Pseudomonas Keratitis

Pseudomonas keratitis is a serious infection of the cornea—the clear, dome-shaped window at the front of the eye—caused by a bacterium called Pseudomonas aeruginosa. This germ can attach to the corneal surface, invade the corneal tissue, and trigger intense inflammation that can melt the corneal layers quickly. The disease can start suddenly, worsen over hours, and, if not treated promptly, can leave a white scar, create a hole in the cornea, or cause permanent vision loss. Doctors consider it an eye emergency because the infection can spread deeply, the cornea can thin fast, and sight can be damaged in a short time. Contact lens wear (especially sleeping in lenses or water exposure with lenses in) is a common setting, but the infection can also happen after trauma, surgery, or in people with a dry or unhealthy eye surface. Evidence-based guidelines emphasize that bacterial keratitis—including Pseudomonas—progresses rapidly and needs early culture and strong topical antibiotics to protect vision. American Academy of Ophthalmology+1NCBI

Pseudomonas keratitis is a serious infection of the clear window at the front of the eye (the cornea) caused mostly by the bacterium Pseudomonas aeruginosa. It can start quickly, spread fast through the cornea, and melt corneal tissue if not treated right away. People who wear contact lenses are at higher risk, especially with poor lens hygiene or if lenses touch water. Typical signs include severe pain, redness, light-sensitivity, a dense white or yellow-green spot in the cornea, and sometimes a layer of pus in the front of the eye (hypopyon). Early, intensive care is essential to protect sight. American Academy of OphthalmologyEyeWikiNCBIVagelos College

Pathophysiology

Pseudomonas aeruginosa sticks to damaged or unprotected corneal cells and forms a slimy protective layer called a biofilm. The bacteria release powerful enzymes and toxins that break down the corneal stroma, the thick middle layer that gives the cornea strength and clarity. The body’s immune response brings many white blood cells into the cornea, which helps fight the germs but also adds swelling, pus, and tissue breakdown. Because Pseudomonas can resist many antibiotics and can move through tissue quickly, the cornea can soften, thin, and even perforate if treatment is delayed. This mix of bacterial tools (like proteases) and strong inflammation explains the fast pace, the pus-filled ulcer, the risk of a ring-shaped abscess, and the sudden drop in vision. NaturePMC

This infection often progresses faster than many other corneal infections. In hours to a day, patients can go from mild irritation to severe pain, thick discharge, a visible white spot or gray-green ulcer, a layered white fluid in the front chamber (hypopyon), and a major drop in vision. The combination of quick tissue melt and antibiotic resistance patterns means waiting is risky; the safest approach is fast diagnosis, microbiology testing when indicated, and immediate, high-frequency topical antibiotics. Clinicians often start with a fourth-generation fluoroquinolone or “fortified” compounded antibiotic drops for severe ulcers, while cultures guide the final choice. American Academy of OphthalmologyPMCMedscape

The classic story is a soft contact lens wearer who sleeps in lenses, cleans them poorly, or wears lenses in the shower, pool, or hot tub. Water exposure plus lenses creates a friendly home for Pseudomonas, and poor case hygiene lets the germ grow and stick to the lens and eye. But the infection also appears after corneal scratches, foreign bodies, ocular surgery, or in people with chronic surface disease or reduced corneal sensation. Population studies and reviews consistently link contact lens wear—especially with water exposure and overnight wear—to microbial keratitis and to Pseudomonas specifically. PMC+1BMJ Ophthalmologyemra.org

Types of Pseudomonas keratitis

1) Contact lens–associated Pseudomonas keratitis.
This is the most common real-world scenario. The infection starts under or around the lens, often after overnight wear or water exposure, and can spread quickly because the lens reduces oxygen and traps bacteria against the cornea. The ulcer may be central or paracentral, and the discharge can be heavy.

2) Trauma-related Pseudomonas keratitis.
Here the cornea is scratched by a foreign body, plant material, sand, or dust contaminated with bacteria. The break in the surface lets Pseudomonas enter, and the infection can take hold in the torn area and move inward.

