Mycotic Ulcer 

A mycotic ulcer is an open, painful sore on the cornea (the clear, dome-shaped “window” at the front of your eye) that is caused by a fungus. “Mycotic” means fungal. “Ulcer” means a loss of surface tissue—like a crater or pit—often with inflamed, infected edges.

A mycotic ulcer is an open sore (ulcer) on the clear front window of the eye (cornea) caused by fungi such as Fusarium, Aspergillus, or Candida. It usually follows eye trauma with plant matter or soil, contact-lens problems, or use of steroid eye drops, and can quickly threaten sight if not treated promptly. Globally, fungal keratitis is common in tropical/subtropical regions and among agricultural workers; estimates suggest ≈1 million cases yearly worldwide, especially in Asia and Africa. PubMedThe Lancet

Typical signs/symptoms include redness, pain, light sensitivity, tearing, decreased vision, and a gray-white corneal ulcer with feathery edges or satellite lesions. Yeast infections (e.g., Candida) often occur in eyes with surface disease or immunosuppression; filamentous molds often follow trauma with vegetation. NCBI

Fungal germs (molds or yeasts) can stick to a damaged spot on the cornea—often after a minor injury from plant material or from contact lens problems—then grow into the corneal layers. As the fungus grows, it kills local cells, draws in immune cells, and makes enzymes and toxins that melt corneal tissue. The result is a white, gray, or yellow spot with fuzzy (feathery) edges, sometimes with tiny satellite spots around it. The eye becomes red, watery, light-sensitive, and painful, and vision can become blurry. If untreated, the ulcer can deepen, perforate (create a hole), and cause serious, sometimes permanent vision loss.

• Cornea: Clear front cover of the eye that focuses light.

• Fungus: A germ like mold or yeast (examples: Fusarium, Aspergillus, Candida).

• Ulcer: A sore where tissue is lost.

• Feathery edges: Soft, fuzzy margins around the ulcer—common in fungal ulcers.

• Satellite lesions: Small, separate white spots near the main ulcer—another fungal clue.

• Hypopyon: Pus settling as a white layer in the front chamber of the eye; may occur in severe ulcers.

Fungal corneal ulcers tend to be slower to start than bacterial ulcers but often harder to treat and slower to heal. Some antifungal eye drops penetrate poorly into the cornea, fungi can be resistant, and treatment often needs to be prolonged. Early recognition and correct diagnosis matter a lot to protect sight.

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Types of mycotic ulcer

1. Filamentous fungal ulcer (mold type)
   Caused by molds such as Fusarium or Aspergillus. Often follows plant-based trauma (e.g., a twig or leaf scratch). Looks dry, gray-white, with feathery edges and satellite lesions. Common in warm, humid, agricultural regions.

2. Yeast ulcer (Candida type)
   Caused by yeasts, especially Candida. More common in eyes with long-standing surface disease (e.g., dry eye, prior scars), steroid use, or in immunocompromised people. Can look more plaque-like (thicker, creamy) and may be slower.

3. Dematiaceous (pigmented) fungal ulcer
   From dark-colored (brown/black) molds like Curvularia or Bipolaris. May show brownish pigmentation in the lesion and also occurs after vegetative trauma.

4. Contact lens–associated fungal ulcer
   Related to poor lens hygiene, sleeping in lenses, or rinsing/storing lenses in water. Can be caused by molds or yeasts. Risk rises if the lens case is contaminated.

5. Post-surgical fungal ulcer
   Occurs after corneal surgery (e.g., LASIK, corneal graft) if fungi contaminate the surface or sutures. Often difficult because surgery alters corneal structure and local immunity.

6. Mixed infection ulcer (fungal + bacterial)
   The ulcer contains both fungus and bacteria. Clues can be mixed appearances (some features of fungal, some of bacterial). Needs broad testing and combined treatment.

7. Deep stromal fungal ulcer
   The fungus has invaded deeper corneal layers (stroma). Surface signs may be subtle, but the infection is extensive underneath, leading to slow response to drops.

8. Superficial fungal keratitis
   Infection mainly on the surface layers (epithelium). May respond faster if treated early and correctly.

