Ocular Candidiasis

Pathophysiology
Types
Causes and risk factors
Symptoms and signs
Diagnostic tests
Non-Pharmacological Treatments
Drug Treatments
Dietary “Molecular” Supplements
Immunity/Regenerative/Biologic
Surgeries / Procedures
Practical Prevention Tips
When to See a Doctor—Right Away
What to Eat—and What to Avoid—During Recovery
Frequently Asked Questions

Ocular candidiasis means a yeast infection in or on the eye. The yeast is most often Candida. The common species is Candida albicans, but other species like C. glabrata and C. parapsilosis can also cause disease. Candida normally lives on our skin, in our mouth, and in the gut without causing harm. It becomes a problem when it overgrows or enters the bloodstream. When Candida reaches the eye, it can infect the retina and choroid (the back of the eye), the vitreous gel (the clear jelly inside the eye), or the front of the eye like the cornea and conjunctiva.

Ocular candidiasis means a yeast (Candida) infection in the eye. Candida normally lives on our skin and in the gut without causing harm. But it can sometimes get into the bloodstream (called candidemia) or the eye surface and infect eye tissues. When the infection is inside the eye (retina, vitreous), doctors call it Candida endophthalmitis. When it is on the clear front window of the eye (the cornea), it’s Candida keratitis. Both need urgent eye specialist care, because delays can lead to scarring or vision loss. The good news: with early, right-dose antifungals and, when needed, precise eye procedures, many people recover useful vision. The LancetAAO+1

Doctors often split ocular candidiasis into two big groups:

Endogenous infection: Candida travels in the bloodstream and seeds the eye from the inside. This often happens in very sick patients, people with intravenous lines, or people with weak immune systems. It commonly starts as Candida chorioretinitis (spots in the retina and choroid). It can spread into the vitreous and cause endophthalmitis (a deep infection filling the eye).
Exogenous infection: Candida enters the eye from the outside after trauma, surgery, or on the surface of the eye (for example, corneal infection called keratitis).

The eye is delicate. Infection can scar the retina or cornea. That scarring can reduce sight or even cause blindness if not treated in time. Many people with ocular candidiasis also have Candida in the blood (candidemia), which is a serious systemic infection. So, this diagnosis is not only about the eye. It can be a warning sign of infection elsewhere in the body.

Pathophysiology

Candida can enter the bloodstream through an IV line, a surgical wound, the gut, or the urinary tract. Once in the blood, the yeast can stick to the tiny blood vessels in the choroid (the layer behind the retina). It forms tiny white inflammatory spots. These can break through into the retina and then into the vitreous. In the vitreous, the yeast and immune cells can create “snowballs” and hazy strings that block vision. If Candida lands on the cornea after a scratch or contact lens injury, it can dig into the corneal layers and make a painful ulcer. Candida also forms biofilm on plastic like contact lenses or intraocular lenses, which makes it harder for the immune system and drugs to clear it.

Types

Candida chorioretinitis (without vitritis)
Yeast causes creamy-white spots in the retina and choroid. Vision can be normal at first if the spots are away from the center.
Endogenous Candida endophthalmitis (with vitritis)
Infection spreads into the vitreous gel. People notice floaters, foggy vision, and sometimes pain. This is more severe and often needs injection or surgery in addition to pills.
Exogenous Candida endophthalmitis (post-surgical)
Candida enters the eye during or after eye surgery (for example, cataract surgery). It can grow on intraocular lenses. Symptoms may be delayed and vague at first.
Post-traumatic Candida endophthalmitis
Candida gets into the eye after penetrating injury (for example, a stick or metal shard). This is an emergency and needs urgent care.
Candida keratitis (corneal infection)
Yeast infects the cornea. It causes pain, light sensitivity, tearing, and a white spot on the clear front window of the eye. It is more common with contact lenses or topical steroid overuse.
Candida conjunctivitis (surface infection)
The conjunctiva gets inflamed with redness and discharge. It is less common and usually mild but can occur in newborns or very immunocompromised people.
Candida canaliculitis / dacryocystitis (tear drainage infection)
Yeast grows in the tear ducts or tear sac. People have tearing, tenderness, and mucus. A small stone or plug may hold the yeast.
Candida scleritis
The white outer coat of the eye (sclera) is infected. It is painful and often follows surgery or trauma.
Candida orbital cellulitis
Yeast spreads to the eye socket (orbit). There is swelling, pain, fever, and sometimes double vision. This is serious and needs hospital care.
Neonatal ocular candidiasis
Premature or very sick newborns with candidemia can develop retinal lesions. Screening is important because babies cannot tell you their symptoms.