3) Post-surgical Pseudomonas keratitis.
After corneal or refractive surgery, sutures, incisions, or epithelial defects can act as doors for bacteria. The early healing period is a vulnerable time because the surface barrier is weak and steroid drops may be used.

4) Hospital- or ICU-related keratitis (exposure keratopathy setting).
Sedated or ventilated patients may not blink fully. The cornea dries and becomes exposed, which weakens the surface and invites infection by aggressive organisms like Pseudomonas.

5) Keratitis in eyes with unhealthy surfaces.
Dry eye disease, severe blepharitis, meibomian gland dysfunction, vitamin A deficiency, or autoimmune surface disease can reduce tear protection and create tiny breaks where bacteria can attach.

6) Neurotrophic keratitis with secondary infection.
When corneal sensation is poor (after herpes, diabetes, or nerve injury), patients may not feel pain, and small defects grow unnoticed. Pseudomonas can colonize these defects and progress quickly.

7) Fulminant acute ulcer (rapid melt).
This pattern features a large, dense creamy infiltrate with overlying epithelial loss, copious discharge, and a hypopyon. It can thin the cornea fast and is the pattern most likely to perforate.

8) Perforated or impending-perforation keratitis.
In advanced cases the cornea can become so thin that aqueous fluid leaks through (positive Seidel sign) or a small hole forms. This is a true emergency that may require urgent surgical support.

9) Mixed-pathogen keratitis with Pseudomonas predominance.
Sometimes other bacteria are present, or the surface also harbors fungi or Acanthamoeba. Cultures guide therapy when features are atypical or the response is poor.

10) Healing and scar phase after Pseudomonas keratitis.
After control of infection, the cornea can scar and become irregular. Vision may remain blurred from haze, thinning, or irregular astigmatism that sometimes needs specialty contact lenses or surgery.

Causes

1. Soft contact lens wear. Lenses can trap bacteria against the cornea and reduce oxygen, making it easier for Pseudomonas to stick and grow. Poor cleaning makes the risk higher. PMC

2. Sleeping in contact lenses. Overnight wear dries the surface and lets bacteria remain in place for many hours, which increases the chance of infection. Frontiers

3. Showering, swimming, or hot tubs while wearing lenses. Water contains microbes that can cling to lenses and move to the cornea; hot tubs are a classic risk. BMJ Ophthalmologyemra.org

4. Dirty or old lens cases. Bacteria form biofilms in cases and then transfer to lenses and the eye; infrequent case replacement increases risk. PMC

5. Homemade saline or tap-water rinsing. Non-sterile liquids carry germs; using them to rinse lenses or cases introduces bacteria to the eye. PMC

6. Corneal trauma (scratches or foreign bodies). A scratch breaks the surface barrier, creating an entry point for bacteria from soil, water, or the skin.

7. Ocular surgery or sutures. Fresh wounds and sutures can harbor bacteria, especially if the surface is slow to heal.

8. Topical steroid use without proper supervision. Steroids can slow surface healing and weaken local immune defenses, allowing bacteria to multiply. American Academy of Ophthalmology

9. Topical anesthetic abuse. Repeated numbing drops damage the corneal surface and reduce healing, which invites infection.

10. Dry eye disease and severe blepharitis. An unstable tear film and inflamed lids reduce natural antibacterial protection and create micro-defects.

11. Meibomian gland dysfunction. Poor oil layer causes evaporation and surface stress, making small defects more likely.

12. Neurotrophic cornea (reduced corneal sensation). When the cornea cannot feel pain, small injuries persist and bacteria can colonize them.

13. Diabetes mellitus. High blood sugar impairs wound healing and local immunity, which makes infections more likely and slower to heal.

14. Systemic immunosuppression. Chemotherapy, steroids, or immune diseases reduce the body’s ability to control bacteria on the eye.

15. Vitamin A deficiency or malnutrition. A poor ocular surface and weak mucosal defenses allow germs to stick and invade.

16. Chronic exposure or poor eyelid closure. Incomplete blinking or nighttime lagophthalmos dries the cornea and promotes surface breakdown.

17. Contaminated cosmetic tools or eye makeup. Shared or old applicators can transfer bacteria to the lid margin and corneal surface.