9. Chronic indolent fungal ulcer
   A long-lasting, slow, smoldering ulcer that improves and worsens in cycles—often seen with yeasts or with inadequate/partial treatment.

10. Endogenous fungal corneal ulcer (rare)
    Fungi spread from within the body (bloodstream) to the eye (usually in very ill or immunocompromised patients), then involve the cornea secondarily. Rare but serious.

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Causes

1. Eye trauma with plant material
   A scratch from a leaf, twig, husk, or hay pushes fungal spores into the cornea.

2. Dust or soil hitting the eye
   Soil often contains molds; micro-abrasions help fungi attach and grow.

3. Contact lens misuse
   Sleeping in lenses, over-wear, or poor cleaning allows fungus to colonize the lens or case.

4. Rinsing lenses or cases with tap water
   Water may carry fungi; never rinse lenses/cases with tap water.

5. Contaminated lens cases
   Old, cracked, or rarely cleaned cases support biofilms that harbor fungi.

6. Topical steroid eye-drop misuse
   Steroids suppress local immune defenses, letting fungi expand.

7. Long-term surface disease (dry eye, neurotrophic cornea)
   A weak surface cannot protect itself, making infection easier.

8. Prior corneal scars or herpetic keratitis history
   Uneven surfaces and reduced sensation make attachment and unnoticed injury easier.

9. Previous corneal surgery (LASIK, grafts, pterygium excision)
   Surgery disrupts normal barriers; sutures can harbor fungi.

10. Chronic antibiotic eye-drop use
    Wipes out normal bacteria that compete with fungi, shifting balance toward fungal overgrowth.

11. Immunosuppression (HIV, chemotherapy, transplant meds)
    Weakened bodily defenses make fungal infections more likely.

12. Diabetes mellitus
    High glucose impairs immune cells and delays healing.

13. Malnutrition (e.g., vitamin A deficiency)
    Poor nutrition weakens ocular surface integrity and immunity.

14. Traditional or home eye remedies
    Non-sterile substances (herbal oils, plant juices) can introduce fungi.

15. Occupational exposure (farming, gardening, carpentry)
    Frequent vegetative/wood dust contact increases risk.

16. Swimming or showering with lenses in
    Water exposure increases chance of microbe adherence to lenses.

17. Chronic blepharitis or meibomian gland dysfunction
    Inflammation and altered tear film destabilize the surface, making infection easier.

18. Chronic ocular allergy with frequent rubbing
    Rubbing causes micro-injuries that can seed infection.

19. Chemical eye injury history
    Alters corneal surface and tears, creating entry points for fungi.

20. Systemic steroid use
    Whole-body immune suppression lowers defense in the eye as well.

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Symptoms

1. Eye pain: Ranges from mild ache to severe, deep pain.

2. Redness: Inflamed blood vessels on the white of the eye (conjunctiva).

3. Tearing (watering): Reflex tears increase to protect and wash the surface.

4. Light sensitivity (photophobia): Bright light causes discomfort or spasm.

5. Blurred vision: The ulcer and swelling block or scatter light.

6. Foreign-body sensation: Feels like grit or sand in the eye.

7. Discharge: Often mucus-like; may be less thick than in some bacterial ulcers.

8. White or gray spot on the cornea: The ulcer itself appears as a whitish infiltrate.

9. Eyelid swelling: Lids puff up due to inflammation.

10. Difficulty opening the eye (blepharospasm): The eye reflexively closes to shield itself.

11. Decreased contrast or halos around lights: Light scatters through the cloudy cornea.

12. Dull, throbbing ache around the eye: From deeper inflammation.

13. Headache on the affected side: Referred pain from eye strain.

14. Feeling of dryness but with tearing: Tear quality is poor; eyes can feel paradoxically dry and watery.

15. Worsening over days rather than hours: Fungal ulcers often smolder and worsen more gradually than many bacterial ulcers.

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Diagnostic tests

Note: Doctors choose tests based on the look of the ulcer, its history (e.g., plant injury, contact lens habits), and severity. Not every patient needs every test. Some are to confirm fungus, some to rule out other causes, and some to assess complications.