Causes and risk factors

Candidemia (yeast in the blood)
This is the main driver of endogenous ocular infection. Any bloodstream Candida can seed the eye.
Central venous catheters
Plastic lines in big veins let Candida stick and grow. Pieces can break off into the blood and reach the eye.
Recent major surgery, especially abdominal
Surgery can let Candida escape from the gut into the blood. Antibiotics and lines add risk.
Total parenteral nutrition (TPN)
Sugary IV nutrition feeds Candida on catheter surfaces and increases candidemia.
Broad-spectrum antibiotics
These kill good bacteria that usually keep Candida in check, so yeast overgrows and can invade.
Immunosuppression (steroids, chemotherapy, biologics)
A weak immune system cannot control yeast growth or stop spread to the eye.
Neutropenia or hematologic malignancy
Low neutrophils or blood cancers reduce front-line immune defense, so Candida can enter blood and tissues.
Uncontrolled diabetes mellitus
High sugar helps Candida grow and weakens immune cells, raising risk of eye infection.
Intravenous drug use
Unclean injections can push Candida or contaminated material into the bloodstream.
Organ transplant
Anti-rejection drugs lower immunity, and catheters and antibiotics increase risk.
Prematurity and NICU stay
Newborns, especially preterm, have immature immunity and many lines, so they are prone to candidemia and eye seeding.
Indwelling urinary or vascular devices
Long-term tubes or ports can grow biofilms of Candida that release yeast into blood.
HIV infection with low CD4
Advanced HIV weakens immune control of fungi, increasing risk of ocular involvement.
Ocular trauma
A scratch or penetrating injury can carry Candida into the cornea or the inside of the eye.
Recent eye surgery (e.g., cataract)
Candida can enter during surgery or grow on implanted intraocular lenses.
Contact lens wear (especially poor hygiene)
Lenses and cases can carry biofilm. A small corneal abrasion allows Candida to invade.
Chronic topical steroid eye drops
Steroids dampen local immunity on the eye surface, letting Candida overgrow.
Severe dry eye or ocular surface disease
A damaged surface loses its barrier function, so yeast can stick and invade.
Oral or esophageal thrush with frequent self-inoculation
Touching the eyes after touching thrush plaques can move yeast to the eye surface.
Gastrointestinal leaks or inflammation (e.g., perforation, pancreatitis)
These allow Candida to escape the gut into the bloodstream and eventually to the eye.

Symptoms and signs

Blurred or dim vision
Inflammation or debris in the eye blocks light and makes sight hazy.
Floaters
Small dark spots or cobwebs drift across vision when yeast and immune cells collect in the vitreous gel.
Eye pain or ache
Infection irritates nerves in the cornea, sclera, or inside the eye.
Redness
Blood vessels open up with inflammation, making the eye look red.
Light sensitivity (photophobia)
An inflamed cornea or iris makes light feel harsh and uncomfortable.
Tearing and watery eye
The eye makes more tears to try to flush irritants.
Decreased central vision
If lesions are near the macula (the sharp vision center), reading and face recognition get worse.
Hazy or foggy view
Vitritis (haze in the jelly) or corneal swelling makes the world look smoky.
Visual field gaps or dark patches
Retinal spots create blind areas in side vision or central vision.
Mucus or discharge
Surface infection (conjunctivitis or keratitis) can produce stringy or thick discharge.
Foreign-body sensation
Corneal infection feels like sand in the eye.
Headache or brow pain
Deep eye inflammation can cause referred pain to the head.
Swollen eyelids
The tissues around the eye get puffy with inflammation or orbital spread.
Fever or chills
Many patients have Candida in the blood, so whole-body symptoms can occur.
Poor vision that changes day to day
Moving debris and variable inflammation can make vision fluctuate.