18. Contaminated eye drops or improper drop-bottle handling. Touching the bottle tip to the eye or lashes can seed bacteria into the bottle and back to the cornea.

19. Contact lens overwear or poor fit. Tight lenses reduce oxygen and rub the epithelium, causing micro-abrasions that bacteria can exploit.

20. Previous corneal disease or scar. Old scars or dystrophies can create rough surfaces where bacteria adhere more easily.

Symptoms

1. Eye pain that builds quickly. The cornea has many nerves, so infection causes sharp pain that can escalate in hours.

2. Redness of the white of the eye. Inflamed blood vessels crowd the area around the cornea, creating a red ring.

3. Blurry or smeared vision. Swelling, discharge, and a central ulcer scatter light and reduce clarity.

4. Tearing or watery eye. The eye tries to wash away irritants, so tears increase.

5. Thick or greenish discharge. Bacteria and white cells create pus and mucus that stick to the lashes.

6. Light sensitivity (photophobia). Inflamed cornea and iris make bright light painful.

7. Foreign-body sensation. The rough ulcer edge feels like grit in the eye.

8. Visible white or gray spot on the cornea. The pus-filled infiltrate can be seen as a white area in the clear cornea.

9. Eyelid swelling and crusting. Inflammation spreads to the lids and lashes, adding heaviness and crusts.

10. Rapid worsening over hours. Unlike many minor irritations, this infection can deteriorate the cornea quickly. WebEye

11. Decreased ability to wear contact lenses. Lenses become intolerable due to pain and discharge.

12. Headache or brow ache. Pain can radiate around the orbit and forehead.

13. Haloes or glare. Irregular corneal surface and edema cause light scatter.

14. Aching with eye movement. Inflammation and pressure on sensitive tissues can make movements uncomfortable.

15. A white fluid level inside the eye (hypopyon)—seen by the doctor. Pus settles in the front chamber and signals a strong response to infection. WebEye

Diagnostic tests

A) Physical examination (simple bedside/clinic observations)

1. Visual acuity (distance and near). Reading chart results set the baseline and track recovery; a sudden drop suggests central involvement.

2. External exam of lids and lashes. The doctor looks for crusting, blepharitis, meibomian blockage, or trauma that could seed the cornea.

3. Slit-lamp biomicroscopy of the cornea. A microscope with a bright beam shows the ulcer’s size, depth, edges, and any ring-shaped abscess; Pseudomonas ulcers often look dense, wet, and suppurative. The exam also checks for surrounding edema and thinning that signal risk of perforation. NCBIWebEye

4. Anterior chamber assessment for cells, flare, and hypopyon. Inflammation inside the eye indicates severe disease and helps decide on culturing and treatment intensity. PMC

5. Intraocular pressure (IOP) measurement. Pressure can be low if the eye is inflamed or leaking, but applanation is avoided if the cornea looks very thin; handheld methods and caution are used.

6. Eyelid eversion and fornix inspection. Flipping the lid reveals hidden foreign bodies or exposed areas that keep scratching the cornea.

B) Manual tests (simple tools and hands-on checks)

7. Fluorescein staining of the cornea. A dye highlights epithelial defects as bright green under blue light; the pattern shows ulcer size and whether there is active leakage.

8. Seidel test for perforation. After fluorescein, a flowing stream of dye indicates aqueous leakage through a thin spot or hole.

9. Corneal sensitivity testing (Cochet-Bonnet esthesiometer). Reduced sensation suggests a neurotrophic cornea, which heals poorly and needs special care.

10. Lid margin and lash sampling/fornix sweep. A sterile swab or sweep can remove debris and, if indicated, provide material for culture.

11. Contact lens and case inspection (chairside review). The clinician examines care habits, checks dates, and may decide to culture the lens and case if they are suspected sources.

C) Laboratory and pathological tests (definitive organism work-up)

12. Corneal scrapings for Gram stain. A small sterile blade or spatula collects cells from the ulcer edge; Gram stain often shows Gram-negative rods in Pseudomonas and guides immediate therapy while cultures grow. American Academy of Ophthalmology

13. Giemsa or modified stains. These can highlight inflammatory cells and rule out atypical organisms when the picture is unclear.