A) Physical Exam tests

1. Visual acuity testing
   Reading letters (or symbols) measures how well you see. Baseline vision helps track progress.

2. Pupil light reflex check (RAPD test)
   A flashlight checks pupil reactions. An abnormal response (relative afferent pupillary defect) suggests deeper or optic pathway issues and flags severe disease.

3. Slit-lamp biomicroscopy of the cornea
   A microscope with a bright, narrow light examines ulcer size, depth, edges, satellite spots, feathery margins, surface texture, and any thinning. It also checks for infiltrates, epithelial defects, and corneal edema.

4. Anterior chamber assessment
   The doctor looks for cells and flare (inflammatory particles and protein in the eye’s front chamber) and for hypopyon (pus level). This indicates severity.

5. Lid eversion and conjunctival exam
   Flipping the eyelid checks for retained foreign bodies, debris, or line-of-sight irritation that could maintain infection.

B) Manual (bedside/office) tests

6. Fluorescein staining (with cobalt-blue light)
   A harmless orange dye highlights scratches and ulcers in bright green under blue light. It maps the epithelial defect and helps monitor healing.

7. Seidel test
   Uses fluorescein to see if aqueous fluid leaks from a corneal hole (perforation). A positive test means urgent care is required.

8. Corneal sensitivity testing (Cochet-Bonnet esthesiometer or cotton wisp)
   Checks nerve function of the cornea. Reduced sensation suggests neurotrophic issues or prior herpes, which change management.

9. Tonometry (intraocular pressure measurement) – with caution
   Measures eye pressure. In severe ulcers or suspected perforation, pressure testing may be deferred or done gently, because pressure can worsen a thin area.

C) Lab and Pathological tests

10. Corneal scraping for KOH (10%) wet mount
    The doctor gently scrapes the ulcer edge with a sterile tool to collect tissue. A potassium hydroxide (KOH) prep under a microscope can quickly show branching fungal filaments (hyphae). It’s fast and low-cost.

11. Gram stain
    Stains the sample to look for bacteria and may show yeast forms. Helpful when infection may be mixed (fungal + bacterial).

12. Giemsa stain
    Another stain that can highlight cellular detail and some fungal elements, aiding recognition.

13. Calcofluor white stain with fluorescence
    A special fluorescent dye that binds to fungal cell walls; under blue/UV light, fungal elements glow, making detection easier.

14. Culture on Sabouraud dextrose agar (SDA)
    The tissue is placed on fungus-friendly media to grow the organism and identify the exact fungus. Cultures can take days to weeks.

15. Culture on blood/chocolate agar (and other media)
    Helps detect bacteria (for mixed infections) and some yeasts, guiding combined therapy.

16. PCR (polymerase chain reaction) for fungal DNA
    A molecular test that looks for fungal genetic material. It can be very sensitive and faster than culture but may not be available everywhere.

D) Electrodiagnostic tests

17. Electroretinography (ERG)
    Measures electrical responses of the retina to light. If the cornea is so cloudy that the retina can’t be seen, ERG helps estimate retinal health for prognosis.

18. Visual evoked potential (VEP)
    Measures the electrical response from eyes to the brain’s visual cortex. Useful in selected severe cases to gauge overall visual pathway function when direct view is impossible.

E) Imaging tests

19. In vivo confocal microscopy (IVCM)
    A special microscope “scans” the living cornea, sometimes showing moving fungal filaments (hyphae) directly in the tissue. It can help confirm fungus and guide treatment.

20. Anterior segment optical coherence tomography (AS-OCT)
    Uses light waves to create cross-section images of the cornea, showing ulcer depth, thinning, and edges. Helpful for monitoring and surgical planning if needed.

Non-pharmacological treatments

1. Immediate eye protection (rigid shield, not a pressure patch) – prevents rubbing/trauma; a moist pressure patch can worsen infection, so shielding is preferred.

2. Stop contact-lens wear – lenses can harbor organisms; stopping removes a reservoir.

3. Strict hand/face hygiene – lowers re-inoculation risk.

4. Avoid topical steroid drops during active fungal infection – steroids worsen fungal growth and delay healing. Mechanism: local immunosuppression and altered flora. PMC

5. Pain and light-control (dark glasses, cycloplegic ordered by clinician) – reduces ciliary spasm and photophobia; improves comfort.