Diagnostic tests

A) Physical examination

Visual acuity test (reading letters)
This measures how clearly you see. It tells the doctor how much vision is affected and helps track improvement or worsening over time.
Pupil examination (checking light reflex and RAPD)
The doctor shines a light to see how the pupils react. Poor reaction or an afferent defect can suggest retinal or optic nerve trouble from infection.
Slit-lamp examination (microscope at the eye)
A bright beam and microscope let the doctor inspect the cornea, anterior chamber, and lens. It can show keratitis, inflammation cells, and early vitreous haze.
Dilated fundus examination (indirect ophthalmoscopy)
Eye drops widen the pupil so the doctor can see the retina and choroid. Creamy-white lesions, hemorrhages, or vitreous clumps suggest Candida involvement.

B) Manual / procedural bedside tests

Corneal scraping for smear and culture
A sterile blade or spatula gently scrapes the corneal ulcer edge. The sample is checked under the microscope and cultured to identify Candida and guide drug choice.
Aqueous tap (anterior chamber paracentesis)
A tiny needle draws a small fluid sample from the front of the eye. It is used for microscopy, PCR, and culture when deeper infection is suspected.
Vitreous tap or diagnostic pars plana vitrectomy
A small amount of vitreous gel is removed with a needle or during surgery. This gives a high-yield sample for culture, stains, and PCR and can also reduce organism load.
Culture of potential sources (e.g., catheter tip, contact lens, lens case, intraocular lens if exchanged)
Testing these items can show the same Candida species, linking the source to the eye infection and confirming biofilm involvement.

C) Laboratory and pathological tests

Blood cultures
Multiple blood samples are sent to the lab. A positive culture confirms candidemia, which strongly supports endogenous ocular infection.
Serum (1→3)-β-D-glucan
This blood test detects a fungal cell wall sugar. A high level suggests invasive fungal infection, including Candida.
Serum mannan antigen and anti-mannan antibodies
These tests look for Candida parts or the body’s response to Candida. They help support the diagnosis when blood cultures are negative.
Fungal culture of ocular fluids (aqueous or vitreous)
Growing Candida from eye fluid gives a definitive diagnosis and helps choose the right antifungal by doing susceptibility testing.
Direct microscopy and special stains (KOH, Calcofluor white, Gram, GMS, PAS)
These show yeast cells or pseudohyphae directly. They are fast and guide early treatment while cultures grow.
PCR for Candida DNA (e.g., ITS region) on ocular fluids
PCR can find small amounts of fungal DNA quickly. It improves detection when culture is slow or negative.

D) Electrodiagnostic tests

Electroretinography (ERG)
ERG measures retinal function using tiny electrodes. It helps when the view is too cloudy to see the retina but you need to know if the retina is still working.
Visual evoked potentials (VEP)
VEP measures the signal from eye to brain. It helps if vision is poor and you need to check whether the optic pathway still conducts signals.

E) Imaging tests

B-scan ocular ultrasonography
This is an ultrasound of the eye. It sees through opaque media (like dense vitritis or cataract) and can show membranes, abscess-like pockets, retinal detachment, or vitreous clumps.
Optical coherence tomography (OCT)
OCT is a cross-section scan of the retina. It shows retinal thickening, subretinal fluid, and chorioretinal lesions from Candida. It is painless and fast.
Fundus photography (including ultra-widefield)
Photos document lesion size and number. They are used to monitor response to treatment over time.
Fluorescein angiography (± indocyanine green angiography)
A dye is injected into a vein. Special photos show blood flow in the retina and choroid. This helps map active lesions, leakage, and ischemia.