14. Bacterial culture on appropriate media. Samples are plated on blood and chocolate agar (and, when available, selective media such as cetrimide) to grow Pseudomonas for identification. Culturing is especially recommended for severe, central, large, or unresponsive ulcers. American Academy of Ophthalmology+1

15. Contact lens and case cultures. Culturing the lens, solution, and case can confirm the source and match it to the corneal isolate.

16. Antibiotic susceptibility testing (disk diffusion or MIC). Lab testing reports which antibiotics work best against the specific strain so drops can be tailored, which is important because Pseudomonas can resist many drugs. Nature

17. Rapid molecular testing (PCR or 16S rRNA sequencing). When cultures are negative or the patient has received antibiotics, molecular tests can detect bacterial DNA and help confirm the diagnosis.

18. MALDI-TOF mass spectrometry identification. Many labs now use MALDI-TOF to identify bacteria directly from culture colonies quickly and accurately.

19. Simple biochemical tests (oxidase and pigment observation). Pseudomonas aeruginosa is oxidase-positive and may produce characteristic pigments; these classic tests still support identification in many labs.

20. Cytology of ulcer scrapings (rarely needed). Microscopic review can document the inflammatory pattern and rule out other causes when results conflict.

D) Electrodiagnostic tests (rare, for special situations)

21. Visual Evoked Potential (VEP). If the cornea is opaque and vision is very poor, a VEP can confirm whether the visual pathway still conducts signals, which can inform long-term prognosis.

22. Electroretinogram (ERG). In extreme cases with suspected endophthalmitis or retinal compromise, an ERG can help confirm whether the retina is functioning, although this is not routine for keratitis.

E) Imaging tests (to map severity and complications)

23. Anterior Segment Optical Coherence Tomography (AS-OCT). AS-OCT is a non-contact scan that measures ulcer depth, shows thinning, and tracks healing over time; it helps judge risk of perforation and guides shielding or glue if needed.

24. B-scan ultrasonography. When the cornea is too opaque to see through, a B-scan checks the vitreous and retina for signs of spread (such as endophthalmitis) and confirms that the back of the eye is intact.

Non-pharmacological treatments (therapies & “other” care)

These are supportive steps and procedures that work alongside prescription eye drops and, when needed, surgery. They do not replace antibiotics.

1. Stop contact lenses immediately and keep the lens, case, and solution for culture. Stopping lens wear removes a continuing source of germs; sending the lens/case helps the lab identify the exact microbe and its drug sensitivities. American Academy of Ophthalmology

2. Urgent eye specialist assessment and corneal scraping for culture. A doctor gently scrapes the ulcer edge to reduce germ load and to culture the organism so treatment can be precisely targeted. American Academy of Ophthalmology

3. Gentle epithelial debridement when indicated. Removing loose, dead surface tissue can lower bacterial burden and improve antibiotic penetration into the cornea. PMC

4. Protective eye shield (no pressure patch). A rigid shield protects the cornea from accidental trauma while allowing oxygen; patches that press on the eye are avoided in active bacterial ulcers. American Academy of Ophthalmology

5. Hospital admission for severe disease or poor adherence. In very painful, large, central, or melting ulcers, admission allows round-the-clock dosing, monitoring, and fast changes to therapy. American Academy of Ophthalmology

6. Strict hand hygiene for anyone touching the drops or eyelids. Clean hands reduce re-seeding bacteria onto the eye during frequent drop schedules. CDC

7. No water to the eye and no showering or swimming exposure. Water contains microbes, including Pseudomonas; keeping water away prevents new contamination during healing. CDCLippincott Journals

8. Sunglasses and dim-light rest for photophobia. Light sensitivity is common; dark lenses reduce pain and eyelid squeezing so the drops can work.

9. Frequent follow-up with documented size/depth/photos. Close review lets the clinician catch worsening early and escalate care in time. American Academy of Ophthalmology

10. Education and written drop timetable. Bacterial ulcers often need drops every 5–60 minutes at first; a written schedule helps adherence and prevents missed doses. PMC

11. Nutrition and hydration support. Good protein and vitamin C intake support collagen repair as the cornea heals; dehydration is avoided to support tear film. PMC

12. Glycemic control in diabetes. Better blood sugar control improves corneal healing and lowers risk of infection spreading; clinicians often coordinate with primary care.