6. Frequent follow-up (initially daily) – monitors size/depth and adjusts therapy rapidly.

7. Mechanical debridement of necrotic epithelium – gently removes fungal load and improves drug penetration. Purpose: reduce organism burden and allow antifungals to reach stroma.

8. Therapeutic corneal scraping for culture/microscopy – doubles as both diagnosis and partial treatment (removes hyphae at the margin). American Academy of Ophthalmology

9. Discontinue non-prescribed/home remedies (rose water, herbal drops, steroids from pharmacy, topical anesthetics) – many are contaminated or harmful.

10. Control of systemic risks (optimize blood glucose; address immunosuppression) – better host response speeds healing. PMC

11. Protect from water exposure (no swimming/pond water) – reduces additional contamination.

12. Nutritional support for wound healing (adequate protein, vitamins A/C/Zinc) – supports epithelium and collagen repair (diet section below).

13. Avoid eye rubbing – prevents epithelial breaks and spread.

14. Limit contact with plant dust/soil during healing – lowers re-exposure risk.

15. UV protection outdoors – reduces photophobia and surface irritation.

16. Adherence coaching (alarms, family reminders) – antifungals are often hourly at first.

17. Tectonic support with tissue adhesive (cyanoacrylate) when thinning/perforation is small – acts like a waterproof patch while medicines work; bandage lens is usually avoided in infectious perforations. PMCEyeWiki

18. Temporary tarsorrhaphy (closing lids partially) – improves ocular surface protection in exposure risk.

19. Amniotic membrane transplantation (AMT) as an adjuvant in severe cases – biologic “bandage” that promotes epithelialization and may reduce inflammation; evidence supports faster healing and better scarring outcomes as an adjunct (quality of evidence low-to-moderate). NatureAnnals of Eye SciencePubMed

20. Photo-activated chromophore corneal cross-linking (PACK-CXL) as an adjunct in selected, therapy-resistant cases – UVA + riboflavin stiffens collagen and has antimicrobial effects; evidence is mixed and evolving, so it’s an add-on, not a replacement for antifungals. PMC+1ScienceDirect

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Evidence-based drug treatments

Important: Doses below reflect common adult regimens used by cornea specialists and in major trials. Exact dosing/compounding varies; pediatric, pregnant, and liver-/kidney-impaired patients require individualized care.

1. Natamycin 5% (topical) – Class: Polyene antifungal. Dose: Hourly while awake for 48 h, then every 1–2 h for 1–2 weeks, then taper over 4–6 weeks based on response. Purpose: First-line for filamentous fungi (Fusarium/Aspergillus). Mechanism: Binds ergosterol → membrane disruption → fungal death. Side effects: Ocular irritation, white surface deposits. Why first-line? In the MUTT I randomized trial, natamycin outperformed voriconazole for smear-positive filamentous ulcers (especially Fusarium). PubMedEyeWikiAmerican Academy of Ophthalmology

2. Voriconazole 1% (topical, compounded) – Class: Triazole. Dose: Hourly initially, then taper over weeks. Purpose: Alternative/adjunct, particularly for non-Fusarium mold or yeast ulcers, and salvage cases. Mechanism: Inhibits fungal 14-α-demethylase (ergosterol synthesis). Side effects: Irritation; systemic use may cause visual disturbances, hepatotoxicity, photosensitivity. Evidence: Less effective than natamycin for filamentous disease in MUTT I; useful as adjunct or for certain organisms. PubMed

3. Amphotericin B 0.15% (topical) – Class: Polyene. Dose: Every 1–2 h initially, then taper; often favored for Candida keratitis. Purpose: Yeast-predominant ulcers and as add-on in severe cases. Mechanism: Ergosterol binding. Side effects: Punctate keratopathy, irritation. American Academy of OphthalmologyEyeWiki