Non-Pharmacological Treatments

These support, but do not replace, antifungal medicine or eye procedures.

Immediate ophthalmology referral (same day if possible).
Purpose: Get expert care before damage progresses.
Mechanism: Early intravitreal therapy or vitrectomy and targeted systemic azoles improve drug delivery to the eye and outcomes. AAO+1
Source control of candidemia (remove/replace the central line, drain obvious abscesses).
Purpose: Stop continuous seeding of the eye.
Mechanism: Removing the “feeder” source lowers fungal load and improves cure rates. Oxford Academic
Optimize blood sugar if you have diabetes.
Purpose: High glucose weakens immune cells and slows healing.
Mechanism: Better neutrophil function and less hospitable tissue environment for Candida. (Standard endocrine practice; widely recommended in invasive candidiasis care.) Oxford Academic
Review and, if safe, reduce immune-suppressing medicines.
Purpose: Let your own defenses participate.
Mechanism: Improved phagocyte function helps clear yeast; this is individualized and physician-guided. Oxford Academic
Strict hand and eye-drop hygiene.
Purpose: Prevent adding bacteria or more fungi to an already stressed eye.
Mechanism: Clean hands, no tip-touching of dropper, and no shared drops reduce inoculation risk. (AAO infection-control norms.) EyeWiki
Stop contact lens wear immediately.
Purpose: Reduce trauma and biofilm risk.
Mechanism: Removing mechanical irritation and contaminated lenses helps the cornea re-epithelialize. EyeWiki
Avoid tap water, swimming pools, and hot tubs during treatment.
Purpose: Keep microbes out.
Mechanism: Tap water and pools can carry organisms that worsen keratitis. EyeWiki
Wear sunglasses outdoors and in bright rooms.
Purpose: Reduce light sensitivity and inflammation.
Mechanism: Lower photophobia and reflex tearing, improving comfort so you can keep up with drops.
Use preservative-free lubricating tears (if your doctor agrees).
Purpose: Soothe the ocular surface and dilute inflammatory debris.
Mechanism: Improves tear film and epithelial healing; does not treat the fungus. EyeWiki
Pain control with safe systemic analgesics (per doctor advice).
Purpose: Keep you comfortable enough to adhere to intense regimens.
Mechanism: Central pain relief; avoid topical anesthetic abuse which harms cornea. NCBI
Protect the eye from accidental rubbing.
Purpose: Prevent corneal abrasion or perforation in ulcerated corneas.
Mechanism: Reduces mechanical trauma while the epithelium heals. NCBI
Adherence coaching and dose-timing tools (alarms, charts).
Purpose: Antifungals often require strict hourly or multi-daily dosing early on.
Mechanism: Better adherence → better outcomes in fungal keratitis/endophthalmitis. NCBI
Hospital infection-control practices (for inpatients).
Purpose: Limit line infections; prompt line review every day.
Mechanism: Fewer catheter days = lower candidemia risk. Oxford Academic
Peri-operative povidone-iodine prep for any eye procedure.
Purpose: Reduce surface microbes before surgery.
Mechanism: Iodine rapidly kills bacteria and fungi on the ocular surface; standard of care worldwide. AAO
Careful steroid stewardship.
Purpose: Avoid worsening fungal replication.
Mechanism: Steroids can flare fungal keratitis; they are generally avoided until the infection is controlled and then only if an ophthalmologist specifically advises. NCBI
Nutrition optimization (protein and micronutrients).
Purpose: Support immune function and tissue repair.
Mechanism: Adequate protein, vitamins A/D/C, zinc, and selenium help epithelial and immune function; this complements—not replaces—antifungals. (See supplement section for safe ranges.) NCBI
Smoking cessation.
Purpose: Improve ocular surface and microcirculation.
Mechanism: Better oxygenation and fewer toxic byproducts aid healing.
Low-vision supports if vision is temporarily reduced.
Purpose: Keep you safe while recovering.
Mechanism: High-contrast lighting, magnifiers, and electronic zoom reduce fall risk.
Close follow-up schedule.
Purpose: Catch progression early.
Mechanism: Fungal infections can deepen; re-exams determine if you need intravitreal injections or surgery. AAO
Treat the systemic infection fully (even if the eye feels better).
Purpose: Prevent relapse into the eye.
Mechanism: Guidelines recommend 4–6 weeks of systemic antifungal therapy for ocular involvement. The Lancet

