pulsation cure PKC?
They don’t treat the phlyctenule itself, but by rehabilitating meibomian glands, they reduce the blepharitis driver, helping prevent future flares. AAO

15) What’s the bottom line for home care?
Do daily lid hygiene, protect your eyes, eat a nutritious diet, and keep your follow-ups. See a doctor promptly for pain, photophobia, or blurred vision.

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 21, 2025.