4. Voriconazole (oral) – Class: Triazole. Dose: Commonly 200 mg twice daily after a loading day (per specialist). Purpose: Add-on for deep/large ulcers, scleral spread, or high-risk organisms. Mechanism: Same as above. Side effects/monitoring: Liver tests, photosensitivity, drug–drug interactions. Evidence: MUTT II showed no overall visual benefit and more adverse events versus placebo; a subgroup with Fusarium had fewer perforations/TPK. Use is selective. PubMedAmerican Academy of OphthalmologyPMC

5. Itraconazole (oral ± compounded topical 1%) – Class: Triazole. Dose: 200 mg twice daily (specialist-guided). Purpose: Alternative systemic azole in resistant cases. Mechanism: Ergosterol synthesis inhibition. Side effects: Hepatotoxicity, drug interactions (CYP3A4). EyeWiki

6. Fluconazole (oral ± topical) – Class: Triazole. Dose: 200–400 mg/day systemically (organism-dependent). Purpose: Especially for Candida ulcers. Mechanism/SE: As above; generally fewer interactions than itraconazole/voriconazole. NCBI

7. Posaconazole (oral ± compounded topical 1%) – Class: Extended-spectrum triazole. Dose: Often 300 mg daily after loading (specialist). Purpose: Salvage therapy for azole-resistant molds. Mechanism/SE: As other azoles; significant interactions. (Evidence mainly case series.) PMC

8. Amphotericin B (intrastromal/intracameral) – Class: Polyene. Dose examples: Intrastromal ~2.5 µg/0.1 mL; intracameral 5–10 µg/0.1 mL (specialist-administered). Purpose: Drug depot near deep, recalcitrant ulcers. Mechanism: Direct high-local antifungal effect. SE: Local toxicity if overdosed. PMC

9. Voriconazole (intrastromal/intracameral) – Class: Triazole. Dose examples: Intrastromal 50 µg/0.1 mL, often in multiple quadrant “pockets.” Purpose: Rescue therapy for deep stromal disease not responding to drops. SE: Rare local toxicity; requires expert technique. PMCMDPIScienceDirect

10. Cycloplegic drops (e.g., atropine 1%) – Class: Antimuscarinic (supportive). Dose: 2–3×/day. Purpose: Pain relief, prevents synechiae. Mechanism: Paralyzes ciliary muscle and iris sphincter. SE: Blurred near vision, light sensitivity.

Notes
• During the first 48 hours, topical antifungals are often given hourly, then tapered according to response; courses commonly last weeks. NCBI
• Avoid topical steroids in the active fungal phase unless a cornea specialist adds them late to control scarring after organism control. PMC

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Dietary, molecular, and supportive” supplements

Evidence for nutrition/supplements in fungal keratitis is supportive/indirect (wound healing, epithelial health, immunity). Always check for drug interactions—especially with azole antifungals.

1. Vitamin A (retinol/beta-carotene) – e.g., carrots, pumpkin, eggs; supplement only if deficient. Function: Supports corneal epithelium and mucins. Mechanism: Epithelial gene regulation.

2. Vitamin C (ascorbate 500–1000 mg/day if tolerated) – Function: Collagen cross-linking and antioxidant protection during stromal healing.

3. Zinc (10–20 mg elemental/day) – Function: Cofactor in epithelial repair and immunity.

4. Vitamin E (200–400 IU/day) – Function: Antioxidant membrane protection.

5. Vitamin D (1000–2000 IU/day as advised) – Function: Immune modulation; correct deficiency.

6. Omega-3 fatty acids (e.g., fish oil 1–2 g EPA/DHA/day) – Function: Tear-film quality, anti-inflammatory support for the ocular surface.

7. Protein sufficiency (lean fish, eggs, dal/lentils, dairy) – Function: Collagen and tissue repair.

8. Probiotics (food-based yogurt/curd) – Function: Gut immune tone; avoid probiotic capsules if immunocompromised unless okayed by your doctor.

9. Hydration (2–3 L/day unless restricted) – Function: Mucosal health and drug distribution.

10. L-arginine (dietary sources: nuts/pulses) – Function: Nitric oxide for wound microcirculation (indirect).

11. Selenium (55 µg/day) – Function: Antioxidant enzymes (glutathione peroxidase).

12. Copper (food-based) – Function: Lysyl oxidase for collagen cross-linking.

13. B-complex (esp. B2 riboflavin in food) – Function: Epithelial metabolism; riboflavin is also the chromophore in PACK-CXL (procedure, not a supplement).