Drug Treatments

Exact choices depend on species (e.g., C. albicans, C. glabrata), susceptibility results, site (cornea vs inside eye), and your kidney/liver status. These are not self-care instructions—they outline what specialists use.

Fluconazole (triazole; oral/IV).
Dose: Often 800 mg loading, then 400–800 mg daily; duration 4–6 weeks for endophthalmitis/chorioretinitis when organism is susceptible.
Purpose: First-line systemic therapy for many Candida with good ocular/vitreous penetration.
Mechanism: Inhibits ergosterol synthesis (fungistatic).
Side effects: Liver enzyme elevation, GI upset, drug interactions (CYP). Oxford Academic
Voriconazole (triazole; IV/PO; also intravitreal—see #7).
Systemic dose: 6 mg/kg IV q12h × 2 doses, then 3–4 mg/kg IV q12h or 200 mg PO q12h (levels & liver tests often monitored).
Purpose: Alternative or step-down therapy with excellent ocular penetration; useful for non-albicans species.
Mechanism: Ergosterol pathway blockade.
Side effects: Visual disturbances, photosensitivity, liver toxicity, drug interactions. JVs Medic’s CornerPMC
Amphotericin B deoxycholate (polyene; IV).
Dose: ~0.7–1 mg/kg/day when used; lipid formulations below.
Purpose: Broad activity; used when azole resistance/intolerance.
Mechanism: Binds ergosterol and forms pores (fungicidal).
Side effects: Kidney toxicity, electrolyte loss (K/Mg), infusion reactions. (Limited vitreous penetration systemically; see intravitreal below.) Oxford Academic
Liposomal Amphotericin B (polyene; IV).
Dose: 3–5 mg/kg/day.
Purpose: Similar spectrum with improved kidney safety profile.
Mechanism: Same as above, liposomal delivery.
Side effects: Infusion reactions, less nephrotoxicity than deoxycholate. Oxford Academic
Flucytosine (antimetabolite; oral) – usually in combination with amphotericin.
Dose: Commonly 25 mg/kg every 6 h; levels and blood counts monitored.
Purpose: Synergy against Candida endophthalmitis; excellent vitreous penetration.
Mechanism: Converts to 5-FU inside fungus → DNA/RNA synthesis block.
Side effects: Bone-marrow suppression, liver enzyme elevation, GI effects. PMC
Topical Amphotericin B 0.15% (compounded eye drops) for Candida keratitis.
Dose: Often hourly for 48 h then tapered over weeks per response.
Purpose: Direct corneal antifungal therapy.
Mechanism: Polyene—membrane pores.
Side effects: Surface toxicity/epithelial defects if overused; dosing individualized. EyeWikiAAONCBI
Intravitreal Amphotericin B (injected into the vitreous).
Dose: 5–10 µg/0.1 mL; can be repeated based on exam.
Purpose: Delivers fungicidal drug directly where systemic medicines penetrate poorly.
Mechanism: High intraocular concentration kills yeast within the vitreous.
Side effects: Retinal toxicity if overdosed; requires expert technique. AAO+1PMC
Intravitreal Voriconazole.
Dose: 100 µg/0.1 mL, repeat guided by retina exam.
Purpose: Alternative intravitreal agent with excellent Candida activity.
Mechanism: Local ergosterol synthesis block.
Side effects: Rare retinal toxicity at standard dosing; requires OR/office injection. AAOAAO Journal
Topical Voriconazole 1% (compounded) for keratitis (often second-line or adjunct).
Dose: Hourly loading then taper over weeks.
Purpose: Useful when amphotericin is not tolerated/ineffective.
Mechanism: Local azole effect on cornea.
Side effects: Surface irritation, photophobia. NCBI
Topical Natamycin 5% (keratitis tool—best for filamentous fungi; may be adjunct in mixed cases; amphotericin is preferred for Candida).
Dose: Hourly then taper 4–6 weeks.
Purpose: Broad topical antifungal for corneal disease.
Mechanism: Polyene binding to ergosterol.
Side effects: Surface irritation; blurred vision from suspension. AAODrug Information Group