13. Manage eyelid disease after the acute phase. Once safe, gentle lid hygiene reduces bacterial load at the lid margin and lowers future risk.

14. Pain coping strategies (rest, mindfulness breathing, cold compress on the brow/cheek—not on the eye). Comfort measures reduce stress and enhance adherence.

15. Avoid topical steroids unless and until your cornea specialist advises. Steroids can worsen infection if used too early; some cases may benefit later under close supervision.

16. Pack-CXL (photoactivated chromophore for infectious keratitis, “PACK-CXL”) as an adjuvant in selected, non-responding cases. Riboflavin plus controlled UV-A can stiffen corneal collagen and has antimicrobial effects; evidence is mixed and it’s considered case-by-case.

17. Avoid contact lens wear until complete medical clearance. Early re-wear risks relapse; your doctor will advise when it is truly safe. American Academy of Ophthalmology

18. Replace or discard old lens cases and cosmetics. These items can harbor biofilms; replacing them prevents re-contamination. CDC

19. Protect the ocular surface during sleep. A shield or physician-directed eyelid taping reduces accidental rubbing during the most fragile phase.

20. Rehabilitation planning once infection is cured. If scarring reduces vision, later options can include specialty contact lenses (e.g., scleral lenses) or surgery for visual rehabilitation. American Academy of Ophthalmology

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Drug treatments

Doses below are typical starting points; your cornea specialist adjusts based on ulcer size, depth, response, and lab results.

1. Fortified tobramycin (aminoglycoside) — Class/Mechanism: 30S ribosome inhibitor, strong anti-pseudomonal activity. Dose/Time: Compounded ~14 mg/mL, often alternating hourly with a β-lactam for severe ulcers; every 5 min for 30 min as a loading dose may be used, then hourly; taper over weeks as healing allows. Purpose: Rapid kill and penetration into the ulcer. Side effects: Surface toxicity/epitheliopathy and stinging; very rarely allergy. PMCScienceDirect

2. Fortified amikacin (aminoglycoside) — Class/Mechanism: 30S inhibitor; sometimes used if gentamicin/tobramycin are not ideal. Dose/Time: Compounded (e.g., 50 mg/mL) hourly initially; taper with improvement. Purpose: Alternative potent gram-negative coverage. Side effects: Surface irritation/epithelial toxicity. ScienceDirect

3. Fortified ceftazidime (β-lactam, 3rd-gen cephalosporin) — Mechanism: Blocks cell-wall synthesis; excellent anti-pseudomonal activity. Dose/Time: Compounded 50 mg/mL, often alternated hourly with an aminoglycoside in severe disease. Purpose: Backbone anti-Pseudomonas agent. Side effects: Mild surface irritation; rare allergy. PMCDe Gruyter Brill

4. Ciprofloxacin 0.3% (fluoroquinolone) monotherapy — Mechanism: DNA gyrase/topoisomerase IV inhibitor; good Pseudomonas activity. Dose/Time: Every 5–15 min for the first hour, then hourly around the clock for 24–48 h; taper with response. Purpose: Effective monotherapy for many bacterial ulcers, including Pseudomonas, with less ocular toxicity than some fortified regimens. Side effects: Bitter taste, mild irritation; rare white corneal precipitate. PubMedPMC

5. Ofloxacin 0.3% (fluoroquinolone) monotherapy — Similar role to ciprofloxacin; dosing and tapering like above. Some series show non-inferiority to fortified combinations with fewer side effects. PMC

6. Gatifloxacin 0.3% or moxifloxacin 0.5% (newer FQs) — Broad spectrum; often preferred for gram-positives, but still used broadly while awaiting culture results. Hourly initially; taper as guided. Note: For classic Pseudomonas, older FQs like ciprofloxacin may retain stronger in-vitro activity; your doctor chooses based on local resistance. MedscapePMC