14. Avoid “ocular miracle” herbals (e.g., undiluted essential oils, raw honey in eye) – contamination risk; not recommended for ulcers.

15. Drug-interaction caution foods – grapefruit/Seville orange can raise azole levels; St. John’s wort lowers them (don’t use). (General azole–CYP3A4 interaction principle).

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Advanced/Regenerative” therapies

1. Autologous serum eye drops (ASEDs, 20–50%) – Patient’s own serum, 4–8×/day. Function: Delivers growth factors (EGF, vitamin A) to promote epithelial healing once infection is controlled. Mechanism: Mimics natural tears.

2. Platelet-rich plasma (PRP) eye drops – Concentrated platelets provide growth factors; dosing similar to ASEDs. Function: Epithelial/stromal healing support.

3. Amniotic membrane transplantation (AMT) – Biologic graft over the ulcer. Function: Anti-inflammatory matrix that speeds epithelialization and may improve scarring as an adjunct to antimicrobials. Evidence supports benefit as adjunct in infectious keratitis (low-to-moderate quality). Dose: Surgical placement; not a “drop.” NatureAnnals of Eye Science

4. Recombinant human nerve growth factor (cenegermin) – For neurotrophic keratopathy component (if present), 6×/day for 8 weeks; not an antifungal, but can aid epithelial closure once infection is controlled.

5. Limbal stem cell–based procedures (e.g., SLET/LSCT) – For eyes left with limbal stem-cell failure after severe ulcers; helps long-term surface stability. (Surgical, not a drug.)

6. PACK-CXL (see above) – Adjunctive UV-riboflavin procedure for select, therapy-resistant ulcers; protocols and efficacy are evolving; not a replacement for antifungals. PMC

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Surgeries

1. Therapeutic penetrating keratoplasty (TPK) – Replaces infected corneal tissue with a donor graft when medical therapy fails or if there is imminent/perforated cornea. Why: Removes organism load, restores globe integrity; about ~10–12% of fungal cases in some tertiary centers need TPK; earlier TPK in severe disease may reduce enucleation and improve outcomes. PMCDove Medical Press

2. Lamellar keratoplasty (DALK or lamellar patch) – Removes the diseased anterior layers while sparing endothelium if infection is superficial. Why: Structural support with potentially lower rejection risk.

3. Amniotic membrane transplantation (AMT) – Adjunct to help epithelial healing and reduce scarring/pain in moderate–severe ulcers. Why: Promotes surface recovery and can shorten hospitalization. PubMed

4. Cyanoacrylate tissue adhesive (“corneal glue”) – For small perforations (<2–3 mm) or severe thinning; often a temporary bridge before definitive grafting; bandage lens is typically avoided in infectious perforations. EyeWikiPMC

5. Tarsorrhaphy (temporary partial eyelid closure) – Protects the cornea in exposure/neurotrophic risk or after keratoplasty to support healing.

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Prevention tips

1. Wear protective eyewear during farming, gardening, or construction.

2. Rinse eyes with clean water after dust/plant injury and seek same-day eye care if pain or blurred vision develops.

3. Never start steroid eye drops without a doctor’s exam. PMC

4. For contact-lens users: perfect hygiene—daily cleaning, no overnight wear unless prescribed, no water exposure/swimming with lenses.

5. Replace lens cases regularly and avoid topping up solutions.

6. Manage diabetes and immunosuppression in partnership with your clinician. PMC

7. Avoid home remedies and non-sterile eye products.

8. Finish the full antifungal course; do not stop when the eye “looks better.”

9. Protect healing eyes from dust/soil and bright sun (shields and sunglasses).

10. Know your region’s risks (humid/rural = higher risk); seek care early after any plant-related eye trauma. PubMed

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When to see a doctor

• Immediately (same day) for eye injury with plant/soil, new corneal pain/redness + blurred vision, white spot on the cornea, discharge, light sensitivity, contact-lens discomfort that doesn’t settle quickly, or any leak/tearing that seems like fluid is seeping.