Why not echinocandins alone? IV echinocandins (caspofungin, micafungin, anidulafungin) are fantastic for bloodstream Candida but penetrate the vitreous poorly and are not recommended as sole therapy when the eye is involved. They may still be part of therapy for candidemia while an azole or intravitreal therapy covers the eye. PMC+1ScienceDirect

Dietary “Molecular” Supplements

Always clear supplements with your clinician; some interact with azoles or affect liver/kidney tests.

Vitamin D3 (about 1,000–2,000 IU daily unless your doctor advises a different dose).
Function: Supports innate immunity and macrophage function.
Mechanism: Modulates antimicrobial peptides and T-cell responses.
Vitamin A (as beta-carotene; avoid excess in pregnancy).
Dose: Near the RDA (700–900 mcg RAE/day) unless deficient.
Function: Corneal/ocular-surface integrity.
Mechanism: Epithelial differentiation and mucin support.
Vitamin C (500 mg daily).
Function: Antioxidant; collagen cross-linking for wound repair.
Mechanism: Scavenges free radicals; cofactor for collagen hydroxylation.
Zinc (10–20 mg elemental/day, short term).
Function: Innate immunity and epithelial repair.
Mechanism: Cofactor for many immune enzymes.
Selenium (100–200 mcg/day).
Function: Antioxidant enzyme cofactor; immune modulation.
Mechanism: Supports glutathione peroxidase.
Omega-3 (EPA/DHA) (~1 g/day).
Function: May reduce surface inflammation and support tear film.
Mechanism: Competes with pro-inflammatory eicosanoids.
Probiotics (e.g., Lactobacillus rhamnosus GG, 10–20 billion CFU/day).
Function: Gut-immune axis support during/after systemic antifungals.
Mechanism: Barrier and cytokine effects; avoid in severe immunosuppression unless approved.
β-Glucans (oat or yeast-derived) (250–500 mg/day).
Function: Immune training of macrophages/monocytes.
Mechanism: Dectin-1 pathway modulation; not a treatment for eye infection, but general immune support. PMC
Lutein + Zeaxanthin (10 mg + 2 mg/day).
Function: Macular antioxidant support during recovery.
Mechanism: Filters blue light; quenches oxidative stress.
N-Acetylcysteine (NAC) (600 mg once or twice daily).
Function: Antioxidant; supports glutathione.
Mechanism: Reduces oxidative stress that can accompany inflammation.

Immunity/Regenerative/Biologic

Not first-line antifungals; specialist-only, used case-by-case. Some are off-label for Candida eye disease.