7. Topical piperacillin-tazobactam (compounded) — Considered for resistant strains after culture results. Dosing is intensive (e.g., hourly) and tailored by the specialist. Purpose: Salvage therapy when standard drugs fail. Side effects: Surface irritation. PubMedScienceDirect

8. Topical colistin/colistimethate (polymyxin E) for MDR Pseudomonas — Used when cultures show multi-drug resistance; compounded (e.g., ~0.19–1.6% based on series) with hourly dosing early on. Purpose: Rescue therapy with activity against some highly resistant isolates. Side effects: Surface toxicity possible. PMC

9. Cycloplegic drops (e.g., atropine 1% or homatropine 2–5%) — Class/Mechanism: Paralyzes the ciliary muscle and dilates the pupil. Dose/Time: Usually 1–3×/day. Purpose: Relieves deep aching pain and prevents iris adhesions while the infection heals. Side effects: Light sensitivity, blurry near vision. EyeWiki

10. Oral doxycycline 100 mg twice daily (adjunct) — Class/Mechanism: Tetracycline antibiotic with anti-collagenase and MMP-9–modulating effects; used to reduce corneal melting risk. Time: Often for 1–2 weeks or as directed. Side effects: GI upset, photosensitivity; avoid in pregnancy/children. Lippincott JournalsPMC

How often are drops used at first? Severe ulcers are typically started with a loading dose (every 5 min for 30 min) and then hourly around the clock for the first 24–48 hours; frequency is tapered only after clear clinical improvement. Your doctor individualizes this schedule. PMC

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Dietary molecular supplements

Supplements do not kill bacteria; they may support the body’s healing after the correct antibiotics are started. Always confirm dosing with your clinician, especially if pregnant, on anticoagulants, or with kidney/liver disease.

1. Vitamin C (ascorbic acid) — Dose: 500–1000 mg/day (oral) is commonly used in eye practice; IV vitamin C may be considered in hospital settings. Function/Mechanism: Cofactor for collagen cross-linking; may reduce corneal thinning and scarring; one clinical study found smaller residual opacity in infectious keratitis with systemic vitamin C. PMC

2. Vitamin A (dietary or medically supervised supplementation if deficient) — Function: Essential for healthy corneal epithelium; deficiency can cause corneal ulcers and melting (keratomalacia). Note: Do not self-dose high vitamin A without supervision. World Health OrganizationIris

3. Omega-3 fatty acids (EPA/DHA) — Dose: Many use ~1000 mg/day combined EPA+DHA from fish oil; evidence for dry-eye support is mixed, but omega-3s can modulate surface inflammation and tear film quality during recovery. New England Journal of MedicinePMC

4. Zinc (e.g., zinc gluconate 15–30 mg/day) — Function: Cofactor in immune function and epithelial repair; older ocular studies and wound-care data support a role in healing, but evidence is indirect for keratitis. PMC

5. Vitamin D (check level; supplement if low) — Function: Immunomodulatory effects that can calm ocular surface inflammation; small studies suggest benefits in dry eye and surface health. PMCLippincott Journals

6. Adequate protein (food or shakes) — Function: Supplies amino acids for new tissue. Protein malnutrition slows corneal and skin wound repair. PMC

7. Arginine (as part of supervised wound-healing formulas) — Dose: Often 3–9 g/day in medical nutrition products; can support collagen deposition and immune responses in general wound literature. Use only with clinician guidance. PubMedScienceDirect

8. Hydration and electrolytes — Function: Good hydration supports tear production and ocular surface physiology during intensive drop therapy.

9. Balanced antioxidants from food (berries, citrus, leafy greens) — Function: Provides vitamin C and other antioxidants that support cellular repair. PMC

10. Avoid high-dose unsupervised supplements that claim to “boost immunity.” Over-supplementation can interact with medicines or delay proper care; the priority is targeted antibiotics plus clinician-directed adjuncts. (General safety guidance.)

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Regenerative / “hard immunity booster” / stem-cell-related therapies

There is no proven “immunity booster drug” that cures Pseudomonas keratitis. The options below support healing the corneal surface after the infection is controlled, and some are used in parallel for stubborn epithelial defects—only under specialist care.