• Emergency if there’s sudden severe pain relief + worsening blur (possible perforation), pus level in the eye (hypopyon), or systemic fever with eye pain.

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What to eat and what to avoid

1. Eat for healing: protein-rich foods (fish such as hilsa/ruhi, eggs, dal), plus vitamin-A foods (carrot, pumpkin, spinach, egg yolk), vitamin-C fruits (guava, amla, citrus), and zinc sources (beans, nuts).

2. Stay well hydrated.

3. Limit refined sugar if you have diabetes (better infection control).

4. Avoid alcohol while on systemic azoles (liver stress).

5. Avoid grapefruit and Seville orange—they can dangerously increase azole levels (CYP3A4).

6. Avoid St. John’s wort—it can reduce azole levels (CYP induction).

7. No raw or homemade eye applications (honey, oils, rose water).

8. Balanced fats: include natural omega-3s (fish, walnuts).

9. Regular small meals if nausea from meds—protect the stomach.

10. Discuss any supplements with your doctor to avoid interactions.

11. Natamycin 5% is first-line for filamentous fungal keratitis. The MUTT I randomized trial found natamycin superior to voriconazole for smear-positive filamentous ulcers (especially Fusarium). PubMed

12. Adding oral voriconazole to topical therapy did not improve overall outcomes and increased adverse events in MUTT II; a Fusarium subgroup showed fewer perforations/transplants—hence selective use. PubMedPMC

13. Intrastromal voriconazole/amphotericin can help deep, refractory ulcers by delivering high drug levels into the stroma. PMC

14. AMT can speed epithelial healing and improve scarring outcomes as an adjunct in infectious keratitis. Nature

15. TPK is timely rescue when medical therapy fails or the cornea perforates; earlier surgery in severe disease may improve outcomes. PMCDove Medical Press

16. PACK-CXL is a promising adjunct but not yet a substitute for antifungals; evidence and protocols are evolving. PMC+1

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Frequently asked questions

1) Is a mycotic ulcer contagious between people?
No, it’s not “catchy” person-to-person. It comes from fungi entering your own cornea (often after trauma or lens problems).

2) How soon should I start treatment?
Immediately. Delay increases the chance of scarring, perforation, and transplant.

3) Why must I use drops so often at first?
Fungi are hard to kill. Hourly drops for 1–2 days (then frequent dosing) keep drug levels high in the cornea where the organisms live. NCBI

4) Can I use steroid drops to reduce redness?
Not during active fungal infection—steroids worsen it. They’re sometimes added later by specialists after the fungus is controlled to limit scarring. PMC

5) How long will treatment last?
Often weeks. Doctors taper slowly to prevent relapse.

6) Will I need surgery?
Most people heal with medicines, but some need corneal glue or a corneal transplant (TPK) if the ulcer is deep, large, or perforated. PMC

7) Are contact lenses safe after I heal?
Ask your cornea specialist. Many patients can wear lenses again later with strict hygiene, but some need glasses if scarring changes corneal shape.

8) Can I go to work while healing?
If your job exposes you to dust/plant debris or needs sharp vision, take leave until your doctor clears you.

9) Does diet really matter?
Diet won’t kill fungi, but protein, vitamins A/C, zinc, and omega-3s support healing tissues.

10) Are “natural” eye drops safe?
No home-made or non-sterile preparations should go in the eye—contamination risk is high.

11) Will I need oral antifungals?
Sometimes, for deep or severe disease. Your doctor weighs benefit vs. side effects (e.g., liver effects, interactions). PubMed

12) What about cross-linking (PACK-CXL)?
It may be used as an add-on in tough cases; it’s not a standard stand-alone cure. PMC

13) Can I drive?
Not until your vision is stable and your clinician says it’s safe.

14) Will my vision fully recover?
Many recover well; others may have a scar. Earlier treatment improves the odds.

15) How do I avoid this in the future?
Eye protection, perfect lens hygiene, and no steroid eye drops without an exam. PMC

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 13, 2025.

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