Filgrastim (G-CSF; injection).
Dose: Often 5 mcg/kg/day short-term until neutrophils recover (individualized).
Function: Shortens neutropenia in patients with low white cells, reducing risk of ongoing seeding from candidemia.
Mechanism: Stimulates neutrophil production and function. (Adjunct in invasive fungal risk—not a direct antifungal.) PMC
Sargramostim (GM-CSF).
Dose: Common regimens 250 mcg/m²/day (varies).
Function/Mechanism: Broad myeloid stimulation; considered in refractory invasive fungal disease with phagocyte defects. PMC
Interferon-γ1b.
Dose: Typical 50 mcg/m² SC three times weekly in chronic granulomatous disease; not routine for candidiasis but occasionally used in complex immunodeficiencies.
Function: Enhances macrophage killing.
Mechanism: Up-regulates oxidative burst. (Specialist, off-label decision.)
Intravenous Immunoglobulin (IVIG).
Dose: Varied (e.g., 0.4 g/kg/day × 3–5 days) in hypogammaglobulinemia; not standard for Candida eye disease.
Function: Passive immunity if antibody-deficient.
Mechanism: Broad opsonization.
Autologous Serum Tears (topical biologic).
Dose: 20–50% drops several times daily.
Function: Promotes corneal epithelial healing after severe keratitis.
Mechanism: Provides growth factors, vitamins, and albumin—regenerative surface support.
Cenegermin (recombinant human nerve growth factor; topical).
Dose: 1 drop six times daily for 8 weeks (labeled for neurotrophic keratopathy).
Function: Helps nerve and epithelial recovery when the cornea is neurotrophic after severe infection.
Mechanism: NGF-mediated regeneration. (Use only if your ophthalmologist diagnoses neurotrophic keratopathy.)

Important: None of the above “adjuncts” replace antifungals or intravitreal therapy when indicated.

Surgeries / Procedures

Intravitreal antifungal injections (amphotericin B 5–10 µg/0.1 mL or voriconazole 100 µg/0.1 mL).
Why: Delivers high drug levels directly into the vitreous where IV drugs may not reach.
How: Office/OR micro-injection after sterilizing the eye; may need repeats. AAO+1
Pars plana vitrectomy.
Why: Remove dense fungal clumps and inflammatory debris, improve view, and allow better drug penetration.
How: Tiny ports remove the infected vitreous gel; often paired with intravitreal antifungal at the end. AAO
Therapeutic penetrating keratoplasty (corneal transplant).
Why: For deep or non-healing Candida keratitis threatening perforation.
How: Diseased corneal button is removed and replaced; antifungal therapy continues to prevent recurrence. EyeWiki
Intrastromal antifungal injections (cornea).
Why: For stubborn, deep corneal ulcers not responding to drops.
How: Tiny amounts of amphotericin B or natamycin are injected into the corneal stroma around the ulcer to raise local drug levels. EyeWiki
Enucleation or evisceration (last resort).
Why: For painful, blind eyes with uncontrollable panophthalmitis to eliminate infection and pain.
How: Surgical removal of the eye (or contents) with later prosthesis fitting in selected cases. (Rare with timely care.)

Practical Prevention Tips

Keep excellent contact lens hygiene; never sleep in lenses unless specifically approved; never rinse with tap water. EyeWiki
At the hospital, review the need for central lines every day and remove early when possible. Oxford Academic
Control diabetes and other chronic illnesses. Oxford Academic
Avoid unnecessary steroids (especially topical steroid eye drops) without specialist advice. NCBI
Limit unnecessary broad-spectrum antibiotics that disrupt normal flora (doctor-guided). Oxford Academic
Make sure surgeons/nurses use povidone-iodine prep before eye procedures. AAO
If you have candidemia, follow your team’s plan for systemic therapy; many experts recommend a careful eye assessment to rule out ocular involvement (practice is evolving, but early detection is crucial when the eye is involved). The LancetOxford Academic
Do not share eye drops or makeup.
Seek help promptly for red eye that worsens on steroids or fails to improve. NCBI
Maintain general wellness: sleep, nutrition, and smoke-free living—your immune system matters.