1. Cenegermin (recombinant human nerve growth factor, 20 µg/mL) — Dose: 1 drop six times daily for 8 weeks. Function: Heals neurotrophic corneal defects by restoring corneal nerve health; used when infection has triggered or unmasked neurotrophic keratopathy. Evidence: Two randomized, vehicle-controlled trials showed higher complete-healing rates. ScienceDirectPMC

2. Autologous serum tears (20–100%) — Dose: Often 4–8×/day (regimens vary). Function: Patient’s own serum contains growth factors (EGF, vitamin A, fibronectin) that promote epithelial healing. Evidence: Reviews and technology assessments support use in severe dry eye and persistent epithelial defects, with generally good safety. AAO JournalAmerican Academy of Ophthalmology

3. Platelet-rich plasma (PRP) eye drops — Dose: Typically 4–8×/day; protocol individualized. Function: Delivers platelet growth factors to speed re-epithelialization; used for persistent epithelial defects after infections or surgery. Evidence: Prospective studies and series support improved healing. PMC+1

4. Matrix-regenerating agent (RGTA; e.g., Cacicol) — Dose: Often every 2–3 days for several weeks. Function: Heparan sulfate mimetic that protects and organizes extracellular matrix to aid epithelial healing. Evidence: Case series suggest benefit in difficult neurotrophic ulcers; evidence base is emerging. PubMedScienceDirect

5. Topical insulin (compounded) for persistent epithelial defect — Dose: Specialist-directed; drops are diluted from regular insulin. Function: Promotes epithelial cell migration and closure in neurotrophic or post-infectious defects. Evidence: Protocols are evolving; clinicians may consider after standard care. Nature

6. Amniotic membrane (device or extract) — see surgery section for in-office membrane placement; as drops (AMEED), protocols vary and evidence is developing. It supplies a biologic scaffold and anti-inflammatory factors to help stubborn defects re-epithelialize.

Important: These regenerative options do not replace antibiotics. They are considered when the surface won’t heal, when nerves are damaged, or when the cornea is at risk of melting/perforating despite infection control.

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Surgeries

1. Therapeutic penetrating keratoplasty (TPK) — The infected, melted central cornea is removed and replaced with a donor corneal button. Why: To eliminate infection not responding to drops and to save the globe when perforation is imminent or present. PMC

2. Deep anterior lamellar keratoplasty (DALK) — Diseased anterior cornea is removed while keeping the patient’s own endothelium. Why: When infection is superficial and controlled but scarring ruins vision; reduces rejection risk compared with a full-thickness graft. PMC

3. Amniotic membrane transplantation (AMT/PROKERA) — A biologic membrane is placed on the cornea in clinic or OR. Why: To cover and heal persistent epithelial defects, reduce inflammation, and stabilize thinning.

4. Temporary tarsorrhaphy — Partially sewing the eyelids together to protect the cornea. Why: To reduce exposure and promote healing when blinking is poor or defects keep reopening. CDC

5. Conjunctival flap (Gundersen flap) — Bringing vascularized conjunctiva over a chronically non-healing cornea. Why: Last-resort tectonic support and pain relief in eyes with poor healing potential. PMC

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Prevention steps

1. Never sleep in contact lenses unless your doctor specifically prescribes it. Overnight wear is a major risk. American Academy of Ophthalmology

2. Keep lenses away from all water (tap, shower, pool, hot tub). Water is not sterile and can carry Pseudomonas. CDCLippincott Journals

3. Wash and dry hands before handling lenses. CDC

4. Rub-and-rinse lenses with fresh solution; never “top off.” Replace solution every time. CDC

5. Replace the lens case at least every 3 months and let it air-dry daily. CDC

6. Use daily disposable lenses if possible to lower risk from case/solution issues. PMC

7. Remove lenses at the first sign of redness, pain, or blurred vision, and arrange an eye exam the same day. American Academy of Ophthalmology

8. Never make homemade saline or solution. Only use sterile commercial products. SELF

9. Do not share eye cosmetics; discard any that touched an infected eye. CDC

10. Regular checkups with your eye-care professional if you wear lenses. American Academy of Ophthalmology

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When to see a doctor

• Immediately (same day) if you have eye pain, light sensitivity, sudden blur, discharge, or a new white spot on the cornea, especially if you wear contact lenses. Pseudomonas ulcers can worsen within hours. Vagelos College