When to See a Doctor—Right Away

Any sudden drop in vision, severe eye pain, or new floaters/light flashes.
Red, light-sensitive eye with a white spot on the cornea or discharge.
If you’ve been told you have Candida in your blood and you notice any eye symptom.
If you use contact lenses and develop a painful red eye not settling in 24 hours.
These can be emergencies; do not wait. Prompt antifungals and, if needed, intravitreal treatment or surgery are time-sensitive. AAO

What to Eat—and What to Avoid—During Recovery

Hydrate well; dehydration worsens surface discomfort.
Prioritize lean proteins (fish, eggs, legumes) to support tissue repair.
Eat colorful produce rich in vitamins A, C, and carotenoids (leafy greens, carrots, citrus).
Include omega-3 sources (fish, flax, walnuts) for anti-inflammatory support.
Ensure micronutrients: zinc (nuts, seeds), selenium (Brazil nuts, seafood).
Consider yogurt/fermented foods if your team is okay with probiotics.
Limit added sugars—high glucose impairs immunity and healing.
Avoid alcohol while on azoles; it stresses the liver.
Avoid grapefruit with certain azoles (e.g., voriconazole) because of interactions.
Avoid raw/undercooked foods if you’re neutropenic or on intense immunosuppression, to lower overall infection risk. JVs Medic’s Corner

Frequently Asked Questions

1) Is ocular candidiasis contagious from person to person?
No. It comes from your own yeast overgrowing, often via the bloodstream, or from contamination of the eye surface—not from normal casual contact.

2) Can it cause permanent vision loss?
Yes, if diagnosis or treatment is delayed, especially with endophthalmitis. Early antifungals and timely intravitreal therapy or vitrectomy greatly improve outcomes. AAO

3) How long will I need treatment?
For internal eye infection, guidelines commonly recommend 4–6 weeks of systemic antifungals, often with intravitreal injections and sometimes vitrectomy. Corneal disease may require weeks of topical therapy. Your doctor tailors the duration to your response and culture results. The Lancet

4) I’m already on an echinocandin for candidemia; is that enough for my eyes?
Usually no. Echinocandins penetrate the vitreous poorly, so azoles (fluconazole/voriconazole) and/or intravitreal therapy are used when the eye is involved. PMC

5) Are steroid eye drops helpful?
Typically avoided in active fungal keratitis/endophthalmitis because they can worsen infection. They may be introduced later in select cases by the ophthalmologist once the fungus is controlled. NCBI

6) What are the most proven eye injections?
Intravitreal amphotericin B (5–10 µg/0.1 mL) and intravitreal voriconazole (100 µg/0.1 mL) are standard options. Choice depends on species, response, and tolerance. AAO

7) Will I need surgery?
If there is dense vitritis, non-clearing lesions, or poor response, vitrectomy is considered to remove infectious debris and improve drug access. Corneal transplants are reserved for deep, non-healing ulcers. AAOEyeWiki

8) Which oral drug gets into the eye best?
Fluconazole and voriconazole have good ocular penetration and are mainstays when the Candida species is susceptible. Oxford AcademicPMC

9) Are there tests besides cultures?
Yes. β-D-glucan can support the diagnosis of invasive candidiasis; mannan/anti-mannan are researched but not FDA-cleared in the U.S. for this purpose. Ocular fluids may undergo microscopy, PCR, and culture. PMC+1

10) Do supplements cure eye Candida?
No. Supplements may support general immunity and healing, but only antifungal drugs and, when needed, procedures cure the infection. (Use supplements only with clinician approval.)

11) Can contact lens wearers get Candida keratitis?
Yes—especially with poor lens hygiene or contaminated solutions. Strict hygiene and no overnight wear reduce risk. EyeWiki

12) Is natamycin the first choice for Candida keratitis?
For Candida on the cornea, amphotericin B 0.15% is often preferred; natamycin is excellent for filamentous fungi and may be used as adjunct in mixed cases. Drug Information Group

13) How often are drops needed?
Early fungal keratitis often needs hourly drops for 48 hours, then a slow taper guided by the exam. Do not change your regimen without your ophthalmologist’s guidance. NCBI

14) Will I need liver or drug-level monitoring?
Often yes for systemic azoles (especially voriconazole) because of drug interactions and liver effects. JVs Medic’s Corner

15) After recovery, can it come back?
Relapse is uncommon if the bloodstream source is controlled and you complete the full treatment course. Some situations require longer therapy or suppressive fluconazole to prevent recurrence, depending on your risks and organism. Oxford Academic

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.