• Urgently if pain worsens after starting drops, if you see a dark “pit” or bulging thin spot, or if a hypopyon develops—these are danger signs for melting or perforation. NCBI

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What to eat” and “what to avoid

Eat more of 

1. Citrus, kiwi, berries, peppers for vitamin C to support collagen. PMC

2. Leafy greens, carrots, eggs, dairy (if tolerated) for vitamin A to support surface cells. World Health Organization

3. Fatty fish (salmon, sardine, mackerel) for omega-3s that may calm surface inflammation. PMC

4. Lean proteins (fish, poultry, legumes, tofu, dairy) to supply healing amino acids. PMC

5. Nuts/seeds and whole grains for minerals (including zinc) that assist healing. PMC

Avoid or limit 

1. Alcohol excess and smoking, which impair wound healing.
2. Sugary drinks and ultra-processed foods that displace nutrient-dense options.
3. Unverified “immune booster” megadoses without your doctor’s OK.
4. Contact lenses until your specialist says it’s safe. American Academy of Ophthalmology
5. Eye makeup until fully healed; then replace old products. CDC

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FAQs

1. Can Pseudomonas keratitis cause blindness?
   Yes—if treatment is delayed or the infection is very aggressive, scarring or perforation can severely reduce vision; early, intensive care prevents this in most cases. NCBI

2. Is it contagious person-to-person?
   Casual spread is unlikely; it usually comes from environmental exposure (especially water or lens cases) to the cornea’s surface. Good hygiene protects others. CDC

3. Why are contact lenses a big risk?
   They can carry microbes and reduce oxygen, and the case/solution can grow biofilms; water exposure adds dangerous germs. American Academy of OphthalmologyLippincott Journals

4. How fast can it worsen?
   Very fast—hours to days—because Pseudomonas produces tissue-damaging enzymes and toxins. PMC

5. Do I always need cultures?
   For moderate to severe ulcers, yes—cultures guide targeted therapy and help if the ulcer fails first-line treatment. American Academy of Ophthalmology

6. Are fluoroquinolones enough on their own?
   Many ulcers respond to monotherapy with ciprofloxacin/ofloxacin; severe Pseudomonas ulcers often start with fortified combination drops. Your doctor chooses based on severity and local resistance. PubMedPMCScienceDirect

7. Why so many drops at first?
   High, frequent dosing quickly overwhelms bacteria in the corneal tissue; dosing is tapered only after clear improvement. PMC

8. Can I use steroid drops?
   Not at the start. Steroids may be considered later in selected bacterial ulcers responding to antibiotics—strictly under specialist supervision.

9. What if initial antibiotics fail?
   Doctors switch based on culture/susceptibilities, add fortified or rescue agents (like piperacillin-tazobactam or colistin), consider adjuvant PACK-CXL, and escalate to surgery if needed. PubMedPMC

10. Why am I taking doxycycline if it doesn’t kill Pseudomonas well?
    It reduces corneal collagen breakdown (anti-MMP effect) and helps prevent melting in severe ulcers. Lippincott Journals

11. Will an amniotic membrane “treat” the infection?
    No—it helps the surface heal and reduces inflammation after antimicrobials start working; it can protect a thin cornea.

12. What about nerve growth factor (cenegermin)?
    It treats neurotrophic keratitis (poor corneal sensation) that prevents healing; some post-infectious cases benefit. ScienceDirect

13. Could I need a corneal transplant?
    If the ulcer perforates or won’t clear despite maximal therapy, a therapeutic transplant (TPK) can remove infection and save the eye. PMC

14. When can I wear contact lenses again?
    Only after your specialist confirms complete healing and safety; many patients switch to daily disposables and stricter hygiene to reduce future risk. PMC

15. Top three prevention rules for the future?
    No sleeping in lenses, keep lenses away from all water, and wash/dry hands before touching lenses—every time. American Academy of OphthalmologyCDC+1

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

Last Updated: August 23, 2025.